Novel Hydroquinone Derivaties

Abstract

The present invention provides novel hydroquinone derivatives of formula (I), processes of preparation, as well as pharmaceutical compositions and methods of treating and / or preventing e.g. autoimmune, immunological, rheumatology, vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic and gastrointestinal disorders, neuroinflammatory and neurodegenerative diseases, neoplasms and cancer associated disorders, hormone related diseases and immunological disorders resulting from viral and bacterial infectious diseases and complications thereof. wherein R 1 is COOR 4, (CH 2 ) n COOR 4, SO 3 H, (CH 2 ) n SO 3 H or CONH-R 10; one of R 2 and R 3 is H and the other is R 5.

Description

FIELD OF THE INVENTION This invention relates generally to novel hydroquinone derivatives, their preparation and to methods of treating disorders by administration of such compounds to a warm-blooded animal in need thereof. 5 The present invention also relates to compounds that are useful in the prevention and / or treatment of autoimmune, immunological, rheumatology, vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic and gastro-intestinal disorders, neuroinflammatory and neurodegenerative diseases, neoplasms and cancer associated disorders, hormone related diseases and immunological disorders resulting from viral and bacterial infectious diseases, and complications thereof. 10 BACKGROUND OF THE INVENTION Some hydroquinone-based derivatives like for example, 2,5-dihydroxybenzenesulfonic acid derivatives and specifically calcium dobesilate, ethamsylate and persilate are known in the art as active agents for the treatment of male sexual dysfunction and other vascular disorders of endothelial origin, both alone and in combination with other agents. For example, US Patent No. 6,147,112 15 describes a method for the use of 2,5-dihydroxybenzenesulfonic acid derivatives, preferably calcium dobesilate, ethamsylate and persilate. Calcium dobesilate or hydroquinone calcium sulfonate, with the chemical name 2,5-dihydroxybenzenesulfonic acid calcium salt, is being sold as Dexium (Delalande) and Doxium (Carrion), and a process for its preparation is described in US Patent No. 3,509,207. There are many drugs that contain phenol or catechol groups which suffer from premature metabolism 20 at the hydroxy group during absorption after oral administration. Previous efforts to protect the hydroxy groups have been generally unsuccessful as the protecting groups employed are either too labile (O=COR or O=CR) or too stable (CH3). It is thus an object of the present invention to provide novel derivatives of hydroquinones, their pharmaceutically acceptable salts and formulations. These novel hydroquinones derivatives have particularly potent anti-fibrotic, anti-inflammatory and anti-25 angiogenic properties. International publication WO2018160618A1 discloses certain substituted hydroquinones, 1,4-quinones, catechols, 1,2-quinones, anthraquinones, and anthrahydroquinones for use as redox mediators in emerging technologies, such as in mediated fuel cells or organic-mediator flow batteries. Richter et al, in Synthesis, 1976, 1976(3), 192-194 disclose Bis-N-arylcarbamates and 2, 5 - 30 Dihydroxy-3,6-bis[N-arylcarboxamido]-1,4-benzoquinones and their preparation from 2,5-Dihydroxy-1,4-benzoquinone and Aryl Isocyanates. Japanese publication JP 51026839A discloses Benzanilides I (R = H, OH) as possessing antitubercular, analgesic, anti-inflammatory, and uric acid-excreting activities: Benzanilides I US granted patent US 3,973,038 also discloses benzoylaniline compounds having general formula: wherein (Ri = OH, acyloxy; R2 = H, OH, lower alkyl, halo, acyloxy; R3 = Cl, Br, lower alkyl; R4 = OH, NH2, lower alkoxy, acyloxy; R5 = H, halo, CO2H, lower alkyl, acyloxy) having in vivo enzyme inhibition properties, in particular, histamine deacetylase and xanthine oxidase None of the prior art documents however disclose the novel class of hydroquinone derivative compounds of the present invention, which are particularly useful for the prevention and / or treatment of a variety of diseases including autoimmune, immunological, rheumatology, vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic and gastro-intestinal disorders, neuroinflammatory and neurodegenerative diseases, neoplasms and cancer associated disorders, hormone related diseases and immunological disorders resulting from viral and bacterial infectious diseases, and complications thereof. The invention also relates to the treatment, prevention, and reduction of metabolic disorders, such as diabetes and obesity. As the levels of blood glucose rise postprandially, insulin is secreted and stimulates cells of the peripheral tissues (skeletal muscles and fat) to actively take up glucose from the blood as a source of energy. Eoss of glucose homeostasis as a result of faulty insulin secretion or action typically results in metabolic disorders such as diabetes, which may be co-triggered or further exacerbated by obesity. Because these conditions are often fatal, strategies to restore adequate glucose clearance from the bloodstream are required. Metabolic disorders, particularly glucose and lipid regulatory disorders, are becoming increasingly prevalent as the populations in industrialized nations age and sedentary lifestyles become more common. Such disorders are frequently interrelated and are often predictors or results of each other. For example, diabetes is caused by a combination of insulin resistance and defective secretion of insulin by pancreatic-P cells. Individuals with insulin resistance often have abdominal obesity, dyslipidemia, hypertension, glucose intolerance and a prothrombitic state (Metabolic syndrome). Correspondingly, obese individuals as a whole are at higher risk for acquiring insulin resistance. The breakdown of a metabolic pathway thus can trigger myriad disorders such as hyperlipidemia, obesity, diabetes, insulin resistance, glucose intolerance, hyperglycemia, metabolic syndrome and hypertension which may in turn trigger further metabolic dysfunction resulting in systemic issues and putting individuals at risk for additional complications and premature morbidity. Glucose and lipid levels are regulated in part by the liver which plays a role in synthesizing, storing, secreting, transforming, and breaking down glucose, proteins and lipids. Disease or traumatic injury can greatly reduce the liver's ability to carry out these normal activities. Thus, most of the clinical manifestations of liver dysfunction stem from cell damage and impairment of the normal liver capacities. Liver dysfunction can result from genetic conditions, inflammatory disorders, toxins such as drugs and alcohol, immunological disorders, vascular disorders or metabolic conditions. Regardless of the cause, liver damage can have a systemic effect on the function of metabolic processes and the regulation of blood glucose and serum lipid levels, exacerbating chronic disease states and leading to increased risks for further disease and morbidity. Both elevated and reduced levels of blood glucose trigger hormonal responses designed to restore glucose homeostasis. Low blood glucose triggers the release of glucagon from pancreatic a-cells. High blood glucose triggers the release of insulin from pancreatic b-cells. ACTH and growth hormones released from the pituitary, act to increase blood glucose by inhibiting uptake by extrahepatic tissues. Glucocorticoids also act to increase blood glucose levels by inhibiting glucose uptake. Cortisol, the major glucocorticoid released from the adrenal cortex, is secreted in response to the increase in circulating ACTH. The adrenal medullary hormone, epinephrine, stimulates production of glucose by activating glycogenolysis in response to stressful stimuli, etabolic disorders that effect glucose and lipid metabolism such as hyperlipidemia, obesity, diabetes, insulin resistance, hyperglycemia, glucose intolerance, metabolic syndrome and hypertension have long term health consequences leading to chronic conditions including cardiovascular disease and premature morbidity. Such metabolic and cardiovascular disorders may be interrelated, aggravating, or triggering each other and generating feedback mechanisms that are difficult to interrupt. Current pharmaceutical treatments for metabolic and cardiovascular disorders include combinations of lipid-lowering drugs, hypoglycemic drugs, anti-hypertensive agents, diet, and exercise. However, complicated therapeutic regimens can cause polypharmacy problems of increased side effects, drug-drug interactions, failure of adherence, and increased medication errors. There is therefore a compelling, unmet need in the art to identify new compounds, formulations, and methods to safely and effectively treat metabolic and cardiovascular disorders and conditions associated with metabolic disorders. Examples of metabolic conditions include, but are not limited to, pain, wound healing, fever, neuroinflammatory and neurodegenerative conditions, inflammation, heat production, homeothermy, breakdown of triglycerides, glycolysis, Krebs cycle, fermentation, photosynthesis, metabolic rate, biotic and abiotic stress, secretions, oxidative stress, stress, neoplastic growth, skin condition, cardiovascular conditions, neuroinflammatory and neurodegenerative conditions, mental and behavioural disorders. Such processes or conditions can occur in a cell, group of cells, or an entire organism. Recent progress in molecular medicine has led to certain improvements in diagnostics and treatment of neoplastic diseases. Despite this partial success, these pathologies remain a considerable challenge. For certain types of cancers, the current therapy in some cases fails for several reasons. On the one hand, it is inherent resistance of tumour cells, their ability of constant mutation and therapy evasion, on the other hand it is also the heterogeneity of the tumour environment. It was shown that tumours of the same type highly differ for individual subjects from the viewpoint of their genomic profde which indicates the necessity of the so-called "personal" therapy. Even a bigger problem is the heterogeneity of mutations in the same tumour, as it has been recently shown for renal tumours, and this situation can be expected for other types of tumours as well. For this reason, it is necessary to search for new approaches and for an invariable intervention point(s) common for all or most malignant cells in the tumour and which preferably affects essential functions in cancer cells. It seems that such an intervention point could be at the metabolic level say for example mitochondria, re., organelles which are fundamental for the generation of energy necessary for all physiological as well as pathophysiological processes in cells. Although tumour cells use, from a major part, the so-called aerobic glycolysis for energy generation, mitochondrial respiration (re., consumption of oxygen linked to ATP formation) is inherent to most (if not all) types of tumours. Hence there is an unmet and compelling need in the art to identify new compounds, formulations, and methods to treat such neoplastic disorders safely and effectively. SUMMARY OF THE INVENTION The present invention provides novel hydroquinone derivatives, novel process of preparation, and novel key intermediates. The present invention also relates to pharmaceutical compositions comprising therapeutically effective amount of such hydroquinone derivatives and pharmaceutically acceptable excipient. The invention further provides a method of treating and / or preventing angiogenic (vascular), inflammatory and / or fibrotic pathobiology, as they have anti-fibrotic, anti-inflammatory and anti-angiogenic effects. The present invention thus finally provides a method of treating and / or preventing a disease or disorder including immunological / rheumatology / vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic & gastro-intestinal disorders, neoplasms and cancer associated disorders comprising administering a subject in a need a therapeutically effective dose of the compounds 4 and / or pharmaceutical compositions of the present invention as described above. In particular, the present invention provides a method of treating and / or preventing a disease or disorder autoimmune, immunological, rheumatology, vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic and gastro-intestinal disorders, neuroinflammatory and neurodegenerative diseases, neoplasms and cancer associated disorders, hormone related diseases and immunological disorders resulting from viral and bacterial infectious diseases and complications thereof. BRIEF DESCRIPTION OF THE FIGURES FIGURE 1:   (A) Confocal immunofluorescence images of vascular permeability assessed by Evans blue dye leakage in retinal whole mounts in a representative mouse from each experimental group. Arrows indicate extravasation location. Scale bars, 30 pm. (B) Quantification of vascular leakage by assessing the number of extravasations per field (0.44 mm2). The effect of Ia-007a eye drops was significant by reducing the vascular leakage to the same level that occur in the non-diabetic control group. *p < 0.01 in comparison with the other groups. FIGURE 2:   (A) Schmidt score is the evaluation of the efficacy of the compounds based on the four histopathology assessment criteria which describe pancreatic injury based on the foilwing scores (number in parenthesis) for the four parameters, (a) Edema Interstitial oedema with scores (0) None (1) Interlobular (2) Lobule involved (3) Isolated island like acinar cells, (b) Inflammatory infiltration = leukocytes infiltration with scores (0) None, (1) < 20%, (2) 20%-50%, (3) > 50%. (c) Parenchymal necrosis = Acinar cell necrosis with scores (0) None, (1) < 5%, (2) 5%-20%, (3) > 20%. (d) Haemorrhage with scores (0) None, (1) 1-2 points, (2) 3-5 points, (3) > 5 points. Schmidt highest score = 10 is caerulein induced + vehicle treatment and lowest score = 0 is non-induced animals. Schmidt score is the total of a+b+c+d scores and **** means statistically significant difference with caerulein induced group as shown in Figure 2. All products show improved Schmidts score compared to caerulein control animals. FIGURES 3A-D: Figures 3A-B represent a disease list with main cytokines involved in selected diseases (Akdis M. et al, J Allergy Clin Immunol 2016;138:984-1010) and Figure 3C represents part of the search results with cytokines and genes ranked by scores and likely to be involved in the selected disease given as an example “diabetic retinopathy” after search in https: / / www.targetvalidation.org / . In Figure 3D, search was performed using VEGFA as the cytokine to find a list of diseases where VEGFA is mentioned. Only part of the diseases where VEGFA is involved are represented in Figure 3D. ref: Open Targets Platform: new developments and updates two years on. Denise Carvalho et al (Nucleic Acids Research, Volume 47, Issue DI, 08 January 2019,   D1056-D1065, https: / / doi.org / 10.1093 / nar / gky 1133). FIGURES 4 (A-D): represent a table listing the conditions and yields of compounds of type la-Id as described in Examples 1.1 to 1.4. Overall yield calculated from starting material 2,5-dihydroxyterephthalic acid. FIGURE 5 (A-C): represent a table listing the conditions and yields of compounds of type Ila-IIc as described in Examples 1.5 to 1.7. FIGURE 6: represent a table listing the conditions and yields of compounds of type Illa and Illb as described in Examples 1.8 and 1.9. FIGURE 7: represent a table listing the conditions and yields of compounds of type IIIc as described in Example 1.10. FIGURE 8: is a table listing deprotection procedures as described in Example 1.12 relative to compounds type V. FIGURE 9: shows non-fasting blood glucose levels (average ± stdev of all animals) in the STZ-induced diabetes model in all animals of each group sampled after at day 0 before dosing, and after 7 and 14 days daily dosing by intravenous or per os routes. FIGURE 10: shows accelerating wound healing in the STZ-induced diabetes model in 3 animals per group sampled after 7 days dosing daily by intravenous or per os routes. FIGURE 11: Figure 11A shows representative images of lung fibrosis at day 21 oftreatment; (Al) noninduced (healthy); A2, Bleomycine induced with vehicle treatment; A3, Bleomycine induced with pirfenidone 100 mg / kg treatment; A4, Bleomycine induced with IVc-059a treatment. Figure 1 IB shows the Ashcroft score of healthy, bleomycine induced non-treated versus pirfenidone versus IVc-059a. DETAIEED DESCRIPTION OF THE INVENTION Disclosed herein are novel compounds useful for the treatment of subjects suffering from a disease, disorder, or dysfunction. Examples of such diseases, disorders, or dysfunctions include without limitation autoimmune, metabolic, inflammatory, degenerative and neoplastic disorders, in particular inflammatory pathologies, angiogenic diseases and / or fibrotic disorders such as diabetic retinopathy, diabetic nephropathy, ankylosing spondylitis, chronic pancreatitis, liver fibrosis, kidney fibrosis, as well as metabolic diseases caused by pancreas dysfunctions. Hereinafter, unless otherwise specified, the collection of diseases, disorders, or dysfunctions that may be treated utilizing the novel compounds disclosed herein are collectively termed "medical conditions." The term "subject," as used herein, comprises any and all organisms and includes the term "patient." A subject to be treated according to the methods described herein may be one who has been diagnosed by a medical practitioner as suffering from a medical condition. Diagnosis may be performed by any suitable means. One skilled in the art will understand that a subject to be treated according to the present disclosure may have been subjected to standard tests to diagnose the medical conditions. As known to 6 the ordinarily skilled artisan, the clinical features of medical conditions of the type disclosed herein vary according to the pathomechanisms. Herein "treating" refers to utilizing the disclosed compounds for therapeutic purposes. Therapeutic treatment may be administered, for example, to a subject suffering from the medical condition in order to improve or stabilize the subject's condition. Thus, in the claims and embodiments described herein, treating refers to a subject undergoing for therapeutic purposes, the methodologies disclosed herein. Prodrugs as used herein refers to any broad pro-drug strategy. For example, prodrug strategies were formally recognized by Adrian Albert in 1958 (Albert, A. Chemical aspects of selective toxicity. Nature, 1958,182,421-422) but started in the early part of the previous century, as exemplified by methenamine, phenacetin and prontosil. Prodrugs generally are molecules with little or no pharmacological activity but have a built-in structural lability, whether by chance or by design, that permits bioconversion in vivo into the active drug. The conversion can occur through a chemical or enzymatic process or a combination of the two. Active molecules are often associated with undesirable physicochemical properties that create considerable challenges for their delivery to the appropriate biological target. Prodrugs can improve metabolic instability which is typically attributed to hepatic metabolism. Similarly, unwanted intestinal metabolism of drugs can be overcomed by selective prodrug strategies. This instability can greatly reduce the total amount of a drug that reaches the systemic circulation and its target. Prodrugs can be used to protect active drugs from this first-pass effect by masking a metabolically labile but pharmacologically essential functional group, such as a phenol, to avoid rapid metabolism. Prodrugs obtained via structural modifications of the drug are designed to influence the inherent physicochemical properties of a molecule to enable its delivery. These developments are not always integrated into the design of new molecules at the discovery phase. Often the analogue optimization, is the preferred path forward. Implementing an early prodrug strategy may result in more rapid clinical development and, ultimately, commercialization of a drug product. Many prodrug strategies can be applied to influence the lipophilicity of a parent drug. Lipophilicity of drugs has been improved by masking its polar and ionized functionalities by short-chain hydrocarbon promoieties. Hydrophilic hydroxyl, carboxyl, phosphate or amine and other negatively or positively charged groups have been successfully converted to more lipophilic alkyl or aryl esters or N-acyl derivatives, which are rapidly hydrolysed back to the parent drugs in the body by ubiquitous esterases or peptidases. The present invention thus provides a compound of Formula (I): ORa Formula (I) wherein: Ra, Rb = H, Cwacyl, arylCi-4alkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C?alkylNHCO, phosphono, phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or Ci-Cgalkoxy carbonyloxy-1 -ethyl; Ri = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, or CONH-Ri0; R2 and R3 are H or R5, with the proviso that when one of R2 and R3 is R5, the other is H and when one of R2 and R3 is H, the other is R5; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; Rs = Rg, R7 or RX; Rg = CONH-R9, CONHCOR9, CONH(CH2)n-R9, or CONHCH(COOR4)(CH2)kR9, heteroaryl-Rg wherein k = 0-4; R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, azoles [5-membered N-containing heterocycles], or fluorine; Rx = (CH2)mX(CH2)pR9; X = O, S, SO2, NH, NAc, or N(CH2)qR9; R9 = aryl or heteroaryl substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles], fluorine, C=O, NHCO-R10; Rio = aryl, or heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles], fluorine; wherein the aryl of R9 and Rio is an aromatic group containing from 6 to 14 carbon atoms, selected among phenyl, naphthyl, biphenyl group; and the heteroaryl R9 and Rio is an aromatic group containing 1 to 14 carbon atoms and one or more nitrogen; and n, m, p and q are independently 1-4. The present invention further provides a compound of formula (I): ORa (I) wherein: Ra, Rb = H, Cwacyl, arylCi-4alkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C?alkylNHCO, phosphono, phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or Ci-Cgalkoxy carbonyloxy-1 -ethyl; Ri = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, or CONH-Ri0; R2 and R3 are H or R5, with the proviso that when one of R2 and R3 is R5, the other is H and when one of R2 and R3 is H, the other is R5; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; Rs = Rg, or R7, Rg = CONH-R9, CONHCOR9, CONH(CH2)n-R9, or CONHCH(COOR4)(CH2)kR9; wherein k = 0-4; R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, azoles [5-membered N-containing heterocycles], or fluorine; R9 = aryl, heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles], fluorine, C=O, or NHCO-R10; Rio = aryl, heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles], or fluorine; wherein the aryl of R9 and Rio is an aromatic group containing from 6 to 14 carbon atoms, selected among phenyl, naphthyl, biphenyl; and the heteroaryl of R9 and Rio is an aromatic group containing 1 to 14 carbon atoms and one or more nitrogen; and n, is independently 1-4. The present invention also provides a compound of formula (I): wherein: Ra, Rb = H, Cwacyl, arylCi-4alkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C?alkylNHCO, phosphono, phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or Ci-Cgalkoxy carbonyloxy-1 -ethyl; Ri = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, or CONH-Ri0; R2 and R3 are H or R5, with the proviso that when one of R2 and R3 is R5, the other is H and when one of R2 and R3 is H, the other is R5; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; Rs = Rs Rs = (CH2)mX(CH2)pR9; X = O, S, SO2, NH, NAc, or N(CH2)qR9; R9 = aryl, heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles], fluorine, C=O, or NHCO-R10; Rio = aryl, heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles], fluorine; wherein the aryl of R9 an Rio is an aromatic group containing from 6 to 14 carbon atoms, selected among phenyl, naphthyl, biphenyl group; wherein the heteroaryl R9 an Rw is an aromatic group containing 1 to 14 carbon atoms and one or more nitrogen; and n, m, p and q are independently 1-4. The expression “alkyl” refers to a saturated, straight-chain or branched hydrocarbon group that contains from 1 to 20 carbon atoms, preferably from 1 to 12 carbon atoms, especially from 1 to 6 (e.g.. 1, 2, 3 or 4) carbon atoms, for example a methyl, ethyl, propyl, iso-propyl, n-butyl, iso-butyl, sec-butyl or tertbutyl. Furthermore, the term alkyl refers to groups in which one or more hydrogen atoms have been replaced by a halogen atom (preferably F or Cl) such as, for example, a 2,2,2-trichloroethyl or a trifluoromethyl group. The expression "acyl" refers to the groups (alkyl)-C(O)-, (aryl)-C(O)-, (heteroaryl)-C(O)-, (heteroalkyl)-C(O)-, and (heterocycloalkyl)-C(O)-, wherein the group is attached to the parent structure through the carbonyl functionality. In some embodiments, it is a C1-C4 acyl radical which refers to the total number of chain or ring atoms of the alkyl, aryl, heteroaryl or heterocycloalkyl portion of the acyloxy group plus the carbonyl carbon of acyl, fe. three other ring or chain atoms plus carbonyl. The expression “aryl” refers to an aromatic group that contains one or more rings containing from 6 to 14 ring carbon atoms, preferably from 6 to 10 (especially 6) ring carbon atoms. The expression "aralkyl" or "arylCi-4alkyl" refers to groups containing both aryl and also alkyl, alkenyl, alkynyl and / or cycloalkyl groups in accordance with the above definitions, but are not limited to benzyl, 2-phenylethyl, 3-phenylpropyl, and 2-naphth-2-ylethyl. An aralkyl group preferably contains one or two aromatic ring systems (1 or 2 rings) containing from 6 to 10 carbon atoms and one or two alkyl, alkenyl and / or alkynyl groups containing from 1 or 2 to 6 carbon atoms and / or a cycloalkyl group containing 5 or 6 ring carbon atoms. The expression “heteroaryl” refers to an aromatic group that contains one or more rings containing from 5 to 14 ring atoms, preferably from 5 to 10 (especially 5 or 6 or 9 or 10) ring atoms, and contains one or more (preferably 1, 2, 3 or 4) oxygen, nitrogen, phosphorus or sulfur ring atoms (preferably O, S or N). Examples are pyridyl (e.g.. 4-pyridyl), imidazolyl (e.g.. 2-imidazolyl), phenylpyrrolyl (e.g.. 3-phenylpyrrolyl), thiazolyl, isothiazolyl, 1,2,3-triazolyl, 1,2,4-triazolyl, oxadiazolyl, thiadiazolyl, indolyl, indazolyl, tetrazolyl, pyrazinyl, pyrimidinyl, pyridazinyl, oxazolyl, isoxazolyl, triazolyl, tetrazolyl, isoxazolyl, indazolyl, indolyl, benzimidazolyl, benzoxazolyl, benzisoxazolyl, benzthiazolyl, pyridazinyl, quinolinyl, isoquinolinyl, pyrrolyl, purinyl, carbazolyl, acridinyl, pyrimidyl, 2,3-bifuryl, pyrazolyl (e.g. 3-pyrazolyl) and isoquinolinyl groups. The expression "benzoheteroaryl" or "benzoheteroaromatic" refers to bicyclic rings comprising a phenyl ring fused to a monocyclic heteroaromatic ring. Examples of benzoheteroaryl include benzisoxazolyl, benzoxazolyl, benzisothiazolyl, benzothiazolyl, benzimidazolyl, benzofuryl, benzothienyl (including S-oxide and dioxide), quinolyl, isoquinolyl, indazolyl, indolyl, and the like. The term “azole” refers to a five membered heteroaryl group having a nitrogen ring atom and between 0 and 3 additional ring heteroatoms selected from N, O or S. Imidazole, oxazole, thiazole and tetrazole are representative azole groups. The expression “cycloalkyl” refers to a saturated or partially unsaturated (for example, a cycloalkenyl group) cyclic group that contains one or more rings (preferably 1 or 2), and contains from 3 to 14 ring carbon atoms, preferably from 3 to 10 (especially 3, 4, 5, 6 or 7) ring carbon atoms. Specific examples of cycloalkyl groups are a cyclopropyl, cyclobutyl, cyclopentyl, group. The expression “optionnally substituted” refers to groups in which at least one, or optionally two, three or more hydrogen atoms may have been replaced by fluorine, chlorine, bromine, iodine atoms, or by OH, =0, SH, =S, NH2, =N0H, N3 or NO2 groups. This expression refers furthermore to groups that may be substituted by at least one, two, three or more unsubstituted C1-C10 alkyl, C2-C10 alkenyl, C2-C10 alkynyl, heteroalkyl, C3-C18 cycloalkyl, C2-C17 heterocycloalkyl, C4-C20 alkylcycloalkyl, C2-C19 heteroalkylcycloalkyl, Cg-Ci8 aryl, C1-C17 heteroaryl, C7-C20 aralkyl or C2-C19 heteroaralkyl groups. This expression refers furthermore especially to groups that may be substituted by one, two, three or more unsubstituted Ci-Cg alkyl, C2-Cg alkenyl, C2-Cg alkynyl, Ci-Cg heteroalkyl, C3-C10 cycloalkyl, C2-C9 heterocycloalkyl, C7-C12 alkylcycloalkyl, C2-C11 heteroalkylcycloalkyl, Cg-Cio aryl, Ci-C9 heteroaryl, C7-C12 aralkyl, or C2-C11 heteroaralkyl groups. According to a preferred embodiment, all alkyl, alkenyl, alkynyl, heteroalkyl, aryl, heteroaryl, cycloalkyl, heterocycloalkyl, alkylcycloalkyl, heteroalkylcycloalkyl, aralkyl and heteroaralkyl groups described herein may optionally be substituted. Preferably, the present invention provides a hydroquinone derivative compound of formula (I), wherein: (A) Ra, Rb = H, Ci-4acyl, arylCi-4alkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C7alkylNHCO, phosphono, phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or C i-Cgalkoxy carbonyloxy-1 -ethyl, Ri = COOR4; R4 = H, Ci-4alkyl, arylCwalkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and R5 = Rg = CONH-R9; or (B) Ra, Rb = H, Ci-4acyl, arylCwalkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C7alkylNHCO, phosphono, phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or C i-Cgalkoxy carbonyloxy-1 -ethyl, Ri = COOR4; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl,     Ci-Cgacyloxy-1-ethyl,     Ci- Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; 5 R3 = H; R2 = R5; and R5 = Rg= CONH-R9. In a first embodiment, the present invention thus includes compounds in accordance with Table 1: Table 1 A. ORa r4ooc^J^h r3 ORb R3 = R5 = CONHR9 Compound No. Compound chemical names Ra Rb R4 R9 la-OOla 4-(2-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-carboxyphenyl la-OOla-Tz 4-(2-(lH-tetrazol-5-yl)phenyl-aminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-(lH-tetrazol-5-yl)phenyl la-OOlc 2,5-dihydroxy -4-(2-sulfophenylaminocarbonyl)benzoic acid H H H 2-sulfophenyl Ia-002a 4-(3-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 3-carboxyphenyl Ia-002a-Tz 4-(3-(lH-tetrazol-5-yl)phenyl-aminocarbonyl)-2,5-dihydroxybenzoic acid H H H 3 -(lH-tetrazol-5 -y l)phenyl Ia-002c 2,5-dihydroxy-4-(3-sulfophenylaminocarbonyl)benzoic acid H H H 3-sulfophenyl Ia-003a 4-(4-carboxyphenyl-aminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-carboxyphenyl Ia-003a-Tz 4-(4-(lH-tetrazol-5-yl)phenyl-aminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-(lH-tetrazol-5-yl)phenyl Ia-003c 2,5-dihydroxy-4-(4-sulfophenylaminocarbonyl)benzoic acid H H H 4-sulfophenyl Ia-004a 4-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 3 -carboxy -4-hydroxyphenyl Ia-005a 4-(4-carboxy-3-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-carboxy-3 -hydroxyphenyl Ia-056a 4-(4-carboxy-2,5-dihydroxyphenylaminocarbonyl)- 2,5-dihydroxybenzoic acid H H H 4-carboxy-2,5-dihydroxyphenyl Ia-006a 4-(2-carboxy -4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-carboxy-4-hydroxyphenyl Ib-OlOa 3,5-bis(2,5-dihydroxy-4-carboxybenzoylamino)benzoic acid H H H COOH h L II ^XOOH OH la-Olla 3-(4-carboxy-2,5-dihydroxybenzamido)phthalic acid; H H H 2,3 -dicarboxyphenyl Ia-012a 2-(4-carboxy-2,5-dihydroxybenzamido)terephthalic acid H H H 2,5-dicarboxyphenyl Ia-013a Compound 36: 2-(4-carboxy-2,5-dihydroxybenzamido)isophthalic acid H H H 2,6-dicarboxyphenyl Ia-014a Compound 38: 4-(4-carboxy-2,5-dihydroxybenzamido)phthalic acid H H H 3,4-dicarboxyphenyl Ia-015a 5-(4-carboxy-2,5-dihydroxybenzamido)isophthalic acid H H H 3.5 -dicarboxyphenyl Ia-016a 2-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid H H H 3 -carboxypyridin-2-yl Ia-017a 2-(4-carboxy-2,5-dihydroxybenzamido)isonicotinic acid H H H 4-carboxypyridin-2-yl Ia-018a 6-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid H H H 5-carboxypyridin-2-yl Ia-019a 6-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid H H H 6-carboxypyridin-2-yl Ia-020a 2-(4-carboxy-2,5 -dihydro xybenzamido)-5 -fluoronicotinic acid H H H 3-carboxy-5-fluoropyridin-2-yl Ia-021a 6-(4-carboxy-2,5-dihydroxybenzamido)pyridine-2,5-dicarboxylic acid H H H 3,6-dicarboxypyridin-2-yl Ia-022a 2-(4-carboxy-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylie acid H H H 3,5 -dicarboxypyridin-2-y 1 Ia-023a 3-(4-carboxy-2,5-dihydroxybenzamido)isonicotinic acid H H H 4-carboxypyridin-3 -yl Ia-024a 5-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid H H H 5-carboxypy ridin-3-yl Ia-025a 5-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid H H H 6-carboxypyridin-3 -yl Ia-026a 3-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid H H H 2-carboxypyridin-3 -yl Ia-027a 5-(4-carboxy-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid H H H 4-carboxy-6-fluoropy ridin-3 -yl Ia-028a 4-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid H H H 3 -carboxypyridin-4-yl Ia-029a 4-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid H H H 2-carboxypyridin-3 -yl Ia-032a 4-(4-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-(carboxymethyl)phenyl Ia-O33a 4-(3-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 3 -(carboxy methy l)pheny 1 Ia-O33a- HyP 2,5-dihydroxy-4-(3 -(1 -hydroxy- lH-pyrazol-4-yl)phenylaminocarbonyl)benzoic acid H H H 3 -(1 -hydroxy- lH-pyrazol-4-yl) phenyl Ia-034a 4-(2-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-(carboxymethyl)phenyl la-OOla- E2-A2 ethyl 4-(2-(ethoxycarbonyl)phenylaminocarbonyl)- 2,5 -diacetoxybenzoate Ac Ac Et 2-(ethoxycarbonyl)phenyl Ia-001a-E2 ethyl 4-(2-(ethoxycarbonyl)phenylaminocarbonyl)-2,5 -dihy droxybenzoate H H Et 2-(ethoxycarbonyl)phenyl la-OOla-Tz- E1-A2 ethyl 4-(2-(lH-tetrazol-5- yl)phenylaminocarbonyl)-2,5-diacetoxybenzoate Ac Ac Et 2-(lH-tetrazol-5-yl)phenyl la-OOla-Tz- E1 ethyl 4-(2-(lH-tetrazol-5- yl)phenylaminocarbonyl)-2,5-dihy droxybenzoate H H Et 2-(lH-tetrazol-5-yl)phenyl Ia-004a-E2 ethyl 2,5-dihydroxy-4-(4-hydroxy-3-(methoxycarbonyl)phenylaminocarbonyl)benzoate H H Et 4-hydroxy-3-(methoxycarbonyl)phenyl Ib-OlOa- E3-A4 ethyl 3,5-bis(2,5-diacetoxy-4-ethoxycarbonylbenzoylamino)benzoate Ac Ac Et cooe O Ofc H L JI Yp^COOEl OAc Ib-OlOa- E3 ethyl 3,5-bis(2,5-dihydroxy-4-ethoxycarbonylbenzoylamino)benzoate H H Et •:aoE’ j5'' ji 11 n- 4J. A A ■ h r. t Y COOEt ('11 Ia-023a-E2 ethyl 3-(4-(ethoxycarbonyl)-2,5-dihydroxybenzamido)isonicotinate H H Et 4-ethoxycarbonylpyridin-3 -yl Ia-056a-E2 Compound 390: Ethyl 4-(4-ethoxycarbonyl-2,5-dihydroxyphenylaminocarbonyl)-2,5-dihy droxybenzoate H H Et 4-ethoxy carbonyl-2,5 -dihydroxyphenyl B. ORa r4o          r2 ORb R2 = R5 = CONHR9 IIa-00 la 3-(2-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-carboxyphenyl IIa-00 la-Tz 3-(2-(lH-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-(lH-tetrazol-5-yl)phenyl Ila-OOlc 2,5-dihydroxy-3-(2-sulfophenylaminocarbonyl)benzoic acid H H H 2-sulfophenyl IIa-002a 3 -(3 -carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 3-carboxyphenyl IIa-002a-Tz 3-(3-( lH-tetrazol-5 -y l)phenylaminocarbony 1)-2,5 -dihydroxybenzoic acid H H H 3 -(lH-tetrazol-5 -y l)phenyl IIa-002c 2,5-dihydroxy-3-(3-sulfophenylaminocarbonyl)benzoic acid H H H 3-sulfophenyl IIa-003a 3-(4-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-carboxyphenyl IIa-003a-Tz 3-(4-( lH-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-(lH-tetrazol-5-yl)phenyl IIa-003c 2,5-dihydroxy-3-(4-sulfophenylaminocarbonyl)benzoic acid H H H 4-sulfophenyl IIa-004a 3-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 3 -carboxy -4-hydroxyphenyl IIa-005a 3-(4-carboxy-3-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-carboxy-3 -hydroxyphenyl IIa-006a 3-(2-carboxy -4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-carboxy -4-hydroxyphenyl nb-OlOa 3,5 -B is (2,5 -dihydroxy-3 -carboxybenzoy lamino)benzoic acid H H H COOH aSi °h A^A, A A jCOOH OH Ila-Olla 3 -(3 -carboxy-2,5-dihydro xybenzamido)phthalic acid H H H 2,3 -dicarboxyphenyl IIa-012a 2-(3-carboxy-2,5-dihydroxybenzamido)terephthalic acid H H H 2,5-dicarboxyphenyl IIa-013a 2-(3-carboxy-2,5-dihydroxybenzamido)isophthalic acid H H H 2.6-dicarboxyphenyl IIa-014a 4-(3-carboxy-2,5-dihydroxybenzamido)phthalic acid H H H 3,4-dicarboxyphenyl na-015a 5-(3-carboxy-2,5-dihydroxybenzamido)isophthalic acid H H H 3,5-dicarboxylie acid IIa-016a 2-(3-carboxy-2,5-dihydroxybenzamido)nicotinic acid H H H 3 -carboxypyridin-2-yl IIa-017a 2-(3-carboxy-2,5-dihydroxybenzamido)isonicotinic acid H H H 4-carboxypyridin-2-yl IIa-018a 6-(3-carboxy-2,5-dihydroxybenzamido)nicotimc acid H H H 5-carboxypyridin-2-yl IIa-019a 6-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid H H H 6-carboxypyridin-2-yl IIa-020a 2-(3 -carboxy-2,5 -dihydro xybenzamido)-5 -fluoronicotinic acid H H H 3-carboxy-5-fluoropyridin-2-yl na-021a 6-(3-carboxy-2,5-dihydroxybenzamido)pyridine-2,5-dicarboxylic acid H H H 3,6-dicarboxypyridin-2-yl IIa-022a 2-(3-carboxy-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylie acid H H H 3,5 -dicarboxypyridin-2-y 1 IIa-023a 3-(3-carboxy-2,5-dihydroxybenzamido)isonicotinic acid H H H 4-carboxypyridin-3 -yl IIa-024a 5-(3-carboxy-2,5-dihydroxybenzamido)nicotinic acid H H H 5-carboxypy ridin-3-yl IIa-025a 5-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid H H H 6-carboxypyridin-3 -yl IIa-026a 3-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid H H H 2-carboxypyridin-3 -yl IIa-027a 5-(3-carboxy-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid H H H 4-carboxy-6-fluoropy ridin-3 -yl IIa-028a 4-(3-carboxy-2,5-dihydroxybenzamido)nicotimc acid H H H 3 -carboxypyridin-4-yl IIa-029a Compound 172: 4-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid; H H H 2-carboxypyridin-3 -yl IIa-032a 3-(4-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 4-(carboxymethyl)phenyl IIa-O33a 3 -(3-(carboxy methyl)phenylaminocarbony 1)-2,5 -dihydroxybenzoic acid H H H 3 -(carboxy methy l)pheny 1 IIa-O33a- Hyp 2,5-dihydroxy-3-(3 -(1 -hydroxy-lH-pyrazol-4-yl)phenylaminocarbonyl)benzoic acid H H H 3 -(1 -hydroxy- lH-pyrazol-4-yl)phenyl IIa-034a 3-(2-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid H H H 2-(carboxymethyl)phenyl Ila-OOlaTz- E1 ethyl 3-(2-(lH-tetrazol-5- yl)phenylaminocarbonyl)-2,5-dihydroxybenzoate H H Et 2-(lH-tetrazol-5-yl)phenyl IIa-034a- E2 ethyl 3-(2- (ethoxycarbonylmethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoate H H Et 2-(2- ethoxycarbonylmethyl)phenyl Preferably, the present invention provides a compound of formula (I), wherein: (A) Ra, Rb = H; 5 Ri=SO3H; R2 = H; R3 = and R5 = R5 = CONH-R9; or (B) 10 Ra, Rb = H; Ri=SO3H; R3 = H; R2 = R5; and R5 = R6=CONH-R9. 15 In a second embodiment, the present invention includes compounds in accordance with Table 2: Table 2 A. HO3S. R3 = R5 = ORa r3 ORb CONHR9 Compound No. Compound chemical names Ra Rb R9 la-OOlb 2-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid H H 2-carboxyphenyl la-OOld 2,5-dihydroxy -4-(2-sulfophenylaminocarbonyl)benzenesulfonic acid H H 2-sulfophenyl Ia-002b 3-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid H H 3-carboxyphenyl Ia-002d 2,5-dihydroxy-4-(3-sulfophenylaminocarbonyl)benzenesulfonic acid H H 3-sulfophenyl Ia-003b 4-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid H H 4-carboxyphenyl Ia-003d 2,5-dihydroxy-4-(4-sulfophenylaminocarbonyl)benzenesulfonic acid H H 4-sulfophenyl Ia-004b 5-(2,5-dihydroxy -4-sulfobenzamido)-2-hydroxybenzoic acid H H 3 -carboxy-4-hydroxyphenyl Ia-005b 4-(2,5-dihydroxy-4-sulfobenzamido)-2-hydroxybenzoic acid H H 4-carboxy-3 -hydroxyphenyl Ia-006b 2-(2,5-dihydroxy-4-sulfobenzamido)-5-hydroxybenzoic acid H H 2-carboxy-4-hydroxyphenyl Ib-OlOb 3,5-bis(2,5-dihydroxy-4-sulfobenzamido)benzoic acid H H COOH O o oh OH la-Ollb 3-(2,5-dihydroxy-4-sulfobenzamido)phthalic acid H H 2,3 -dicarboxyphenyl Ia-012b 2-(2,5-dihydroxy-4-sulfobenzamido)terephthalic acid H H 2,5-dicarboxyphenyl Ia-013b 2-(2,5-dihydroxy-4-sulfobenzamido)isophthalic acid H H 2,6-dicarboxyphenyl Ia-014b 4-(2,5-dihydroxy-4-sulfobenzamido)phthalic acid H H 3,4-dicarboxyphenyl Ia-015b 5-(2,5-dihydroxy-4-sulfobenzamido)isophthalic acid H H 3.5 -dicarboxypheny 1 Ia-016b 2-(2,5-dihydroxy-4-sulfobenzamido)nicotinic acid H H 3 -carboxypyridin-2-y 1 Ia-017b 2-(2,5-dihydroxy-4-sulfobenzamido)isonicotinic acid H H 4-carboxypyridin-2-yl Ia-018b 6-(2,5-dihydroxy-4-sulfobenzamido)nicotinic acid H H 5 -carboxypyridin-2-y 1 Ia-019b 6-(2,5-dihydroxy-4-sulfobenzamido)picolinic acid H H 6-carboxypyridin-2-yl Ia-020b 2-(2,5-dihydroxy-4-sulfobenzamido)-5-fluoronicotinic acid H H 3 -carboxy-5 -fluoropy ridin-2-y 1 Ia-021b 6-(2,5-dihydroxy-4-sulfobenzamido)pyridine-2,5-dicarboxylic acid H H 3,6-dicarboxypyridin-2-yl Ia-022b 2-(2,5-dihydroxy-4-sulfobenzamido)pyridine-3,5-dicarboxylic acid H H 3,5-dicarboxypyridin-2-yl Ia-023b 3-(2,5-dihydroxy-4-sulfobenzamido)isonicotinic acid H H 4-carboxypyridin-3-yl Ia-024b 5-(2,5 -dihydroxy-4-sulfobenzamido)nicotinic acid H H 5 -carboxypyridin-3 -y 1 Ia-025b 5-(2,5 -dihydro xy-4-sulfobenzamido)picolinic acid H H 6-carboxypyridin-3-yl Ia-026a 3-(2,5-dihydroxy-4-sulfobenzamido)picolinic acid H H 2-carboxypyridin-3-yl Ia-027b 5-(2,5-dihydroxy-4-sulfobenzamido)-2-fluoroisonicotinic acid H H 4-carboxy-6-fluoropyridin-3-yl Ia-028b 4-(2,5-dihydroxy-4-sulfobenzamido)nicotinic acid H H 3 -carboxypyridin-4-y 1 Ia-029b 4-(2,5-dihydroxy-4-sulfobenzamido)picolinic acid H H 2-carboxypyridin-3-yl Ia-032b (4-(2,5-dihydroxy-4-sulfobenzamido)phenyl)acetic acid H H 4-(carboxymethyl)phenyl Ia-O33b (3-(2,5-dihydroxy-4-sulfobenzamido)phenyl)acetic acid H H 3 -(carboxymethy l)pheny 1 Ia-034b (2-(2,5-dihydroxy-4-sulfobenzamido)phenyl)acetic acid H H 2-(carboxymethyl)phenyl B. ho3s. R2 = R5 = ORa ''pH ORb CONHR9 IIa-00 lb 2-(2,5-dihydroxy-3-sulfobenzamido)benzoic acid H H 2-carboxyphenyl IIa-00 Id 2,5-dihydroxy-3-(2- sulfophenylaminocarbonyl)benzenesulfonic acid H H 2-sulfophenyl IIa-002b 3-(2,5-dihydroxy-3-sulfobenzamido)benzoic acid H H 3-carboxyphenyl IIa-002d 2,5 -dihydro xy-3 -(3-sulfophenylaminocarbonyl)benzenesulfonic acid H H 3-sulfophenyl IIa-003b 4-(2,5-dihydroxy-3-sulfobenzamido)benzoic acid H H 4-carboxyphenyl IIa-003d 2,5-dihydroxy-3-(4- sulfophenylaminocarbonyl)benzenesulfonic acid H H 4-sulfophenyl IIa-004b 5-(2,5-dihydroxy-3-sulfobenzamido)-2-hydroxybenzoic acid H H 3 -carboxy-4-hydroxyphenyl IIa-005b 4-(2,5-dihydroxy-3-sulfobenzamido)-2-hydroxybenzoic acid; H H 4-carboxy-3 -hydroxyphenyl IIa-006b 2-(2,5-dihydroxy-3-sulfobenzamido)-5-hydroxybenzoic acid H H 2-carboxy-4-hydroxyphenyl lib-010b 3-(2,5-dihydroxy-3-sulfobenzamido)-5-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid H H COOH A'A Q OH A A .so,4 4 L OH Ila-Ollb 3-(2,5-dihydroxy-3 -sulfobenzamido)phthalic acid; H H 2,3 -dicarboxyphenyl IIa-012b 2-(2,5-dihydroxy-3-sulfobenzamido)terephthalic acid H H 2,5-dicarboxyphenyl IIa-013b 2-(2,5-dihydroxy-3-sulfobenzamido)isophthalic acid H H 2,6-dicarboxyphenyl IIa-014b 4-(2,5-dihydroxy-3-sulfobenzamido)phthalic acid H H 3,4-dicarboxyphenyl IIa-015b 5-(2,5-dihydroxy-3-sulfobenzamido)isophthalic acid H H 3.5 -dicarboxypheny 1 IIa-016b 2-(2,5-dihydroxy-3-sulfobenzamido)nicotinic acid H H 3 -carboxypyridin-2-y 1 IIa-017b 2-(2,5-dihydroxy-3-sulfobenzamido)isonicotinic acid H H 4-carboxypyridin-2-yl IIa-018b 6-(2,5-dihydroxy-3-sulfobenzamido)nicotinic acid H H 5 -carboxypyridin-2-y 1 IIa-019b 6-(2,5-dihydroxy-3-sulfobenzamido)picolinic acid H H 6-carboxypyridin-2-yl IIa-020b 2-(2,5-dihydroxy-3-sulfobenzamido)-5-fluoronicotinic acid H H 3 -carboxy-5 -fluoropy ridin-2-y 1 IIa-021b 6-(2,5-dihydroxy-3-sulfobenzamido)pyridine-2,5-dicarboxylic acid; H H 3,6-dicarboxypyridin-2-yl IIa-022b 2-(2,5-dihydroxy-3-sulfobenzamido)pyridine-3,5-dicarboxylic acid H H 3,5-dicarboxypyridin-2-yl WO 2021 / 180655                                                 PCT / EP2021 / 055791 21 IIa-023b 3-(2,5 -dihydro xy-3 -sulfobenzamido)isonicotinic acid H H 4-carboxypyridin-3-yl IIa-024b 5-(2,5-dihydroxy-3 -sulfobenzamido)mcotinic acid H H 5 -carboxypyridin-3 -y 1 IIa-025b 5-(2,5-dihydroxy-3 -sulfobenzamido)picolinic acid H H 6-carboxypyridin-3-yl IIa-026b 3-(2,5-dihydroxy-3 -sulfobenzamido)picolinic acid H H 2-carboxypyridin-3-yl IIa-027b 5-(2,5-dihydroxy-3-sulfobenzamido)-2-fluoroisonicotinic acid H H 4-carboxy-6-fluoropyridin-3-yl IIa-028b 4-(2,5-dihydroxy-3-sulfobenzamido)mcotinic acid H H 3 -carboxypyridin-4-y 1 IIa-029b Compound 173: 4-(2,5-dihydroxy-3-sulfobenzamido)picolinic acid H H 2-carboxypyridin-3-yl IIa-032b (4-(2,5-dihydroxy-3-sulfobenzamido)phenyl)acetic acid H H 4-(carboxymethyl)phenyl IIa-O33b (3-(2,5-dihydroxy-3-sulfobenzamido)phenyl)acetic acid H H 3 -(carboxymethy l)pheny 1 IIa-034b (2-(2,5-dihydroxy-3-sulfobenzamido)phenyl)acetic acid H H 2-(carboxymethyl)phenyl Preferably, the present invention provides a hydroquinone derivative compound of formula (I), wherein: (A) Ra, Rb = H; Ri = (CH2)nCOOR4; R4 = H, Cwalkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl,     Ci-Cgacyloxy-1-ethyl,     Ci- Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and R5 = Rg = CONH-R9; Or (B) Ra, Rb = H; Ri = (CH2)nCOOR4; R4 = H, Cwalkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl,     Ci-Cgacyloxy-1-ethyl,     Ci- Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R3 = H; R2 = R5; and R5 = Rg= CONH-R9. In a third embodiment, the present invention includes compounds in accordance with Table 3: Table 3 A. ORa Ri\A^h r3 ORb R3 = R5 = R6 = CONH-R9 Compound No. Compound chemical names RI Ra Rb R9 Illa-OOla 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid CH2COOH H H 2-carboxyphenyl IIIa-OOla-Tz (2-(lH-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid CH2COOH H H 2-(lH-tetrazol-5-yl)phenyl Illa-OOlc (2,5-dihydroxy -4-(2-sulfophenylaminocarbonyl)phenyl)acetic acid CH2COOH H H 2-sulfophenyl IIIa-002a 3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid; CH2COOH H H 3-carboxyphenyl IIIa-002c (2,5-dihydroxy-4-(3-sulfophenylaminocarbonyl)phenyl)acetic acid; CH2COOH H H 3-sulfophenyl IIIa-003a 4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid; CH2COOH H H 4-carboxyphenyl IIIa-003c 2-(2,5-dihydroxy-4-(4-sulfophenylaminocarbonyl)phenyl)acetic acid; CH2COOH H H 4-sulfophenyl IIIa-004a Compound 216: 5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid CH2COOH H H 3-carboxy-4-hydroxyphenyl IIIa-005a 4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid CH2COOH H H 4-carboxy-3-hydroxyphenyl IIIa-006a 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-5-hydroxybenzoic acid CH2COOH H H 2-carboxy-4-hydroxyphenyl Illb-010a 3,5 -B is (2,5 -dihydroxy -4 -carboxymethylbenzoylamino)benzoic acid CH2COOH H H COOH O OH ri OH Illa-Olla 3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid CH2COOH H H 2,3 -dicarboxypheny 1 ma-012a 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)terephthalic acid CH2COOH H H 2,5-dicarboxyphenyl ma-013a 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid CH2COOH H H 2,6-dicarboxyphenyl IIIa-014a 4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid CH2COOH H H 3.4-dicarboxypheny 1 ma-015a 5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid CH2COOH H H 3.5-dicarboxyphenyl IIIa-016a 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid CH2COOH H H 3 -carboxypyridin-2-yl IIIa-017a 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotimc acid CH2COOH H H 4-carboxypyridin-2-yl ma-018a 6-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid CH2COOH H H 5-carboxypyridin-2-yl IIIa-019a 6-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid CH2COOH H H 6-carboxypyridin-2-yl IIIa-020a 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-5-fluoronicotinic acid CH2COOH H H 3-carboxy-5-fluoropyridin-2-yl IIIa-021a 6-(4-(carboxymethyl)-2,5-dihydroxybenzamido)pyridine-2,5-dicarboxylic acid CH2COOH H H 3,6-dicarboxypyridin- 2-yl IIIa-022a 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylic acid CH2COOH H H 3,5 -dicarboxypyridin- 2-yl IIIa-023a 3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotinic acid; CH2COOH H H 4-carboxypyridin-3 -yl IIIa-024a 5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid CH2COOH H H 5 -carboxypy ridin-3 -y 1 IIIa-025a 5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid CH2COOH H H 6-carboxypyridin-3 -yl IIIa-026a 3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid CH2COOH H H 2-carboxypyridin-3 -yl IIIa-027a 5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid CH2COOH H H 4-carboxy-6-fluoropyridin-3 -y 1 IIIa-028a 4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid; CH2COOH H H 3 -carboxypyridin-4-yl IIIa-029a 4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid; CH2COOH H H 2-carboxypyridin-3 -yl IIIa-032a (4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid CH2COOH H H 4-(carboxymethyl)pheny 1 IIIa-O33a (3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid CH2COOH H H 3- (carboxymethyl)pheny 1 IIIa-034a (2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid CH2COOH H H 2-(carboxymethyl)pheny 1 IIIa-001a-E2 methyl 2-(4-(ethoxycarbonylmethyl)-2,5-dihydroxybenzamido)benzoate CH2COOEt H H 2-(methoxycarbonyl)phe nyl IIIa-OOlaTz- E1 Compound 383: ethyl (4-(2-(lH-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihy droxypheny l)acetate; CH2COOEt H H 2-(lH-tetrazol-5-yl)phenyl IIIa-015a-E3 diethyl 5-(4-( ethoxycarbonylmethyl)-2,5-dihydroxybenzamido)isophthalate CH2COOEt H H 3,5-diethoxycarbonylphen yi mb-010a-E3 methyl 3,5-bis(4-(ethoxycarbonylmethyl)- 2,5-dihydroxybenzamido)benzoate CH2COOEt H H LU 0 0 o B. ORa Riy4zR2 < n ORb R2 = R5 = R6 = CONHR9 IVa-OOla 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid CH2COOH H H 2-carboxyphenyl IVa-OOlc (2,5-dihydroxy -3-(2-sulfophenylaminocarbonyl)phenyl)acetic acid CH2COOH H H 2-sulfophenyl IVa-002a 3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid CH2COOH H H 3-carboxyphenyl IVa-002c (2,5-dihydroxy-3-(3-sulfophenylaminocarbonyl)phenyl)acetic acid CH2COOH H H 3-sulfophenyl IVa-003a 4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid CH2COOH H H 4-carboxyphenyl IVa-003c (2,5-dihydroxy-3-(4-sulfophenylaminocarbonyl)phenyl)acetic acid CH2COOH H H 4-sulfophenyl IVa-004a 5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid CH2COOH H H 3-carboxy-4-hydroxyphenyl IVa-005a 4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid CH2COOH H H 4-carboxy-3-hydroxyphenyl IVa-006a Compound 295: 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-5-hydroxybenzoic acid; CH2COOH H H 2-carboxy-4-hydroxyphenyl IVb-OlOa 3,5 -B is (2,5 -dihydroxy -3 -carboxymethylbenzoylamino)benzoic acid CH2COOH H H COOH 0 OH OH IVa-Olla 3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid CH2COOH H H 2,3 -dicarboxypheny 1 IVa-012a 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)terephthalic acid CH2COOH H H 2,5-dicarboxyphenyl IVa-013a 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid CH2COOH H H 2,6-dicarboxyphenyl IVa-014a 4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid CH2COOH H H 3.4-dicarboxypheny 1 IVa-015a 5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid CH2COOH H H 3.5-dicarboxyphenyl IVa-016a 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid CH2COOH H H 3 -carboxypyridin-2-yl IVa-017a 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotinic acid CH2COOH H H 4-carboxypyridin-2-yl IVa-018a 6-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid CH2COOH H H 5-carboxypyridin-2-yl IVa-019a 6-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid CH2COOH H H 6-carboxypyridin-2-yl IVa-020a 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-5-fluoronicotinic acid CH2COOH H H 3-carboxy-5-fluoropyridin-2-yl IVa-021a 6-(3-(carboxymethyl)-2,5-dihy droxybenzamido)py ridine-2,5 -dicarboxylic acid CH2COOH H H 3,6-dicarboxypyridin- 2-yl IVa-022a 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylic acid CH2COOH H H 3,5 -dicarboxypyridin- 2-yl IVa-023a 3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotinic acid CH2COOH H H 4-carboxypyridin-3 -yl IVa-024a 5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid CH2COOH H H 5 -carboxypy ridin-3 -y 1 IVa-025a 5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid CH2COOH H H 6-carboxypyridin-3 -yl IVa-026a 3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid CH2COOH H H 2-carboxypyridin-3 -yl IVa-027a 5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid CH2COOH H H 4-carboxy-6-fluoropyridin-3 -y 1 IVa-028a 4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid CH2COOH H H 3 -carboxypyridin-4-yl IVa-029a 4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid CH2COOH H H 2-carboxypyridin-3 -yl IVa-032a (4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid CH2COOH H H 4- (carboxymethyl)phenyl IVa-O33a (3 -(3-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid CH2COOH H H 3- (carboxymethyl)phenyl IVa-034a (2 -(3-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid CH2COOH H H 2- (carboxymethyl)phenyl Preferably, the present invention provides a hydroquinone derivative compound of formula (I), wherein: (A) Ra, Rb = H, Ci-4acyl, arylCi-4alkyl, Cg-CwarylCO, HOOC(CH2)nCO, Ci-CvalkylNHCO, phosphono, 5 phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or Ci-Cgalkoxy carbonyloxy-1 -ethyl; Ri = CONH-Rio; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-10 Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and R5 = Rg = CONH-R9; Or (B) Ra, Rb = H, Ci-4acyl, arylCi-4alkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C?alkylNHCO, phosphono, phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or Ci-Cgalkoxy carbonyloxy-1 -ethyl; 5 Ri = CONH-Rio; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R3 = H; R2 = R5; and 10   R5 = Rg = CONH-R9 In a fourth embodiment, the present invention includes compounds in accordance with Table 4: Table 4 A. ORa R10HNOC^^L^H R3 ORb R3 = R5 = R6 = CONH-R9 Compound No. Compound chemical names Ra Rb RIO R9 Ic-OOla- Tz / l-004a 5-(4-(2-(lH-tetrazol-5- yl)phenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxy benzoic acid H H 3-carboxy-4-hydroxyphenyl 2-(lH-tetrazol-5-yl)phenyl Ic-OOla- Tz(2) Ni,N4-bis(2-(lH-tetrazol-5-yl)phenyl)-2,5-dihydroxyterephthalamide H H 2-(lH-tetrazol-5-yl)phenyl 2-(lH-tetrazol-5-yl)phenyl Ic-007a 5-(4-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxy benzoic acid; H H 3-carboxy-4-hydroxyphenyl 3-carboxy-4-hydroxyphenyl Ic-007b 5-(2,5-dihydroxy-4-(4-hydroxy-3-sulfophenylaminocarbonyl)benzami do)-2-hydroxy benzenesulphonic acid H H 4-hydroxy-3-sulfonylphenyl 4-hydroxy-3-sulfonylphenyl Ic-008a 4-(4-(4-carboxy-3-hydroxyphenylaminocarbonyl)-2,5- H H 4-carboxy-3-hydroxyphenyl 4-carboxy-3-hydroxyphenyl dihydroxybenzamido)-2-hydroxy benzoic acid Ic-008b 4-(2,5-dihydroxy-4-(3-hydroxy-4-sulfophenylaminocarbonyl)benzami do)-2-hydroxy benzenesulphonic acid H H 3-hydroxy-4-sulfonylphenyl 3-hydroxy-4-sulfonylphenyl Ic-009a 2-(2,5-dihydroxy-4-(4-hydroxy-2-carboxyphenylaminocarbonyl)benza mido)-5-hydroxy benzoic acid H H 2-carboxy-4-hydroxyphenyl 2-carboxy-4-hydroxyphenyl Ic-009b 2-(2,5-dihydroxy-4-(4-hydroxy-2-sulfophenylaminocarbonyl)benzami do)-5-hydroxy benzene sulphonic acid H H 4-hydroxy-2-sulfophenyl 4-hydroxy-2-sulfophenyl Ib-OOla- Tz / l-004a- E1 methyl 5-(4-(2-(lH-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoate; H H 4-hydroxy-3-(methoxycarbonyl)ph enyl- 2-(lH-tetrazol-5-yl)phenyl Ic-007a- E2-A4 methyl 5-(2,5-diacetoxy-4-(4-acetoxy-3-(methoxycarbonyl)phenylaminocarb onyl) benzamido)-2-acetoxybenzoate; Ac Ac 4-acetoxy-3-(methoxycarbonyl)ph enyl 4-acetoxy-3-(methoxycarbonyl)phenyl Ic-007a-E2 methyl 5-(2,5-dihydroxy-4-(4-hydroxy-3-(methoxycarbonyl)phenylaminocarb onyl) benzamido)-2-hydroxybenzoate; H H 4-hydroxy-3-(methoxycarbonyl)ph enyl 4-hydroxy-3-(methoxycarbonyl)phenyl Ic-007a-pive2 1-(2,2-dimethylpropanoyloxy)ethyl 5-[[4-[[3-[l-(2,2- dimethylpropanoyloxy)ethoxycarbo nyl]-4-hydroxy-phenyl]carbamoyl]-2,5 -dihydroxy -benzoy 1] amino] -2 -hydroxybenzoate H H 3-[l-(2,2- dimethylpropanoylox y)ethoxycarbonyl]-4-hydroxyphenyl 3-[l-(2,2- dimethylpropanoyloxy)eth oxycarbonyl]-4-hydroxy-phenyl Ic-009a-E2 : methyl 2-(2,5-dihydroxy-4-(4-hydroxy-2- (methoxycarbonyl)phenylaminocarb onyl) benzamido)-5-hydroxybenzoate H H 4-hydroxy-2-(methoxycarbonyl)ph enyl 4-hydroxy-2-(methoxycarbonyl)phenyl B. ORa R10HNOC^U^.R2 I^H ORb R2 = R5 = R6 = CONH-R9 lie-007a 5-(3-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxy benzoic acid H H 3-carboxy-4-hydroxyphenyl 3-carboxy-4-hydroxyphenyl lie-007b 5-(2,5-dihydroxy-3-(4-hydroxy-3-sulfophenylaminocarbonyl)benzami do)-2-hydroxy benzenesulphonic acid H H 4-hydroxy-3-sulfophenyl 4-hydroxy-3-sulfophenyl lie-008a 4-(3 -(3 -hydroxy -4-carboxyphenylaminocarbony 1)-2,5 -dihydroxybenzamido)-2-hydroxy benzoic acid H H 3 -hydro xy -4-carboxyphenyl 3-hydroxy-4-carboxyphenyl lie-008b 4-(2,5-dihydroxy-3-(3-hydroxy-4-sulfophenylaminocarbonyl)benzami do)-2-hydroxy benzenesulphonic acid H H 3-hydroxy-4-sulfophenyl 3-hydroxy-4-sulfophenyl lie-009a 2-(3 -(2-carboxy -4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-5-hydroxyl benzoic acid H H 2-carboxy-4-hydroxyphenyl 2-carboxy-4-hydroxyphenyl lie-009b 2-(2,5-dihydroxy-3-(4-hydroxy-2-sulfophenylaminocarbonyl)benzami do)-5-hydroxy benzenesulphonic acid H H 4-hydroxy-2-sulfophenyl 4-hydroxy-2-sulfophenyl Preferably, the present invention provides a hydroquinone derivative compounds of formula (I), wherein: (A) Ra, Rb = H; 5 Ri = COOR4; (CH2)nCOOR4; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-l-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and R5 = Re = CONHCOR9; Or (B) Ra, Re = H; 5 Ri = COOR4; (CIDnCOORi; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-l-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R3 = H; R2 = R5; and 10 R5 = Rg = CONHCOR9. In a fifth embodiment, the present invention includes compounds in accordance with Table 5: Table 5 A. OH r3 OH R3 = R5 = R6 = CONHCORs Compound No. Compound chemical names RI R9 Ia-040a N-(l,3,4,5-tetrahydroxycyclohexylcarbonyl) 4-carboxy-2,5-dihydroxybenzamide COOH OH ..... Ia-041a N-(4-carboxy-2,5-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxy-benzamide COOH 2,5-dihydroxy-4-carboxyphenyl Ia-042a N-(3-carboxy-2,5-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxy-benzamide COOH 2,5-dihydroxy-3-carboxyphenyl Ia-043a N-(3,4-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxybenzamide COOH 3,4-dihydroxyphenyl Ia-044a N-(3,5-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxybenzamide COOH 3,5-dihy droxypheny 1 IIIa-040a N-(l,3,4,5-tetrahydroxycyclohexylcarbonyl) 3-carboxy-2,5-dihydroxybenzamide CH2COOH OH OH 101-1 ma-041a N-(4-carboxy-2,5-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxy-benzamide CH2COOH 2,5-dihydroxy-4-carboxyphenyl IIIa-042a N-(3-carboxy-2,5-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxy-benzamide CH2COOH 2,5-dihydroxy-3-carboxyphenyl IIIa-043a N-(3,4-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxybenzamide CH2COOH 3,4-dihydroxyphenyl IIIa-044a N-(3,5-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxybenzamide CH2COOH 3, 5-dihy droxypheny 1 B. OH R OH R2 = R5 = R6 = CONHCOR9 IIa-040a N-(l,3,4,5-tetrahydroxycyclohexylcarbonyl) 4-carboxymethyl-2,5-dihydroxybenzamide COOH •UM Ila-04 la N-(4-carboxy-2,5-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxy-benzamide COOH 2,5-dihydroxy-4-carboxyphenyl IIa-042a N-(3-carboxy-2,5-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxy-benzamide COOH 2,5-dihydroxy-3-carboxyphenyl IIa-043a N-(3,4-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxybenzamide COOH 3,4-dihydroxyphenyl IIa-044a N-(3,5-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxybenzamide COOH 3,5-dihy droxypheny 1 IVa-040a N-(l,3,4,5-tetrahydroxycyclohexylcarbonyl) 3-carboxymethyl-2,5-dihydroxybenzamide CH2COOH OH JL>dh OH   ....... IVa-041a N-(4-carboxy-2,5-dihydroxybenzoyl) 3-carboxymethy 1-2,5-dihydroxy-benzamide CH2COOH 2,5-dihydroxy-4-carboxyphenyl IVa-042a N-(3-carboxy-2,5-dihydroxybenzoyl) 3-carboxy methy 1-2,5-dihydroxy-benzamide CH2COOH 2,5-dihydroxy-3-carboxyphenyl IVa-043a N-(3,4-dihydroxybenzoyl) 3-carboxymethyl-2,5-dihydroxybenzamide CH2COOH 3,4-dihydroxyphenyl IVa-044a N-(3,5-dihydroxybenzoyl) 3-carboxymethyl-2,5-dihydroxybenzamide CH2COOH 3,5-dihy droxypheny 1 Preferably, the present invention provides a hydroquinone derivative compound of formula (I), wherein (A) Ra, Rb = H; Ri = COORp (CH2)nCOOR4; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-l-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and R5 = Rg = CONH(CH2)n-R9; Or (B) Ra, Rb = H; Ri = COOR4; (CH2)nCOOR4; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-l-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R3 = H; R2 = R5; and R5 = Rg = CONH(CH2)n-R9. In a sixth embodiment, the present invention includes compounds in accordance with Table 6: Table 6 A. OH r3 OH R3 = R5 = R6 = CONH(CH2)n-R9 Compound No. Compound chemical names RI n R9 Ia-035a 4-(3,4-dihydroxyphenyhnethylaminocarbonyl)-2,5-dihydroxybenzoic acid; COOH 1 3,4-dihydroxyphenyl Ia-035a-2 4-(2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid; COOH 2 3,4-dihydroxyphenyl Ia-037a 4-(3,5-dihydroxyphenyhnethylaminocarbonyl)-2,5-dihydroxybenzoic acid; COOH 1 3,5 -dihydroxyphenyl Ia-038a 4-((4,5 -dihydro xy-3 -oxocyclohex-1 -enyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid; COOH 1 4,5-dihydroxy-3-oxocyclohex-l-enyl) Ia-039a 2,5-dihydroxy-4-((3,4,5-trihydroxycyclohexyl)methylaminocarbonyl)benzoic acid COOH 1 3,4,5- trihydroxy cyclohexyl) Ia-053a 4-(2-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxybenzoic acid COOH 1 2-carboxyphenyl Ia-054a 4-(3-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxybenzoic acid COOH 1 3-carboxyphenyl Ia-055a 4-(4-carboxyphenylmethylaminocarbonyl) 2,5-dihydroxybenzoic acid COOH 1 4-carboxyphenyl IIIa-035a 3-(3,4-dihydroxyphenyhnethylaminocarbonyl)-2,5-dihydroxybenzoic acid CH2COOH 1 3,4-dihydroxyphenyl IIIa-037a 3-(2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid CH2COOH 1 3,5 -dihydroxyphenyl IIIa-038a 3-(3,5-dihydroxyphenyhnethylaminocarbonyl)-2,5-dihydroxybenzoic acid CH2COOH 1 4-((4,5-dihydroxy-3-oxocyclohex-l-enyl) IIIa-039a 3-((4,5 -dihydro xy-3 -oxocyclohex-1 -enyl)methylaminocarbony 1)-2,5 -dihydroxybenzoic acid CH2COOH 1 3,4,5- trihydroxy cyclohexyl) IIIa-053a 2,5-dihydroxy-3-((3,4,5-trihydroxycyclohexyl)methylaminocarbonyl)benzoic acid CH2COOH 1 2-carboxyphenyl IIIa-054a 3-(2-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid CH2COOH 1 3-carboxyphenyl IIIa-055a 3-(3-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid CH2COOH 1 4-carboxyphenyl B. OH OH R2 = R5 = R6 = CONH(CH2)n-R9 IIa-035a 3-(4-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid COOH 1 3,4-dihydroxyphenyl IIa-035a-2 (4-(3,4-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid COOH 2 3,4-dihydroxyphenyl IIa-037a (4-(3,5-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid COOH 1 3,5 -dihydroxyphenyl IIa-038a (4-((4,5-dihy droxy-3-oxocyclohex-l-enyl)methylaminocarbonyl)-2,5-dihydroxyphenyl) acetic acid COOH 1 4,5-dihydroxy-3-oxocyclohex-l-enyl) IIa-039a Compound 191: (2,5-dihydroxy-4-((3,4,5-trihydroxycyclohexyl)methylaminocarbonyl)phenyl)acetic acid COOH 1 3,4,5- trihydroxy cyclohexyl IIa-053a (4-(2-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid COOH 1 2-carboxyphenyl IIa-054a (4-(3-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid COOH 1 3-carboxyphenyl IIa-055a (4-(4-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid COOH 1 4-carboxyphenyl IVa-035a (3-(3,4-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid CH2COOH 1 3,4-dihydroxyphenyl IVa-037a (3-(3,5-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid CH2COOH 1 3,5 -dihydroxyphenyl IVa-038a (3 -((4,5-dihydroxy-3 -oxocyclohex-1 -enyl)methylaminocarbonyl)-2,5-dihydroxyphenyl) acetic acid CH2COOH 1 4,5-dihydroxy-3-oxocyclohex-l-enyl) IVa-039a (2,5-dihydroxy-3-((3,4,5-trihydroxycyclohexyl)methylcarbonylamino)phenyl)acetic acid CH2COOH 1 3,4,5-trihydroxy cyclohexyl IVa-053a (3-(2-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid CH2COOH 1 2-carboxyphenyl IVa-054a (3-(3-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid CH2COOH 1 3-carboxyphenyl IVa-055a (3-(4-carboxyphenyhnethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid CH2COOH 1 4-carboxyphenyl Preferably, the present invention provides a hydroquinone derivative compound of formula (I), wherein: Ra, Rb = H; Ri = SO3H; 5 R2 = H; R3 = R5; and R5 = Re = CONH(CH2)n-R9. According to a seventh embodiment, the present invention includes compounds in accordance with Table 7 below: 10 Table 7 OH HO3S^xL^H r3 OH R3 = R5 = CONH(CH2)n-R9 Compound No. Compound chemical names n R9 Ia-053b 2-((2,5-dihydroxy-4-sulfobenzamido)methyl)benzoic acid 1 2-carboxyphenyl Ia-054b 3-((2,5-dihydroxy-4-sulfobenzamido)methyl)benzoic acid 1 3-carboxyphenyl Ia-055b 4-((2,5-dihydroxy-4-sulfobenzamido)methyl)benzoic acid 1 4-carboxyphenyl Preferably, the present invention relates to a hydroquinone derivative compound of formula (I) wherein: (A) Ra, Rt, = H; Ri = COOR4; (CH2)nCOOR4; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-l-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and R5 = Rg = CONHCH(COOR4)(CH2)k-R9; Or (B) Ra, Rt = H; Ri = COOR4; (CH2)nCOOR4; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-l-ethyl, Ci-Cgalkoxycarbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-l-ethyl, or (oxodioxolyl)methyl; R3 = H; R2 = Rs; and R5 = Rg = CONHCH(COOR4)(CH2)k-R9 According to an eighth embodiment, the present invention includes compounds in accordance with Table 8 below: Table 8 A. oh r3 OH Rs = Rs = Rs = CONHCH(COOR4)(CH2)kR9 Compound No. Compound chemical names RI R4 k R9 Ia-035a-3 4-(l-carboxy-2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid COOH H 1 3,4-dihydroxyphenyl Ia-036a 4-(carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid COOH H 0 3,4-dihydroxyphenyl IIIa-036a 3-(l-carboxy-2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid CH2COOH H 0 3,4-dihydroxyphenyl B. I 0 OH R2 = Rs = Rs = CONHCH(COOR4)(CH2)kR9 IIa-035a-3 3-(carboxy (3,4-dihydroxyphenyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid COOH H 1 3,4-dihydroxyphenyl IIa-036a (4-(carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)- 2,5-dihydroxyphenyl)acetic acid COOH H 0 3,4-dihydroxyphenyl IVa-036a (3-(carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)- 2,5-dihydroxyphenyl)acetic acid CH2COOH H 0 3,4-dihydroxyphenyl In a specific embodiment, the present invention provides a hydroquinone derivative compounds of formula (I), wherein (A) 5 Ra, Rb = H; Ri = COOR4; (CH2)nCOOR4; SO3H, (CH2)nSO3H, or CONH-Rw; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-10 Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and Rs = Rg = heteroaryl-Rg; Or (B) 15 Ra, Rb = H; Ri = COOR4; (CH2)nCOOR4; SO3H, (CH2)nSO3H, or CONH-R10; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; 5 R3 = H; R2 = R5; and Rs = Rg = heteroaryl-Rg. According to a ninth embodiment, the present invention includes compounds in accordance with Table 9: 10 Table 9 A. OH Ri\U-^H r3 OH R3 = R5 = R6 = heteroaryl-R9 Compound No. Compound chemical names RI Heteroaryl-R9 Ia-045a 4,6-Bis(4-carboxy-2,5-dihydroxyphenyl)-l,3,5-triazin-2- one COOH Ch Ch Ia-046a 4-(4-carboxy-2,5-dihydroxyphenyl)-6-(3-carboxy-2,5-dihydroxyphenyl)-l,3,5-triazin-2-one COOH OH u xjl V 'll N K OH Ia-047a 4-(4-carboxy-2,5-dihydroxyphenyl)-6-(3,4-dihydroxyphenyl)-l,3,5-triazin-2-one COOH ..... in Ia-048a 4-(4-carboxy-2,5-dihydroxyphenyl)-6-(3,5-dihydroxyphenyl)-l,3,5-triazin-2-one COOH OH Tf H      0H Y 0 Ia-049a 4,6-Bis(4-carboxy-2,5-dihydroxyphenyl)-l,3,5-triazine COOH OH Jx COOH c:h Ia-050a 2-(4-Carboxy-2,5-dihydroxyphenyl)-4-(3-carboxy-2,5-dihydroxyphenyl)-1,3,5-triazine COOH OH OH Ia-051a 2-(4-Carboxy-2,5-dihydroxyphenyl)-4-(3,4-dihydroxyphenyl)-1,3,5-triazine COOH X X Ia-052a 2-(4-Carboxy-2,5-dihydroxyphenyl)-4-(3,5-dihydroxyphenyl)-1,3,5-triazine COOH OH IIa-046a 4,6-Bis(3-carboxy-2,5-dihydroxyphenyl)-l,3,5-triazin-2- one COOH X O o IIa-050a 4-(3-Carboxy-2,5-dihydroxyphenyl)-6-(4-carboxy-2,5-dihydroxyphenyl)-l,3,5-triazin-2-one COOH c...... z— X \,„ / X o o o x ma-045a 4-(3-Carboxy-2,5-dihydroxyphenyl)-6-(3,4-dihydroxyphenyl)-l,3,5-triazin-2-one CH2COOH OH J^OOOH Hi 1 |f 1 ¥ T oh 6 IIIa-046a 4-(3-Carboxy-2,5-dihydroxyphenyl)-6-(3,5-dihydroxyphenyl)-l,3,5-triazin-2-one CH2COOH OH H A ¥Nr t H N OH T O IIIa-047a 4,6-Bis(3-carboxy-2,5-dihydroxyphenyl)-l,3,5-triazine CH2COOH OH Y HIa-048a 2-(3-Carboxy-2,5-dihydroxyphenyl)-4-(4-carboxy-2,5-dihydroxyphenyl)-1,3,5-triazine CH2COOH OH h fl Y H N i IIIa-049a 2-(3-Carboxy-2,5-dihydroxyphenyl)-4-(3,4-dihydroxyphenyl)-1,3,5-triazine CH2COOH OH JL^cooh N fj 1 Jl OH IIIa-050a 2-(3-Carboxy-2,5-dihydroxyphenyl)-4-(3,5-dihydroxyphenyl)-1,3,5-triazine CH2COOH OH . >1 JL OH ma-051a 2-(3-Carboxymethyl-2,5-dihydroxyphenyl)-4-(3,4-dihydroxyphenyl)-1,3,5-triazine CH2COOH )—■— ■■ \ HIa-O52a 2-(3-Carboxymethyl-2,5-dihydroxyphenyl)-4-(3,5-dihydroxyphenyl)-1,3,5-triazine CH2COOH OH nJ ? B. OH OH R2 = R5 = R6 = heteroaryl-R9 IIa-045a 4-(4-Carboxymethyl-2,5-dihydroxyphenyl)-6-(3,4-dihydroxyphenyl)-l,3,5-triazin-2-one COOH o o iz Yo IIa-047a 4-(4-Carboxymethyl-2,5-dihydroxyphenyl)-6-(3,5-dihydroxyphenyl)-l,3,5-triazin-2-one COOH OH I F      UH Y O IIa-048a 2-(4-Carboxy-2,5-dihydroxyphenyl)-4-(4-carboxymethyl- 2,5 -dihydro xypheny 1)-1,3,5 -triazine COOH Uh - 3 Ji If Y CH ‘K ., N r o IIa-049a 2-(3-Carboxy-2,5-dihydroxyphenyl)-4-(4-carboxyinethyl- 2,5 -dihydro xypheny 1)-1,3,5 -triazine COOH OH N JL 1 N^N Oh Ila-05 la 2-(4-Carboxymethyl-2,5-dihydroxyphenyl)-4-(3,4-dihydroxyphenyl)-1,3,5-triazine COOH J 1 T ' IIa-052a 2-(4-Carboxymethyl-2,5-dihydroxyphenyl)-4-(3,5-dihydroxyphenyl)-1,3,5-triazine COOH Oh YA H IVa-045a 4-(4-Carboxy-2,5-dihydroxyphenyl)-6-(3-carboxyinethyl- 2,5 -dihydro xypheny 1)-1,3,5 -triazin-2-one CH2COOH OH J. ,COOH '1 [ ' if / 1     \ - Il II I N.H OH IVa-046a 4-(3-Carboxy-2,5-dihydroxyphenyl)-6-(3-carboxyinethyl- 2,5 -dihydro xypheny 1)-1,3,5 -triazin-2-one CH2COOH OH OH n O ''COOH IVa-047a 4-(3-Carboxymethyl-2,5-dihydroxyphenyl)-6-(3,4-dihydroxyphenyl)-l,3,5-triazin-2-one CH2COOH H | IT Ah IVa-048a 4-(3-Carboxymethyl-2,5-dihydroxyphenyl)-6-(3,5-dihydroxyphenyl)-l,3,5-triazin-2-one CH2COOH OH Y o IVa-049a 2-(4-Carboxy-2,5-dihydroxyphenyl)-4-(3-carboxyinethyl- 2,5 -dihydro xypheny 1)-1,3,5 -triazine CH2COOH OH A ,COOH A x IVa-050a 2-(3-Carboxy-2,5-dihydroxyphenyl)-4-(3-carboxyinethyl- 2,5 -dihydro xypheny 1)-1,3,5 -triazine CH2COOH OH 0'1 IVa-051a 2-(3-Carboxymethyl-2,5-dihydroxyphenyl)-4-(3,4-dihydroxyphenyl)-1,3,5-triazine CH2COOH IVa-052a 2-(3-Carboxymethyl-2,5-dihydroxyphenyl)-4-(3,5-dihydroxyphenyl)-1,3,5-triazine CH2COOH XX 1 Y ^°H '4 N Preferably, the present invention provides a hydroquinone derivative compound of formula (I), wherein: (A) Ra, Rb = H; Ri = COOR4; (CH2)nCOOR4; SO3H, (CH2)nSO3H, CONH-Rw; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl;; R2 = H; R3 = R5; and Rs = R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, azoles [5-membered N-containing heterocycles], or fluorine; Or (B) Ra, Rb = H; Ri = COOR4; (CH2)nCOOR4; SO3H, (CH2)nSO3H, or CONH-R10; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; R3 = H; R2 = R5; and Rs = R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, azoles [5-membered N-containing heterocycles], or fluorine. According to a tenth embodiment, the present invention includes compounds in accordance with Table 10: Table 10 A. OH r3 OH R3 = R5 = R7 Compound No. Compound chemical names RI R3 Id-030a 2-(4-Carboxy-2,5-dihydroxyphenyl)-lH-benzo[d]imidazole-4-carboxylic acid COOH N   COOH Id-030a-E2 Methyl 2-(4-ethoxycarbonyl-2,5-dihydroxyphenyl)- IH-benzo [d] imidazole -4-carboxylate COOEt N   COOMe H' X— / Id-030b 2-(2,5-Dihydroxy-4-sulfophenyl)-lH-benzo[d]imidazole-4-carboxylic acid SO3H N   COOH Id-03 la 2-(4-Carboxy-2,5-dihydroxyphenyl)-lH-benzo[d]imidazole-5-carboxylic acid COOH N < %—COOH Id-03 lb 2-(2,5-Dihydroxy-4-sulfophenyl)-lH-benzo[d]imidazole-5-carboxylic acid SO3H ||_^^-COOH IIId-030a 2-(3 -Carboxy -2,5-dihydroxypheny 1)- 1H-benzo[d]imidazole-4-carboxylic acid CH2COOH N   COOH I"1         Xj— IIId-031a 2-(2,5-Dihydroxy-3-sulfophenyl)- 1H-benzo[d]imidazole-4-carboxylic acid CH2COOH y—COOH B. Ri^ R2 OH / Lr2 '']XH OH = R5 = R7 IId-030a 2-(3 -Carboxy -2,5-dihydroxypheny 1)- 1H-benzo[d]imidazole-5-carboxylic acid COOH COOH IId-030b 2-(2,5-Dihydroxy-3-sulfophenyl)- 1H-benzo[d]imidazole-5-carboxylic acid SO3H COOH H    \-s / nd-031a 2-(4-(Carboxymethyl)-2,5-dihydroxyphenyl)-lH-benzo[d]imidazole-4-carboxylic acid COOH J|—1^ J-—COOH IId-030a 2-(4-(Carboxymethyl)-2,5-dihydroxyphenyl)-lH-benzo[d]imidazole-5-carboxylic acid SO3H %—cooh I”! IVd-030a 2-(3-(Carboxymethyl)-2,5-dihydroxyphenyl)-lH-benzo[d]imidazole-4-carboxylic acid CH2COOH N   COOH IVd-031a 2-(3-(Carboxymethyl)-2,5-dihydroxyphenyl)-lH-benzo[d]imidazole-5-carboxylic acid CH2COOH Ji A—cooh H Preferably, the present invention provides a hydroquinone derivative compound of formula (I), wherein: (A) Ra, Rb = H, Cwacyl, arylCi-4alkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C?alkylNHCO, phosphono, 5 phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or Ci-Cgalkoxy carbonyloxy-1 -ethyl; Ri = COOR4; (CH2)nCOOR4; SO3H, (CH2)nSO3H, or CONH-R10; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl 10 (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci- Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; R2 = H; R3 = R5; and R5 = Rs = (CH2)mX(CH2)pR9; wherein X = O, S, SO2, NH, NAc, or N(CH2)qR9; 15 Or (B) Ra, Rb = H, Ci-4acyl, arylCi-4alkyl, Cg-CioarylCO, HOOC(CH2)nCO, Ci-C?alkylNHCO, phosphono, phosphonooxymethyl, Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxycarbonyloxymethyl, or Ci-Cgalkoxy carbonyloxy-1 -ethyl; 5 Ri = COOR4; (CH2)nCOOR4; SO3H, (CH2)nSO3H, or CONH-R10; R4 = H, Ci-4alkyl, arylCi-4alkyl, functionalized Ci-Cgalkyl including morpholino-Ci-Cgalkyl, pyrrolidino-Ci-Cgalkyl, N-methylpiperazino-Ci-Cgalkyl, Cg-Cioaryl including o-methoxyphenyl (guaiacol ester), Ci-Cgacyloxymethyl, Ci-Cgacyloxy-1-ethyl, Ci-Cgalkoxy carbonyloxymethyl, Ci-Cgalkoxycarbonyloxy-1 -ethyl, or (oxodioxolyl)methyl; 10 R3 = H; R2 = R5; and R5 = Rs = (CH2)mX(CH2)pR9; wherein X = O, S, SO2, NH, NAc, or N(CH2)qR9. According to an eleventh embodiment, the present invention includes compounds in accordance with 15 Table 11: Table 11 A. ORa R3 ORb R3 = (CH2)mX(CH2)pR9 No. Compound chemical names RI Ra Rb m X P R9 nic-056a Bis(4-carboxy-2,5-dihydroxyphenylmethyl)amine COOH H H 1 NH 1 4-carboxy-2,5-dihydroxyphenyl nic-056b 4-((2,5-Dihy droxy-4-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid SO3H H H 1 NH 1 4-carboxy-2,5-dihydroxyphenyl IIIc-056c Compound 267: 4-((2,5-Dihydroxy-3-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid COOH H H 1 NH 1 2,5-dihydroxy-3-sulfophenyl nic-056d Bis(2,5-dihydroxy-4-sulfophenylmethyl)amine SO3H H H 1 NH 1 2,5-dihydroxy-4-sulfophenyl nic-057a N,N-Bis(4-carboxy-2,5-dihydroxyphenylmethyl)acetamide COOH H H 1 NH(COCH3) 1 4-carboxy-2,5-dihydroxyphenyl nic-057b N-(2,5-dihydroxy-4-sulfophenylmethyl) N-(4-carboxy-2,5-dihydroxyphenylmethyl) acetamide SO3H H H 1 NH(COCH3) 1 4-carboxy-2,5-dihydroxyphenyl nic-057c N-(2,5-dihydroxy-3-sulfophenylmethyl) N-(4-carboxy-2,5-dihy droxyphenylmethyl) acetamide COOH H H 1 NH(COCH3) 1 2,5-dihy droxy-3-sulfophenyl nic-057d N,N-Bis(2,5-dihy droxy-4-sulfophenylmethyl)acetamide SO3H H H 1 NH(COCH3) 1 2,5-dihy droxy-4-sulfophenyl nic-058a 4-((2,5-Dihy droxy-4-carboxyphenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid COOH H H 1 S 1 4-carboxy-2,5-dihydroxyphenyl nic-058b 4-((2,5-Dihydroxy-4-sulfopheny l)methy lthiomethyl)-2,5 -dihydroxybenzoic acid SO3H H H 1 s 1 4-carboxy-2,5-dihydroxyphenyl nic-058c 4-((2,5-Dihydroxy-3-sulfopheny l)methy lthiomethyl)-2,5 -dihydroxybenzoic acid COOH H H 1 s 1 2,5-dihy droxy-3-sulfophenyl IIIc-058d 4-((2,5-Dihy droxy-4-sulfopheny l)methy Ithiomethy 1)-2,5 -dihydroxybenzenesulfonic acid; SO3H H H 1 s 1 2,5-dihy droxy-4-sulfophenyl nic-059a 4-((2,5-Dihy droxy-4-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid; COOH H H 1 SO2 1 4-carboxy-2,5-dihydroxyphenyl IIIc-059b 4-((2,5-Dihy droxy-4-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid; SO3H H H 1 SO2 1 4-carboxy-2,5-dihydroxyphenyl nic-059c 4-((2,5-Dihy droxy-3-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid COOH H H 1 SO2 1 2,5-dihy droxy-3-sulfophenyl IIIc-059d 4-((2,5-Dihy droxy-4-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzenesulfonic acid SO3H H H 1 SO2 1 2,5-dihy droxy-4-sulfophenyl IIIc-060a 4-((2,5-Dihy droxy-4-carboxyphenyl)methoxymethyl)-2,5-dihydroxybenzoic acid COOH H H 1 0 1 4-carboxy-2,5-dihydroxyphenyl IIIc-060b 4-((2,5-dihy droxy-4-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid; SO3H H H 1 0 1 4-carboxy-2,5-dihydroxyphenyl IIIc-060c 4-((2,5-dihy droxy-3-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid COOH H H 1 0 1 2,5-dihy droxy-3-sulfophenyl IIIc-060d 4-((2,5-Dihy droxy-4-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzenesulfonic acid SO3H H H 1 0 1 2,5-dihy droxy-4-sulfophenyl IIIc-061a Tris (4-carboxy-2,5-dihydroxyphenylmethyl)amine COOH H H 1 N(CH2)qR9 q= 1: R9 = 4-carboxy-2,5-dihydroxyphenyl 1 4-carboxy-2,5-dihydroxyphenyl inc-061a-E3 Tris (4-ethoxycarbonyl-2,5-dihydroxyphenylmethyl)amine COOEt H H (CH2)qR9 q= 1: R9 = 4-ethoxycarboxy-2,5-dihydroxyphenyl 1 4-ethoxycarbonyl-2,5-dihydroxyphenyl B. OR< ORI R2 = (CH2)mX(C a xR2 a H2)PR9 IVc-056a Bis(3-carboxy-2,5-dihydroxyphenylmethyl)amine COOH H H 1 NH 1 3-carboxy-2,5-dihydroxyphenyl IVc-056b 3-((2,5-Dihy droxy-3-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid SO3H H H 1 NH 1 3-carboxy-2,5-dihydroxyphenyl IVc-056c 3-((2,5-Dihy droxy-4-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid COOH H H 1 NH 1 2,5-dihydroxy-3-sulfophenyl IVc-056d Bis(2,5-dihydroxy-3-sulfophenylmethyl)amine SO3H H H 1 NH 1 2,5-dihydroxy-4-sulfophenyl IVc-057a N,N-Bis(3-carboxy-2,5-dihydroxyphenylmethyl)acetamide COOH H H 1 NH(COCH3) 1 3-carboxy-2,5-dihydroxyphenyl IVc-057b N-(2,5-dihydroxy-3-sulfophenylmethyl) N-(3-carboxy-2,5-dihydroxyphenylmethyl) acetamide SO3H H H 1 NH(COCH3) 1 3-carboxy-2,5-dihydroxyphenyl IVc-057c N-(2,5-dihydroxy-4-sulfophenylmethyl) N-(3-carboxy-2,5-dihydroxyphenylmethyl) acetamide COOH H H 1 NH(COCH3) 1 2,5-dihydroxy-3-sulfophenyl IVc-057d N,N-Bis(2,5-dihydroxy-3-sulfophenylmethyl)acetamide SO3H H H 1 NH(COCH3) 1 2,5-dihydroxy-4-sulfophenyl IVc-058a 3-((2,5-Dihy droxy-3-carboxyphenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid COOH H H 1 S 1 3-carboxy-2,5-dihydroxyphenyl IVc-058b 3-((2,5-Dihydroxy-3-sulfopheny l)methy lthiomethyl)-2,5 -dihydroxybenzoic acid SO3H H H 1 s 1 3-carboxy-2,5-dihydroxyphenyl IVc-058c 3-((2,5-Dihy droxy-4-sulfopheny l)methy Ithiomethy 1)-2,5 -dihydroxybenzoic acid COOH H H 1 s 1 2,5-dihydroxy-3-sulfophenyl IVc-058d 3-((2,5-Dihydroxy-3-sulfopheny l)methy lthiomethyl)-2,5 -dihydroxybenzenesulfonic acid SO3H H H 1 S 1 2,5-dihy droxy-4-sulfophenyl IVc-059a 3-((2,5-Dihy droxy-3-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid COOH H H 1 SO2 1 3-carboxy-2,5-dihydroxyphenyl IVc-059b 3-((2,5-Dihy droxy-3-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid SO3H H H 1 SO2 1 3-carboxy-2,5-dihydroxyphenyl IVc-059c 3-((2,5-Dihy droxy-4-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid COOH H H 1 SO2 1 2,5-dihy droxy-3-sulfophenyl IVc-059d 3-((2,5-Dihy droxy-3-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzenesulfonic acid SO3H H H 1 SO2 1 2,5-dihy droxy-4-sulfophenyl IVc-060a 3-((2,5-Dihy droxy-3-carboxyphenyl)methoxymethyl)-2,5-dihydroxybenzoic acid COOH H H 1 0 1 3-carboxy-2,5-dihydroxyphenyl IVc-060b 3-((2,5-dihy droxy-3-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid SO3H H H 1 0 1 3-carboxy-2,5-dihydroxyphenyl IVc-060c 3-((2,5-dihy droxy-4-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid COOH H H 1 0 1 2,5-dihy droxy-3-sulfophenyl IVc-060d 3-((2,5-Dihy droxy-3-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzenesulfonic acid SO3H H H 1 0 1 2,5-dihy droxy-4-sulfophenyl IVc-061a Tris (3-carboxy-2,5-dihydroxyphenylmethyl)amine COOH H H 1 N(CH2)qR9 q= 1: r9 = 3-carboxy- 2,5-dihydroxyph enyl 1 3-carboxy-2,5-dihydroxyphenyl IVc-059a- E2-A4 Methyl 3-((2,5-diacetoxy-3-methoxycarbonylphenyl)methylsulfonylmet hyl)-2,5-diacetoxybenzoate COOMe Ac Ac 1 SO2 1 2,5-diacetoxy-3-(methoxycarbonyl)phenyl IVc-059a-E2 Methyl 3-((2,5-dihy droxy-3-methoxycarbonylphenyl)methylsulfonylmet hyl)-2,5-hydroxybenzoate COOMe H H 1 SO2 1 2,5-dihy droxy-3-(methoxycarbonyl)phenyl IVc-059a-mpe2 2-Morpholinoethyl 3-((2,5-dihydroxy-3-(2-morpholinoethoxycarbonyl)phenyl)methyls ulfonylmethyl)-2,5-hydroxybenzoate COOR R=2-morphol inoethyl H H 1 SO2 1 2,5-dihy droxy-3-(2-morpholinoethoxycarbonyl) phenyl IVc-061a-E3 Tris (3-carboxy-2,5-dihydroxyphenylmethyl)amine COOEt H H 1 N(CH2)qR9 q= 1: r9 = 1 3-ethoxy carbonyl-2,5-dihydroxyphenyl 3-ethoxycarbo nyl-2,5-dihydroxyphenyl According to yet another embodiment, the present invention includes compounds in accordance with Table 12: Table 12 Compound No. Compound chemical names Structures V-OOla 4-(3-(2,5-dihydroxy-4-carboxyphenylcarbamoyl)-5-hydroxybenzamido)-2,5-dihydroxy benzoic acid OH                OH ““A, o o JyCOOH Wu OH V-OOla diethyl ester 4-(3-(4-(ethoxycarbonyl)-2,5- dihydroxyphenylcarbamoyl)-5-hydroxybenzamido)-2,5-dihydroxybenzoic acid ethyl ester OH                OH EtOOC^A.            A^COOEt UU !h h U H OH V-002a 2-hydroxy-5-(3 -hydroxy-5-(4-hydroxy-3 -carboxyphenylcarbamoyl)benzamido)benzoic acid COOH             COOH XX A JU OH V-002a diethyl ester 5-(3-(3 -(ethoxy carbonyl)-4-hydroxyphenylcarbamoyl)-5-hydroxybenzamido)-2-hydroxy benzoic acid ethyl ester COOEt              COOEt ho^A^           J\^oh 0     0 r T OH V-003a 4,4'-carbonylbis(azanediyl)bis(2,5-dihydroxybenzoic acid) QH H H QH 1 ri ri f j T Y 1 HOx^x^ O V^A^OH O OH        OH O V-003a diethyl ester Diethyl 4,4'-carbonylbis(azanediyl)bis(2,5-dihydroxybenzoate) ?H H H ?H jVynxS EtOxA^ O A=A / OEt O OH        OH O The present invention also relates to a process for the preparation of the hydroquinone derivative compound of formula (I), which comprises: Step (a): Coupling of hydroquinone-derived carboxylic acid, protected at the phenolic functions, with an aniline carrying diverse functional groups, by way of the corresponding acyl chloride or using an amide coupling agent such as TCFH in the presence of NMI; Step (b): Deprotection of the ester functions typically by a saponification reaction; and 5 Step (c): Deprotection of the phenolic functions typically by catalytic hydrogenation. Or, alternatively, Step (d): Reduction of the hydroquinone-derived carboxylic acid, protected at the phenolic functions, to produce a benzylic alcohol (e) Activation of the benzylic alcohol function and substitution with a benzylic nucleophile (alcohol, 10 thiol, primary or secondary amine) carrying diverse functional groups; (f) Deprotection of the ester functions typically by a saponification reaction; and (g) Deprotection of the phenolic functions typically by catalytic hydrogenation. The process is schematically represented below: 15 The hydroquinone derivative compounds of the present invention may be present as optically active forms (stereoisomers), E / Z isomers, enantiomers, racemates, diastereoisomers thereof, and hydrates and solvates thereof. Solvates of the compounds are due to the mutual attraction between the molecules of the compound and the inert solvent used. Solvates e.g. monohydrate, dihydrates or alcoholates. The hydroquinone derivatives of the present invention may also be present as pharmaceutically acceptable salts, wherein the parent hydroquinone derivatives are modified by preparing acidic or basic salts thereof. Examples of pharmaceutically acceptable salts include, among others, mineral or organic acid salts of basic residues, such as amines; and alkaline or organic salts of acidic residues, such as carboxylic acids and the like. Pharmaceutically acceptable salts may include conventional non-toxic salts or quaternary ammonium salts which are suitable for all routes of administration of the compounds, for example, from non-toxic organic or inorganic acids. For example, said conventional non-toxic salts include those derived from inorganic acids, such as hydrochloric, hydrobromic, sulfuric, sulfamic, phosphoric, nitric and the like; and salts prepared from organic acids such as acetic, propionic, succinic, glycolic, stearic, lactic, malic, tartaric, citric, ascorbic, pamoic, maleic, hydroxyleleic, phenylacetic, glutamic, benzoic, salicylic, sulfanyl, 2-acetoxy -benzoic, fumaric, toluene sulfonic, methanesulfonic, ethanedisulfonic, oxalic, isethionic, trifluoroacetic and the like. Pharmaceutically acceptable salts are described for cations and anions “Pharmaceutical salts: A summary on doses of salt formers from the Orange Book. Saal C, European Journal of Pharmaceutical Sciences, 2013, 49, 614-623. By way of examples of cations, we may cite aluminum, arginine, benzathine, calcium, chloroprocaine, choline, diethanolamine, diethylamine, ethanolamine, ethylenediamine, lysine, magnesium, histidine, lithium, meglumine, potassium, procaine, sodium, triethylamine, zinc, by way of examples of anions, we may cite acetate, aspartate, benzene sulfonate, benzoate, besylate, bicarbonate, bitartrate, bromide, camsylate, carbonate, chloride, citrate, decanoate, edetate, esylate, fumarate, gluceptate, gluconate, glutamate, glycolate, hexanoate, hydroxynaphthoate, iodide, isethionate, lactate, lactobionate, malate, maleate, mandelate, mesylate, methylsulfate, mucate, napsylate, nitrate, octanoate, oleate, pamoate, pantothenate, phosphate, polygalacturonate, propionate, salicylate, stearate, acetate, succinate, sulfate, tartrate, teoclate, tosylate. Alternatively, zwiterions may be used as salts such as free amino-acids arginine or lysine as cationic counterions and glutamate or aspartate as anionic counterions. Short peptides (2 to 20 amino acids) as repeated units of Arginine or Lysine and their combinations with other neutral amino acids. These cationic cell penetrating peptides (CPP) may be used as enhancers for the penetration of drug into cells. Pharmaceutically acceptable salts of the compounds useful in the present invention may be for example synthesized from the parent compound containing a basic or acidic moiety by conventional chemical procedures. Generally, said salts can be prepared by reacting the free acid or the basic forms of these compounds with a stoichiometric amount of the appropriate base or acid in water or in an organic solvent, or in a mixture of the two; In general, non-aqueous media such as ether, ethyl acetate, ethanol, isopropanol, or acetonitrile are preferred. In Remington’s Pharmaceutical Sciences, 17th ed., Mack Publishing Company, Easton, PA, 1985, p. 1418, whose disclosure is incorporated herein by reference, lists of suitable salts are presented. Suitable dosages according to the invention and as described herein in the various embodiments may vary depending upon the condition, age and species of the subject, and can be readily determined by those skilled in the art. The total daily dosages employed in both veterinary and human medicine will suitably be in the range 0.01 -2000 mg / kg body weight, preferably from 0.1-1000 mg / kg body weight, preferably from 1-100 mg / kg and these may be administered as single or divided doses, and in addition, the upper limit can also be exceeded when this is found to be indicated. Such dosage may be adjusted to the individual requirements in each case including the specific compounds being administered, the route of administration, the condition being treated, as well as the patient being treated. However, the compounds can also be administered as depot preparations (implants, slow-release formulations, etc.) weekly, monthly or at even longer intervals. In such cases the dosage may be much higher than the daily one and may be adapted to the administration form, the body weight, and the concrete indication. The appropriate dosage can be determined by conducting conventional model tests, preferably animal models. In general, in the case of oral or parenteral administration to adult humans weighing approximately 70 kg, a daily dosage of about 10 mg to about 10.000 mg, preferably from about 200 mg to about 1000 mg, should be appropriate, although the upper limit may be exceeded when indicated. It is to be understood that the above therapeutically effective dosages need not be the result of a single administration and are usually the result of the administration of a plurality of unit doses. Those unit doses can in turn comprise portions of a daily or weekly dosage, and thus, the therapeutically effective dose is determined over the period of treatment (contacting). For example, for oral administration, the daily dose can be about 0.04 to about 1.0 mg / kg of body weight, more preferably about 0.04 to about 0.20 mg / kg / day, more preferably still at about 0.05 to about 0.15 mg / kg / day, and most preferably about 0.1 mg / kg body weight. In general, the amount of active substance administered can vary over a relatively wide range to achieve, and preferably maintain, the desired plasma concentration. Unit dosage forms of the active ingredient can contain about 0.1 milligrams to about 15 milligrams thereof. A preferred unit dosage form contains about 0.1 to about 1 milligram of agent and can be administered 2 to 5 times per day. However, it should be noted that other alternative routes like continuous infusion at a rate designed to maintain the above-described plasma concentration is also contemplated. Duration of a particular treatment can also vary, depending on severity of the disease, whether the treatment is intended for an acute manifestation or for prophylactic purposes, and like considerations. Typical administration lasts for a time period of about 5 to about 14 days, with a 7-day time course being usual. Courses (cycles) of administration can also be repeated at monthly intervals, or parenteral unit dosages can be delivered at weekly intervals. Oral unit dosages can be administered at intervals of one to several days to provide the determined therapeutically effective dose. The appropriate dosage of the compounds of the invention will depend on the type of disease to be treated, on the severity and course of the disease, on whether the agent is administered for preventive or therapeutic purposes, of the patient's medical history, and of the response to the compounds, and of the criteria of the responsible physician. The determination of the appropriate dose or route of administration is clearly within the capabilities of a current physician. Animal experiments provide a reliable guide for the determination of effective doses for human therapy. The inter-species scaling of effective doses can be carried out following the principles established by Mordenti, J. and Chappell, W. "The use of interspecies scaling in toxicokinetics", in Toxicokinetics and New Drug Development, editors Yacobi et al., Pergamon Press, New York, 1989, pp. 42-96. The present invention further provides a pharmaceutical composition comprising (i) a therapeutically effective amount of the hydroquinone derivative compound of formula (I) or a pharmaceutically acceptable salt, or a prodrug, or stereoisomer thereof, and (ii) a pharmaceutically acceptable excipient or excipients. The pharmaceutical excipients according to the present invention may be selected from the group consisting of conventional excipients, such as but no limited to solubilizers, binders, fdlers, disintegrants, lubricants, pH modifiers, permeation enhancers, release modifiers, preservatives, coating agents, carriers, taste masking agents and combinations thereof. The pharmaceutical composition of the compounds of the present invention with one or more pharmaceutical components, may be formulated with said excipients as liquid medicines, solid or semisolid medicines, and / or gaseous medicines. When they are present in solid formulations, these may include without any limitations, granules, pellets, tablets, capsules, powders, films, lozenges, crushable tablets, dissolvable tablets, disintegrating tablets, dispersible tablets, film coated tablets, and controlled, sustained, extended, or modified release formats of any of the above-mentioned solid formats. Such formulations may also be in the forms of immediate release, delayed release, or modified release. Further, immediate release compositions may be conventional, dispersible, chewable, mouth dissolving, or flash melt preparations, and modified release compositions that may comprise hydrophilic or hydrophobic, or combinations of hydrophilic and hydrophobic, release rate controlling substances to form matrix or reservoir or combination of matrix and reservoir systems. The compositions may be prepared using any one or more of techniques such as direct blending, dry granulation, wet granulation, homogenization, milling, micronization, extrusion and spheronization. Compositions may be presented as uncoated, fdm coated, sugar coated, powder coated, enteric coated, and modified release coated. When they are present in liquid formulations, these may include without any limitations, any liquid forms such as solutions, suspensions, nanosuspensions, dispersions, colloids, emulsions, lotions, creams, ointments, tinctures, and freeze-dried compositions. When they are present in gaseous formulations these may include without any limitations, milled powder or blend, micronized powder, or blend, nanosuspensions, aerosols, sprays, droplets, mists, nebulised solutions, or suspensions, and / or atomized vapors. Pharmaceutical compositions according to the present invention may further comprise any additives such as vehicles, binding agents, perfumes, flavoring agents, sweeteners, colorants, antiseptics, antioxidants, stabilizing agents, and surfactants, if desired. Pharmaceutical compositions and compounds according to the present invention may be formulated for administration via enteral routes, such as oral routes; parenteral routes via injections such as intravenous, subcutaneous, intraocular, intramuscular, or intraperitoneal injections; topical routes, such as ocular routes, mucosal and transmucosal routes, including sublingual / buccal routes; as well as as pulmonary, nasal, intranasal, intrabronchial, intrapulmonary routes. Ocular routes of administration include topical ocular administration, intraocular, intravitreal, or retrobulbar administration. Preferred formulations of the compounds according to the present invention comprise liquid oral formulations, ocular formulations, and intravenous and intraperitoneal formulations. Liquid oral formulations are solution and suspension formats for oral drug administration are common, convenient, and deemed safe. They can be used to deliver relatively large quantities of drug and are frequently used for the paediatric population and for those who experience difficulties in swallowing tablets or capsules. Introduction via the gastrointestinal tract provides fast dissolution and drug absorption, however tolerability and interaction with other materials in the tract must be considered. Properties of the active pharmaceutical ingredient (API) can lend themselves to be formulated in simple aqueous based oral solutions however when API are poorly soluble, formulations need to be designed around the molecule to enhance solubility and bioavailability. Introduction of surfactant, solvents, buffers, and oils increase solubility and reduce precipitation and / or degradation on interaction with gastric fluids. Where suspensions are required, particle size is often reduced and controlled to enhance drug solubility, permeation and ultimately drug absorption. As formulation development progresses, preservatives and flavours are introduced to enable patient conformity and shelf-life appropriateness. Ocular formulations are ophthalmic formulations are delivered directly to the eye and are frequently liquids in solution or suspension formats. Administration to the eye avoids metabolism by the gastrointestinal tract and can be used for drugs which are poorly absorbed when given orally. Eye drops are sterile and isotonic with a nominal pH of 4-8 to avoid eye irritation. Excipients including solubilizing agents, chelating agents, polymers, surfactants, permeation enhancers and cyclodextrins are added to the formulation to improve stability, modify viscosity, or increase solubility, permeability, and bioavailability of poorly soluble drugs. Intravenous formulations allow rapid absorption after parenteral drug delivery of the entire dose reaching the patients system for an immediate response. This mode of introduction avoids metabolism by the gastrointestinal tract and can be used for drugs which are poorly absorbed when given orally. Injections are typically sterile, isotonic water-based solutions and are designed to not induce pain on administration. For poorly soluble drugs, formulations are modified with organic co-solvents, surfactants, and buffers to increase solubility with nano-suspension formulations also being acceptable. For those molecules which are unstable in solution, formulations can be lyophilised for dilution at the point of use. The present invention also provides kits, comprising a composition comprising a therapeutically effective dose of one or more compounds of the present invention or the formulations thereof as well as a delivery device for administration of the said composition or formulation and further comprising a package insert incorporating manual instructions for usage. To prepare the present pharmaceutical compositions, the active ingredient according to the invention may be mixed with a pharmaceutical acceptable carrier, adjuvant and / or excipient, according to conventional pharmaceutical compounding techniques. Pharmaceutically acceptable carriers that can be used in the present compositions encompass any of the standard pharmaceutical carriers, such as a phosphate buffered saline solution, water, and emulsions, such as an oil / water or water / oil emulsion, and various types of wetting agents. Compositions can additionally contain solid pharmaceutical excipients such as starch, cellulose, talc, glucose, lactose, sucrose, gelatin, malt, rice, flour, chalk, silica gel, magnesium stearate, sodium stearate, glycerol monostearate, sodium chloride, dried skim milk and the like. Liquid and semisolid excipients may be selected from glycerol, propylene glycol, polyethylene glycol, water, ethanol, and various oils, including those of petroleum, animal, vegetable or synthetic origin, e.g., peanut oil, soybean oil, mineral oil, sesame oil, etc. Liquid carriers, particularly for injectable solutions, include water, saline, aqueous dextrose, and glycols. For examples of carriers, stabilizers, and adjuvants, see Remington's Pharmaceutical Sciences, edited by E. W. Martin (Mack Publishing Company, 18th ed., 1990). The compositions also can include stabilizers and preservatives. Examples of pharmaceutically acceptable solvents that may be used in the present composition may be found in reference books such as the Handbook of Pharmaceutical Excipients (Ninth Edition, Pharmaceutical Press, London and American Pharmacists Association, Washington, 2020), Aulton's Pharmaceutics, The Design and Manufacture of Medicines. (Fifth edition, Editors: Kevin Taylor and Michael Aulton, Elsevier, 2017), "Ullmann's Encyclopedia of Industrial Chemistry, 6th Ed." (various editors, 1989-1998, Marcel Dekker) and in "Pharmaceutical Dosage Forms and Drug Delivery Systems" (ANSEL et al., 1994 et 2011, WILLIAMS & WILKINS). Non-limiting examples of pharmaceutically-acceptable solvents that may be used in the present composition include, but are not limited to, propylene glycol (also known as 1 ,2-dihydroxypropane, 2-hydroxypropanol, methyl ethylene glycol, methyl glycol or propane- 1 ,2-diol), ethanol, methanol, propanol, isopropanol, butanol, glycerol, polyethylene glycol (PEG), glycol, Cremophor EL or any forms of polyethoxylated castor oil, dipropylene glycol, dimethyl isosorbide, propylene carbonate, N-methylpyrrolidone, glycofurol, tetraethyleneglycol, propylene glycol fatty acid esters, and mixtures thereof. The compounds according to the invention have demonstrated anti-fibrotic, anti-inflammatory, and antiangiogenic effects. Several diseases listed herein after involving not only one but two or even the three targets. Disease Categories showing pre-dominant angiogenic (vascular), inflammatory and / or fibrotic pathobiology. In some embodiments the present invention is directed to pro-drugs of the compounds according to the present invention. Benefits of such prodrugs are obtained by methods known to a person of skill in art, for example by adding the appropriate cleavable functional groups that would generate for example, a better aqueous solubility for parenteral delivery or for oral delivery. Pro-drugs for molecules of the invention exhibiting very polar and charged properties is especially preferred as these functional groups may positively influence the passive permeability across biological membranes. The main obstacles for polar and charged drugs is their poor membrane permeability which often leads to low and variable oral absorption and to low oral bioavailability. Furthermore, oral absorption of polar and charged drugs is often associated with substantial interspecies variability. Poorly permeable drugs also have low exposure levels in specific target organs even after topical administration. Improving membrane permeability has been one of the most fruitful areas of prodrug research to date. Different prodrug strategies have been developed for the drugs according to the invention to overcome topical route barriers onto the eye, oral mucosa barriers, transprter effects or other topical uses. Prodrug strategies were formally recognized by Adrian Albert in 1958 (Albert, A. Chemical aspects of selective toxicity. Nature, 1958, 182, 421-422) but started in the early part of the previous century, as exemplified by methenamine, phenacetin and prontosil. Prodrugs are molecules with little or no pharmacological activity but have a built-in structural lability, whether by chance or by design, that permits bioconversion in vivo into the active drug. The conversion can occur through a chemical or enzymatic process or a combination of the two. Active molecules are often associated with undesirable physicochemical properties that create considerable challenges for their delivery to the appropriate biological target. Prodrugs obtained via structural modifications of the drug are designed to influence the inherent physicochemical properties of a molecule to enable its delivery. These developments are not always integrated into the design of new molecules at the discovery phase. Often the analogue optimization, is the preferred path forward. Implementing an early prodrug strategy may result in more rapid clinical development and, ultimately, commercialization of a drug product. Prodrug strategies for the most common functional groups on parent drugs are described in Rautio J, 2018 (Jarkko Rautio et al, Nature Reviews Drug Discovery, 2018, 17, 559-587). This review describes the expanding role of prodrugs in contemporary drug design and development and the prodrug strategies for the most common functional groups on parent drugs. Benefits of prodrugs are obtained by adding the appropriate cleavable functional groups that would generate for example, a better aqueous solubility for parenteral delivery or for oral delivery. On the other hand, for very polar and charged molecules, these functional groups may positively influence the passive permeability across biological membranes. The main obstacles for polar and charged drugs is their poor membrane permeability which often leads to low and variable oral absorption and to low oral bioavailability. Furthermore, oral absorption of polar and charged drugs is often associated with substantial interspecies variability. Poorly permeable drugs also have low exposure levels in specific target organs even after topical administration. Improving membrane permeability has been one of the most fruitful areas of prodrug research to date. Many prodrug strategies can be applied to influence the lipophilicity of a parent drug. Lipophilicity of drugs has been improved by masking its polar and ionized functionalities by short-chain hydrocarbon promoieties. Hydrophilic hydroxyl, carboxyl, phosphate or amine and other negatively or positively charged groups have been successfully converted to more lipophilic alkyl or aryl esters or N-acyl derivatives, which are rapidly hydrolysed back to the parent drugs in the body by ubiquitous esterases or peptidases. The majority of lipophilic prodrugs have been developed to improve membrane permeability and oral absorption. The same prodrug strategy can be applied to improve topical administration of parent drugs that are absorbed through the skin or eye. During topical administration on the eye, the prodrug readily penetrates the cornea after instillation where it is hydrolysed predominately by ocular carboxylesterase. Prodrugs can also exploit carrier-mediated transport. These transporters are membrane proteins that play an important role in controlling the intake and efflux of crucial polar endogenous nutrients. Their specificity is not limited to endogenous substrates, and drugs that bear a close structural resemblance to endogenous substrates, can also be carried across cell membranes by transporters. Carrier-mediated transport is particularly important for polar and charged drugs, as they have negligible passive diffusion across biological membranes. Prodrugs that can take advantage of carrier-mediated transport mechanisms offer intriguing targets in drug design. Similarly, prodrugs can bring improved metabolic stability. Prodrugs can improve metabolic instability which is typically attributed to hepatic metabolism. Similarly, unwanted intestinal metabolism of drugs can be overcomed by selective prodrug strategies. This instability can greatly reduce the total amount of a drug that reaches the systemic circulation and its target. Prodrugs can be used to protect active drugs from this first-pass effect by masking a metabolically labile but pharmacologically essential functional group, such as a phenol, to avoid rapid metabolism. To solve the problem of insufficient plasma levels and prolong the duration of action, drugs are usually controlled by formulations, such as suspensions and polymeric matrices, which control drug release and avoid peak effects and prolong their actions. Prodrugs can be used to achieve controlled release of an active drug by modifying its aqueous solubility and dissolution properties in a way that affects the release rate of the active drug, the rate of absorption or its tissue distribution. Prodrugs have been especially useful in the development of several subcutaneous or intramuscular sustained-release depot injections, which maintain therapeutic plasma levels of a parent drug for weeks to months. These prodrugs are typically fatty acid esters, such as decanoates, palmitates, enanthates, cypionates or valerates, that are formulated in an oil-based vehicle, which results in the slow release of the prodrug and, hence, modulates the disposition of the parent drug. The high lipophilicity of these prodrugs also results in binding to blood and tissue proteins, which slows enzymatic conversion and consequently results in the slow appearance of an active drug in the systemic circulation. Better targeting and lower side effects is often achieved with prodrugs targeting cleaved in an acidic environment of a tumor tissue, in endosomes or lysosomes with an acid labile prodrug. A similar approach is also achieved using site-specific enzymes and the prodrug is predominately cleaved in the desired organ or tissue where the enzyme is at the highest concentration. For charged drugs, the intracellular cleavage leads to high cellular concentration of the negatively or positively charged drug which stay confined in the target cell. Different prodrug strategies have been developed for the drugs according to the invention to overcome topical route barriers onto the eye, oral mucosa barriers, transporter effects or other topical uses. Drugs according to the invention are bearing charged polar groups. The problem to solve depends on the route of administration and the need for a long or short duration of drug action. Examples of prodrugs that are cleaved by mouse as well as human tissue and blood esterases have been synthesized successfully. The compounds of the invention carry carboxylic functions and phenol groups. A wide diversity of prodrugs derived from these functions can be considered : for exemple, carboxylic acids have been converted most frequently into esters: simple alkyl esters (methyl, ethyl, isopropyl and longer chains), functionalized alkyl esters such as morpholinoalkyl esters, pyrrolidinoalkyl esters, N-methylpiperazino-alkyl esters, also aryl esters such as guaiacol derived esters; mixed acetal esters such as acyloxymethyl (or 1-ethyl) or alkoxycarbonyloxymethyl (or 1-ethyl) esters and (oxodioxolyl)methyl esters are also efficient prodrug functions for carboxylic acids. A diversity of esters and functionalized ethers have been used as prodrugs based on phenols: simple aliphatic esters, aromatic esters, hemiesters of dicarboxylic acids, amino acid esters, carbamate esters, phosphate monoesters, phosphonooxymethyl ethers, acyloxymethyl (or 1-ethyl) ethers, alkoxycarbonyloxymethyl (or 1-ethyl) ethers, aminoacyloxymethyl ethers, and the like. Therefore, the present invention provides a method of treating and / or preventing a disease or disorder autoimmune, immunological, rheumatology, vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic and gastro-intestinal disorders, neuroinflammatory and neurodegenerative diseases, neoplasms and cancer associated disorders, hormone related diseases and immunological disorders resulting from viral and bacterial infectious diseases and complications thereof, comprising administering a subject in a need a therapeutically effective dose of the compounds and / or pharmaceutical compositions of the present invention as described above. Pharmaceutical compositions and methods according to the present invention are particularly suitable for a subject which is a human or non-human animal subject. Compounds according to the invention may target diseases basis on their individual cytokine profiles as described in BIODATA provided for several compounds (See Figures 3A-D). The following web site Open Targets Platform (URL: https: / / www.targetvalidation.org / , Denise Carvalho et al, Nucleic Acids Research, Volume 47, Issue DI, 08 January 2019, D1056-D1065, https: / / doi.org / 10.1093 / nar / gkyll33) gives a complete picture based on current bibliographic information and can be searched by disease or cytokine. Two typical examples: (a) disease specific search for diabetic retinopathy leads to the following cytokines described with a high correlation with the disease (Figure 3C). The three top cytokines are as an example for diabetic retinopathy search indicate VEGFA score = 1 (vascular endothelial growth factor A), HFE score = 1 (homeostatic iron regulator) and TNF score = 0.86 (tumor necrosis factor) and (b) searching for VEGFA: leads to nervous system disease, vascular disease, eye disease, retinopathy and several other diseases shown in Figure 3D. To illustrate the potency of compounds on small group of inflammatory cytokines, the effects of the compounds were assessed on human whole blood (Example 3.6) and their IC50 values on inhibition of LPS induced inflammation (Table 13, in pM). Table 13: Compound GM-CSF IFNy IL-lb IL-2 IL-4 IL-5 IL-6 IL-9 IL-10 IL-12p70 IL-13 IL-17A IL-17F IL-18 IL-21 IL-33 TGFbeta TNFa TNF|3 la-OOla 100 30.5 34.4 94.3 100 100 1.24 5.63 100 1.5 26.4 0.1 14.7 100 100 19.3 100 0.02 13.20 la-OOla-Tz 100 100 100 7.99 100 100 0.75 8.63 26.1 32.4 32.1 0.11 46.5 100 100 23.6 100 0.63 53.00 la-OOla- Tz / 004a 3.4 0.61 100 4.91 100 100 3.04 8.48 19.5 12.2 1.5 0.02 2.4 46.6 0.3 1.67 100 0.002 3.02 lc-001a-Tz2 100 1.38 100 9.45 100 100 0.52 9.13 100 29.1 0.12 0.31 0.15 33.9 32 0.23 100 0.1 0.41 la-OOlc 100 0.44 100 12.8 100 100 0.95 46.9 1.9 0.44 86.1 0.09 89.7 100 100 100 100 0.05 29.70 la-003a-Tz 100 2.95 100 43 100 100 1.41 3.62 6.94 1.26 89.6 0.07 83.9 100 1.49 72.2 100 0.18 55.00 lc-007a 100 1.44 100 100 100 100 0.09 27.1 12.5 0.49 30.1 0.04 22.9 100 1.9 18.4 100 0.27 6.52 Ib-OlOa 100 2.22 33.3 2.74 100 100 1.02 11.58 100 0.27 100 0.42 100 100 67.8 31.3 100 0.31 49.30 lb-010a-E3 100 2.79 100 36.2 100 100 0.24 26.8 100 0.84 33 0.52 34.2 100 100 20 100 0.98 38.20 la-015a 2.76 100 100 7.08 100 100 0.77 1.47 5.27 0.12 0.15 0.05 0.15 100 57.2 0.24 100 0.17 0.30 llc-007a 26 0.11 100 12.8 100 100 0.05 2.14 17.9 3.37 0.25 0.01 0.26 100 9.41 0.18 100 0.03 0.29 llc-009a 100 0.54 100 19.6 100 100 0.27 18.9 11.31 100 0.13 0.001 0.13 2.95 8.01 0.29 100 0.11 6.94 lla-053a 100 1.04 100 1.67 100 100 2.2 1.41 100 0.27 29.9 100 28.8 100 100 12.1 100 0.02 91.50 IHa-OOlaTz 100 18.9 100 100 100 100 1.98 3.01 7.78 0.48 0.15 0.17 0.16 T1J 3 0.14 100 0.31 0.23 llla-013a 27.8 0.15 100 57.1 100 100 3.55 11.9 37.3 0.5 0.37 0.15 0.41 100 1.63 1.11 100 0.51 0.89 lllc-057a 100 0.9 16.2 24.2 100 100 0.19 11.1 100 0.73 4.73 1.32 5.06 100 1.56 2.93 100 0.15 1.58 lllc-061a 31.2 2.48 100 100 100 100 0.18 8.85 17.9 37.2 0.31 0.04 0.32 32.4 6.38 0.31 100 0.03 0.81 IVc-058a 100 10.6 27.5 3.82 100 100 0.21 31.1 16.4 4.23 55.9 0.1 86.8 100 3.2 33.9 100 0.18 59.30 IVc-059a 100 4.34 38.6 21.2 100 100 0.11 0.4 1.31 42 100 0.16 100 100 1.87 27.5 100 0.16 0.33 IVc-O59a-E2- A4 1.83 3.5 14.1 10.4 100 100 0.99 2.9 16.8 51.4 18.7 0.02 25.8 100 100 23.2 100 0.3 19.40 Immunological / rheumatology / vascular disorders may include for example peritonitis, Kawasaki disease (KD), Takayasu arteritis (TA), microscopic polyangiitis (MP), giant cell arteritis (GCA), 5 antiphospholipid syndrome (APS), Behcet’s Disease (BD), granulomatosis with polyangiitis (GPA) or Wegener's granulomatosis (WG), eosinophilic granulomatosis with polyangiitis, Churg-Strauss syndrome (EGPA), and rosacea (RO). Rheumatology’s disorders in particular affect joints tendons, ligaments and bones with pain, loss of motions, and inflammation. These include many types of arthritis such as osteoarthritis (OA), rheumatoid arthritis (RA), lupus, spondyloarthropathies: ankylosing spondylitis (AS) and psoriatic arthritis (PsA), Sjogren’s syndrome, Gout, scleroderma, Infectious arthritis, juvenile idiopathic arthritis, polymyalgia rheumatica. Peritonitis is an inflammation of the peritoneum usually due to a bacterial or fungal infection. There are two types of peritonitis. First type is spontaneous peritonitis which may develop as a complication of liver disease, such as cirrhosis, or of kidney disease. Secondary peritonitis may result from abdomen perforation, or as a complication of other medical conditions. Left untreated, peritonitis can lead to severe, potentially life-threatening infection. Kawasaki Disease causes inflammation in the walls of medium-sized arteries throughout the body. It primarily affects children. The inflammation tends to affect the coronary arteries, which supply blood to the heart muscle. Kawasaki disease is sometimes called mucocutaneous lymph node syndrome because it also affects lymph nodes that swell during an infection, skin, and the mucous membranes inside the mouth, nose and throat. Takayasu Arteritis is a rare type of vasculitis, a group of disorders that cause blood vessel inflammation. In Takayasu's arteritis, the inflammation damages the aorta and its main branches. The disease can lead to narrowed or blocked arteries, or to aneurysm. Takayasu's arteritis can also lead to arm or chest pain, high blood pressure, and eventually heart failure or stroke. Medications are needed to control the inflammation in the arteries and prevent complications. Granulomatosis with polyangiitis is an uncommon disorder that causes inflammation of the blood vessels in the nose, sinuses, throat, lungs and kidneys. Formerly called Wegener's granulomatosis, this condition is one of a group of blood vessel disorders called vasculitis. It slows blood flow to some organs. The affected tissues can develop areas of inflammation called granulomas, which can affect how these organs work. Without treatment, the condition can be fatal. Giant cell arteritis is an inflammation of the lining of the arteries. Most often, it affects the arteries in the head, especially in the temples. For this reason, giant cell arteritis is sometimes called temporal arteritis. Giant cell arteritis frequently causes headaches, scalp tenderness, jaw pain and vision problems. Untreated, it can lead to blindness. Antiphospholipid syndrome occurs when the immune system mistakenly creates antibodies that make blood much more likely to clot. This can cause dangerous blood clots in the legs, kidneys, lungs and brain. In pregnant women, antiphospholipid syndrome also can result in miscarriage and stillbirth. There is no cure for antiphospholipid syndrome. Only medications available can reduce risk of blood clots. Behcet's disease, also called Behcet's syndrome, is a rare disorder that causes blood vessel inflammation. The disease can lead to numerous signs and symptoms that can seem unrelated at first. They can include mouth sores, eye inflammation, skin rashes and lesions, and genital sores. Current treatment may help reducing the symptoms of Behcet's disease and to prevent serious complications, such as blindness. Churg-Strauss syndrome is a disorder marked by blood vessel inflammation. This inflammation can restrict blood flow to organs and tissues, sometimes permanently damaging them. This condition is also known as eosinophilic granulomatosis with polyangiitis (EGPA). Asthma is the most common sign of Churg-Strauss syndrome. The disorder can also cause other problems, such as hay fever, rash, gastrointestinal bleeding, and pain and numbness in hands and feet. Churg-Strauss syndrome has no cure. Current medications include steroids and other powerful immunosuppressant drugs to help to control symptoms. Rosacea is a common skin condition that causes redness and visible blood vessels in the face. It may also produce small, red, pus-filled bumps. These signs and symptoms may flare up for weeks to months and then go away for a while. Rosacea can be mistaken for acne, other skin problems or natural ruddiness. There is no cure for rosacea, but treatment can control and reduce the signs and symptoms. Osteoarthritis is the most common form of arthritis, affecting millions of people worldwide. It occurs when the protective cartilage wears down over time. Although osteoarthritis can damage any joint, the disorder most commonly affects joints in hands, knees, hips and spine. Osteoarthritis symptoms can usually be managed, although the damage to joints cannot be reversed. Lupus is an autoimmune disease. It causes the immune system to produce proteins called autoantibodies that attack own tissues and organs, including the kidneys. Lupus nephritis is a frequent complication in people who have systemic lupus erythematosus (commonly known as lupus). Lupus nephritis occurs when lupus autoantibodies affect structures of the kidneys. This causes kidney inflammation and may lead to blood in the urine, protein in the urine, high blood pressure, impaired kidney function or even kidney failure. Scleroderma is a group of rare diseases that involve the hardening and tightening of the skin and connective tissues. There are many different types of scleroderma. In some people, scleroderma affects only the skin. But in many people, scleroderma also harms structures beyond the skin, such as blood vessels, internal organs and the digestive tract (systemic scleroderma), there is no cure for scleroderma. Sjogren's syndrome is a disorder of the immune system identified by its two most common symptoms: dry eyes and a dry mouth. The condition often accompanies other immune system disorders, such as rheumatoid arthritis and lupus. In Sjogren's syndrome, the mucous membranes and moisture-secreting glands of the eyes and mouth are usually affected first — resulting in decreased tears and saliva. Infectious or septic arthritis is a painful infection in a joint that can come from germs that travel through the bloodstream from another part of the body. Septic arthritis can also occur when a penetrating injury, such as an animal bite or trauma, delivers germs directly into the joint. People who have artificial joints are also at risk of septic arthritis. Knees are most commonly affected, but septic arthritis also can affect hips, shoulders and other joints. The infection can quickly and severely damage the cartilage and bone within the joint, so prompt treatment is crucial. Juvenile idiopathic arthritis, formerly known as juvenile rheumatoid arthritis, is the most common type of arthritis in children under the age of 16. Juvenile idiopathic arthritis can cause persistent joint pain, swelling and stiffness. Some children may experience symptoms for only a few months, while others have symptoms for many years. Some types of juvenile idiopathic arthritis can cause serious complications, such as growth problems, joint damage, and eye inflammation. Polymyalgia rheumatica is an inflammatory disorder that causes muscle pain and stiffness, especially in the shoulders and hips. Signs and symptoms of polymyalgia rheumatica usually begin quickly and are worse in the morning. Most people who develop polymyalgia rheumatica are older than 65. This condition is related to another inflammatory condition called giant cell arteritis. Ophthalmologic disorders may include for example and without any limitations, age macular degeneration (AMD or ARMD, dry and wet forms), pterygium (PTE), diabetic retinopathy (DR), diabetic macular edema (DME), Stargardt disease (SD), proliferative vitreoretinopathy (PVR), dry eye syndrome (DYS), endophthalmitis, central serous chorioretinopathy (CSC), retinitis pigmentosa (RP), glaucoma and glaucoma associated complications, and uveitis (UVE). Wet macular degeneration is a chronic eye disorder that causes blurred vision or a blind spot in the visual field. It is generally caused by abnormal blood vessels that leak fluid or blood into the macula. The macula is in the part of the retina responsible for central vision. Wet macular degeneration is one of two types of age-related macular degeneration. The wet type always begins as the dry type. Dry macular degeneration is more common and less severe. It also causes blurred or reduced central vision, due to thinning of the macula. Dry macular degeneration may first develop in one or both eyes and then affect both eyes. Vision loss is typically central but is retained in the peripheral vision. Diabetic retinopathy is a diabetes complication that affects eyes. It is caused by damage to the blood vessels of the retina. At first, diabetic retinopathy may cause no symptoms or only mild vision problems. Eventually, it can cause blindness. The condition can develop in anyone who has type 1 or type 2 diabetes. DME is a serious eye complication which occurs when microaneurysms protrude from the vessel walls, leaking or oozing fluid and blood into the retina, thereby causing edema in the macula. Stargadt disease is an eye disease that causes vision loss in children and young adults. It is an inherited disease and thus is passed on to children from their parents. Stargardt disease is a form of macular degeneration and is often called juvenile macular degeneration. PVR is a disease that develops as a complication of rhegmatogenous retinal detachment. PVR occurs in about 8-10% of patients undergoing primary retinal detachment surgery and prevents the successful surgical repair of rhegmatogenous retinal detachment. PVR can be treated with surgery to reattach the detached retina but the visual outcome of the surgery is very poor. Dry eye disease is a common condition that occurs when tears are not able to provide adequate lubrication of the eyes. Tears can be inadequate and unstable for many reasons. For example, dry eyes may occur if you do not produce enough tears or if you produce poor-quality tears. This tear instability leads to inflammation and damage of the eye's surface. Endophthalmitis is an inflammation of the inside of the eye which may occur after eye injection or surgery. Signs are typically: blurred vision or other changes in vision, eye pain, redness of the eye, sensitivity of the eye to light, or tearing. Retinitis pigmentosa (RP) is a group of rare, genetic disorders that involve a breakdown and loss of cells in the retina, which is the light sensitive tissue that lines the back of the eye. Common symptoms include difficulty seeing at night and a loss of side (peripheral) vision. Glaucoma is a group of eye conditions that damage the optic nerve, the health of which is vital for good vision. This damage is often caused by an abnormally high eye pressure. Glaucoma is one of the leading causes of blindness for people over the age of 60. It can occur at any age but is more common in older adults. Many forms of glaucoma have no warning signs. The effect is so gradual with no change in vision until the condition is at an advanced stage. Uveitis is a form of eye inflammation. It affects the middle layer of tissue in the eye wall or uvea. Uveitis warning signs often come on suddenly and get worse quickly. They include eye redness, pain, and blurred vision. Possible causes of uveitis are infection, injury, or an autoimmune or inflammatory disease. Uveitis can be serious, leading to permanent vision loss. Compounds and pharmaceutical compositions according to the present invention may also be used in a method of treating and / or preventing retinal neurodegenerative disease selected from the group consisting of diabetic retinopathy, age-related macular degeneration, glaucoma, and retinitis pigmentosa. Retinal neurodegenerative diseases refer to retinal conditions characterized by progressive neuronal loss. Diabetic retinopathy, age-related macular degeneration, glaucoma, and retinitis pigmentosa are considered retinal diseases in which neurodegeneration plays an essential role. According to this preferred embodiment, the compounds according to the present invention may be combined with other active agents to enhance the therapeutic efficacy of the condition to be treated and particularly with dipeptidyl peptidase-4 inhibitor (DPPIV) or a pharmaceutically acceptable salt thereof, for use in the topical eye treatment and / or prevention of a retinal neurodegenerative disease. The DPPIV inhibitor may be selected from the group consisting of sitagliptin, saxagliptin, vildagliptin, linagliptin, anagliptin, teneligliptin, alogliptin, trelagliptin, gemigliptin, omarigliptin, its pharmaceutically acceptable salts, and mixtures thereof. Compounds according to the present invention may be also advantageously combined with anti-VEGF treatment in order to reduce the number of intraocular anti-VEGF antibody injections needed by the patients. Administration to the patients having retinal neurodegenerative diseases, such as for example diabetic retinopathy, age related macular degeneration slows the progression of these diseases and reduces the anti-VEGF pharmacotherapy that patients need. Fibrotic disorders may include for example and without any limitations, cystic fibrosis, retroperitoneal fibrosis, idiopathic pulmonary fibrosis, combined pulmonary fibrosis & emphysema (CPFE), eosinophilic angiocentric fibrosis, intestinal fibrosis, ovarian fibrosis, nephrotenic systemic fibrosis, oral submucous fibrosis (OSMF) and liver fibrosis. Cystic fibrosis (CF) is an inherited disorder that causes severe damage to the lungs, digestive system, and other organs in the body. It affects the cells that produce mucus, sweat and digestive juices. Instead of acting as lubricants, the secretions plug up tubes, ducts, and passageways, especially in the lungs and pancreas. Pulmonary fibrosis is a lung disease that occurs when lung tissue becomes damaged and scarred. This thickened, stiff tissue makes it more difficult for the lungs to work properly. The scarring associated with pulmonary fibrosis can be caused by a multitude of factors. The lung damage caused by pulmonary fibrosis cannot be repaired, but medications and therapies can sometimes help ease symptoms and improve quality of life. Emphysema is a lung condition that causes shortness of breath. The alveoli are damaged, and overtime, the inner walls of the alveoli weaken and rupture, creating larger air spaces instead of many small ones. This reduces the surface area of the lungs and, in turn, the amount of oxygen that reaches the bloodstream. Damaged alveoli do not work properly, leading to old air being trapped, and leaving no room for fresh, oxygen-rich air to enter. Metabolic & gastro-intestinal disorders may include for example and without any limitations, diabetes induced complications: diabetic nephropathy (DN), diabetic retinopathy (DR), diabetic cardiomyopathy (DCDM), or diabetic foot ulcer (DFU). Hepatic diseases may include Nonalcoholic fatty liver disease (NAFLD), non alcoholic steatic hepatosis (NASH), primary biliary cholangitis (PBC), hepatic fibrosis or cirrhosis (HF), inflammatory bowel disease (IBD): ulcerative colitis, Crohn’s disease, intestinal fibrosis. In addition to diabetic nephropathy, other kidney diseases may include polycystic kidney disease (PKD), chronic kidney disease (CKD), nephrogenic systemic fibrosis (NSF), and pancreatitis (acute and chronic). Diabetic nephropathy is a serious kidney-related complication of type 1 diabetes and type 2 diabetes. It is also called diabetic kidney disease. About 25% of people with diabetes eventually develop kidney disease. Diabetic nephropathy affects kidneys' ability to do their usual work of removing waste products and extra fluid from the body. Over many years, the condition slowly damages kidneys' delicate filtering system, and may progress to kidney failure, also called end-stage kidney disease. Kidney failure is a lifethreatening condition. Nonalcoholic fatty liver disease (NAFLD) is an umbrella term for a range of liver conditions affecting people who drink little to no alcohol. As the name implies, the main characteristic of NAFLD is too much fat stored in liver cells. The most common form of chronic liver disease. Some individuals with NAFLD can develop nonalcoholic steatohepatitis (NASH), an aggressive form of fatty liver disease, which is marked by liver inflammation and may progress to advanced scarring (cirrhosis) and liver failure. This damage is similar to the damage caused by heavy alcohol use. Primary biliary cholangitis is a chronic autoimmune disease in which the bile ducts in the liver are slowly destroyed. When the bile ducts are damaged, bile can back up in the liver and sometimes lead to irreversible cirrhosis. A combination of genetic and environmental factors triggers the disease. IBD describes disorders that involve chronic inflammation of the digestive tract. Types of IBD include ulcerative colitis which involves ulcers along the superficial lining of the colon and rectum, as well as Crohn's disease which is characterized by inflammation of the lining of the digestive tract, which often can involve the deeper layers of the digestive tract. Both ulcerative colitis and Crohn's disease usually are characterized by diarrhea, rectal bleeding, abdominal pain, fatigue, weight loss, and sometimes lead to life-threatening complications. Neoplasms and cancer associated disorders may include for example and without any limitations, pancreatic cancer: mostly fibrotic, renal cell carcinoma, radiation induced fibrosis, primary myelofibrosis, desmoplasia, fibrosarcoma, hepatocellular carcinoma, retinoblastoma, intra-ocular lymphoma, and melanoma (desmoplastic, conjunctival, uveal). The invention also relates to the treatment, prevention, and reduction of viral infections via binding to virus proteins heparan sulfate binding sites. The compounds according to the invention interact with the heparan sulfate binding region of Growth factors (FGF, VEGF and other growth factors) and Growth factor receptors (FGFR, VEGFR and others). Many viruses are known to interact with mammalian cells using their affinity to heparan sulfate moieties bound to cell membranes. Viruses bearing on their surface proteins heparan sulfate (HS) binding domains use this HS affinity as one of the main entrance doors to approach and infect cells and bind to heparan sulfate attached to the cells. When attached to HS viruses are able to infect cells using various invading mechanisms specific to each virus. The strong interaction of the compounds according to the invention with the heparan binding domain of proteins and specifically viral proteins is preventing viral infection of blood cells, endothelial cells lining blood vessels and organs as well as surface epithelial cells present in the mouth, nasal mucosa, and lungs and also in the gastrointestinal tract. Several virus species are known with high affinity to heparan sulphates such as but not limited to respiratory syncytial virus, human metapneumovirus, influenza (H1N1 and the like), human rhinovirus (HRV), rhinosyncitial virus (RV), chikungunya virus, coronavirus such as CoV, SARS-CoV, MERS-Cov, COVID-19 (SARS-CoV-2 and their variants). HS is a necessary co-factor for SARS-CoV-2 infection. HS interacts with the receptor-binding domain of the SARSCoV-2 spike glycoprotein, adjacent to ACE2, shifting the spike structure to an open conformation to facilitate ACE2 binding. Viral and bacterial infectious diseases may also include septic shock, inflammation in the eye such as endophthalmitis due to surgery or infection. EXAMPLES EXAMPLE 1: Synthesis of the compounds and intermediates Example 1.1: Molecules of type la: Monoamides, 25 examples SYNTHESIS OF PRECURSORS Scheme 1. Synthetic Intermediates KI-1 and KI-6 Procedures: Synthesis of KI-1 an KI-6 (steps [1],[2]) Diethyl 2,5-bis(benzyloxy)terephthalate (KI-0) (Step [1]). Potassium carbonate-325 mesh (326.1 g, 2.4 mol) was added portion wise to a stirred solution of diethyl 2,5-dihydroxyterephthalate (200.0 g, 0.79 mol) in DMF (800.0 mL) at ambient temperature over 15 min. Benzyl bromide (280.0 mL, 2.4 mol) was then added to the reaction flask in a dropwise manner over 30 min, and the resulting mixture was heated at 100 °C for 2 h, resulting in the formation of a thick cream-coloured precipitate. The reaction mixture was cooled down to ambient temperature and treated with a solution of saturated aqueous ammonium chloride (2 L). The resulting suspension was stirred for 30 min, then filtered. The solid material was washed with a solution of saturated aqueous ammonium chloride (2 x 200 mL). The solid was then suspended in ethanol (400 mL), filtered and dried in the vacuum oven to give the desired product as a white solid (341.0 g, 0.785 mol, 99.8%) UPLC-MS (acidic method, 2 min): rt = 1.36 min, no ionization observed, peak area >95% 'H NMR (400 MHz, DMSO-J6) 5 7.51-7.44 (m, 6H), 7.44-7.36 (m, 4H), 7.36-7.28 (m, 2H), 5.17 (s, 4H), 4.29 (q, J= 7.1 Hz, 4H), 1.26 (t, J= 7.1 Hz, 6H). 2,5-Bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid (KI-1) and 2,5-bis(benzyloxy)terephthalic acid (KL6) (step [2]) A solution of potassium hydroxide (14.2 g, 0.25 mol) in water (200.0 mL) was rapidly added to a solution of diethyl 2,5-bis(benzyloxy)terephthalate (100 g, 0.23 mol) in 1,4-dioxane (1 L), and the resulting mixture was stirred overnight at ambient temperature. The solvent was removed in vacuo, resulting in the formation of a white slurry. The crude was suspended in EtOH (500 mL) and filtered and the collected solid was dried in vacuum oven to afford pure diethyl 2,5-bis(benzyloxy)terephthalate (23.0 g, 0.053 mol, 23%) UPLC-MS (acidic method, 2 min): rt = 1.36 min, no ionization observed, peak area 98% The ethanolic filtrate was concentrated to give an oil. Ethyl acetate (500 mL) was added to form a precipitate which was filtered and washed with ethyl acetate (200 mL) to afford 2,5-bis(benzyloxy)terephthalic acid (KI-6) as white solid (18.9 g, 0.042 mol, 18%). UPLC-MS (acidic method, 2 min): rt = 1.22 min, m / z 377.1 [M-H]“, peak area 95% ‘HNMR (400 MHz, DMSO-tL) 5 7.52-7.45 (m, 4H), 7.41-7.33 (m, 4H), 7.33-7.26 (m, 4H), 5.13 (s, 4H). The filtrate was washed with a saturated solution of aqueous sodium carbonate (200 mL), aqueous 1 M hydrochloric acid (500 mL) and brine (500 mL), then dried (L^SCL), filtered and concentrated to dryness to give 2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid (KI-1) as a white solid (53 g, 0.130 mol, 57.0%). UPLC-MS (acidic method, 2 min): rt = 1.22 min, m / z 405.3 [M-H]", peak area 96% 1HNMR(400 MHz, DMSO-^) 5 7.52-7.27 (m, 13H), 5.17 (s, 4H), 4.28 (q, J= 7.1 Hz, 2H), 1.26 (t, J = 7.1 Hz, 3H). LARGE SCALE PROTOCOLE FOR THE SYNTHESIS OF KI-1 A 10 L jacketed vessel was charged with diethyl 2,5-bis(benzyloxy)terephthalate (500.00 g, 1.15 mol), 1,4-dioxane (2.5 L), potassium hydroxide (71.00 g, 1.26 mol) and water (500 mL). The reaction mixture was stirred overnight at room temperature. LCMS Analysis showed the reaction had gone half-way to completion, showing also the by-product (di-acid) and starting material (di-ester) in the ratio of (diester:mono-acid:diacid = 28:58:14). (diacid: 4.44 rt, monoacid: 5.08 rt, diester: 5.68 rt). At this stage solvent was removed in vacuo. The crude product was taken into a 2:1 mixture of ethanokwater (3 L), in a 10 L jacketed vessel, stirred overnight and filtered in order to give: Solid: (diester:mono-acid:diacid = 86:12:2, 110.00 g, colourless solid) Filtrates: (diester:mono-acid:diacid 3:63:34) The filtrates were concentrated in vacuo in order to afford an oil. This oil was taken up in ethyl acetate (2.5 L), stirred overnight in a 10 L jacketed vessel and filtered in order to give a white solid (150.00 g). Solid: (diester:mono-acid:diacid = trace: 40:60). The filtrates were collected, washed with a saturated aqueous solution of sodium bicarbonate (100 mL), IN hydrochloric acid solution (200 mL) and brine (200 mL), dried over anhydrous sodium sulfate and filtered. The solvent was removed under reduced pressure to afford the desired product, 2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid (KI-1), as a white solid, which was dried in the vacuum oven at 50°C for 48h (225.00 g, 49% yield) (yields vary between 49-65%). Scheme 2: Synthetic Intermediate KI-IBn OH                       OBn                        OBn KI-OBn        31%            KI-IBn contains 16% KI-OBn Procedure: Synthesis of KI-IBn: 2,5-Bis(benzyloxy)-4-(benzyloxycarbonyl)benzoic acid (KI-IBn). To a solution of 2,5-dihydroxytere-phthalic acid (1.97 g, 10 mmol) in DMF (20 mL) at 0°C was added sodium hydride (2.0 g, 50 mmol) under stirring, then benzyl bromide (5.95 mL, 50 mmol, 5 eq) dropwise over 5 min, and the resulting mixture kept at room temp, for 2h. The mixture was then heated at 60°C for 18 h. The reaction mixture was cooled down to ambient temperature and treated cautiously with MeOH (5 mL). The mixture was concentrated under reduced pressure, and the residual material co-evaporated with heptane (3x). The residue was taken in DCM (30 mL), the organic phase washed with IM HC1 (25 mL), the separated aqueous layer was extracted with DCM (3x30 mL) and the combined organic phases dried (MgSO4) and concentrated. The crude solid was recrystallized from EtOH ( 30 mL) to afford pure KI-OBn (2.286g, 41%). A sample of KI-OBn (282 mg, 0.5 mmol) was added to a mixture of 1,4-dioxane (10 mL) and lithium hydroxide hydrate (22 mg, 0.52 mmol), and the mixture was heated to 80°C for 3 d. The mixture was cooled down to room temp., taken in AcOEt (30 mL) and the solution washed with IM HC1 (2 mL). The organic phase was dried and concentrated, and the residue submitted to column chromatography to afford monoester KI-IBn contaminated by about 16% of diester KI-OBn. KI-OBn: 1HNMR(400 MHz, CDCh): 5 7.51 (s, 2H), 7.36-7.30 (m, 20H), 5.34 (s, 4H), 5.11 (s, 4H). KI-IBn: 'H NMR (250 MHz, CDCh): 5 7.86 (s, 1H), 7.61 (s, 1H), 7.41-7.30 (m, 20H), 5.36 (s, 2H), 5.26 (s, 2H), 5.16 (s, 2H). SYNTHESIS OF MONOAMIDES Scheme 3. Synthesis of Monoamides la General procedure A for Amide Coupling [3A] > Coupling via acyl chloride, from KI-1 or KI-6 Model Reaction (Ia-013a) Dimethyl 2-(2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoylamino)isophthalate. 2,5-Bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid (KI-1, 1.1g, 2.8 mmol) was dissolved in thionyl chloride (6 mL), and the resulting mixture was stirred for 5 min. A few drops of DMF were added, and the resulting mixture was stirred at ambient temperature for 18 h. Excess thionyl chloride was removed in vacuo and the residue was co-distilled with toluene (3 x 20 mL) to afford the acyl chloride. A solution of the acyl chloride in DCM (10 mL) was rapidly added to a solution of amine (dimethyl 2-aminoisophthalate, 210 mg, 3.1 mmol) and N, A-diisopropylethylamine (0.53 mL, 3.045 mmol) in DCM (10 mL) at ambient temperature and the reaction was stirred for 18 h. The reaction was diluted with DCM (70 mL) and was washed with a 1 M aqueous hydrochloric acid (100 mL), water (100 mL), dried (Na2SO4), fdtered and concentrated to give the crude product, which was purified by silica gel chromatography eluting with a gradient of ethyl acetate (0 to 25%) in iso-hexane to the desired product as a white solid (1.24 g, 2.075 mmol, 75%). UPLC-MS (acidic method, 2 min): rt = 1.37 min; m / z = 598.2 [M+H]+, peak area >95% ‘HNMR (400 MHz, DMSO- d6) 5 11.60 (s, 1H), 8.02 (d, J= 7.8 Hz, 2H), 7.69 (s, 1H), 7.59 - 7.23 (m, 12H), 5.49 (s, 2H), 5.19 (s, 2H), 4.28 (q, J= 7.1 Hz, 2H), 3.71 (s, 6H), 1.26 (t, J= 7.1 Hz, 3H). General procedure B for Amide Coupling [3B] > Coupling using a condensation agent, from KI-1 or KI-6 Model Reaction (la-OOla) Methyl 2-(2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoylamino)benzoate. 1-Methylimidazole (13.0 mL, 163 mmol) was added to a mixture of 2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid (KI-1, 12.95 g, 32 mmol) and methyl anthranilate (5.729 g, 38 mmol, 1.190 eq) in MeCN (150 mL) at ambient temperature. Chloro-A'.A',A",A"-tetramethylformamidinium hexafluorophosphate(TCFH) (10.728 g, 0.038 mol) was added portionwise over 30 min, and the resulting mixture was stirred overnight at ambient temperature. The reaction mixture was treated with 1 M aqueous hydrochloric acid (700 mL). The resulting suspension was stirred for 10 min, then fdtered. The solid material was washed with water (2 x 200 mL). The solid was then suspended in ethanol (200 mL), fdtered, washed with ether (100 mL) and dried in the vacuum oven to give the desired product as a white solid (14.7 g, 27 mmol, 86%) UPLC-MS (acidic method, 2 min): rt = 1.43 min; m / z = 540.2 [M+H]+, peak area >99% 1HNMR(400MHz, DMSO-7tf) 5 11.87 (s, 1H), 8.65 (d, 7= 8.4 Hz, 1H), 7.98 (dd,7=8.0, 1.7 Hz, 1H), 7.81-7.61 (m, 2H), 7.59-7.12 (m, 12H), 5.41 (s, 2H), 5.20 (s, 2H), 4.28 (q,7=7.1 Hz, 2H), 3.74 (s, 3H), 1.27 (t, 7= 7.1 Hz, 3H).O General Deprotection procedures [4], [5] Saponification Model reaction (Ia-013a) 2-(2,5-Bis(benzyloxy)-4-carboxybenzoylamino)isophthalic acid. The solution of lithium hydroxide (42 mg, 1 mmol) in water (4 mL) was added to the solution of dimethyl 2-(2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoylamino)isophthalate (100 mg, 0.167 mmol) in THF (6 mL) and the resulting mixture was stirred at ambient temperature for 18 h. Additional LiOH (6 eq) in water (4 mL) was added to the reaction mixture which was stirred for an additional 23 h. After completion, water (50 mL) was added to the reaction and the mixture was washed with ethyl acetate (50 mL). The aqueous layer was acidified with a 1 M aqueous hydrochloric acid to pH=2 and extracted with ethyl acetate (2X 50 mL). The organic layers were collected, dried (Na2SO4), filtered and concentrated to give the title compound as a white solid (82 mg, 0.151 mmol, 91%). UPLC-MS (acidic method, 2 min): rt = 1.02 min; m / z = 542.1 [M+H]+, peak area >95% ‘HNMR (400 MHz, DMSO-tL) 5 13.18 (s, 2H), 11.74 (s, 1H), 8.00 (d, 7= 7.8 Hz, 2H), 7.71 (s, 1H), 7.58 - 7.43 (m, 5H), 7.40 - 7.24 (m, 7H), 5.47 (s, 2H), 5.14 (s, 2H). Debenzylation Model reaction (Ia-013a) 2-(2,5-Dihydroxy-4-carboxybenzoylamino)isophthalic acid (Ia-013a). Pd / C (94 mg, 10%) was added to a solution of 2-(2,5-bis(benzyloxy)-4-carboxybenzoylamino)isophthalic acid (0.94 g, 1.74 mmol) in a 10:30 mixture of EtOH and DCM. The mixture was placed under hydrogen at atmospheric pressure at ambient temperature and stirred for 18 h. After completion, the mixture was filtered through Celite, which was washed with DCM and MeOH. The filtrate and washings were combined and concentrated under reduced pressure to afford the desired product Ia-013a as a yellow solid (644 mg, 1.69 mmol, 98%). UPLC-MS (acidic method, 4 min): rt = 0.91 min; m / z =362.0 [M+H]+, peak area >98% ’H NMR (DMSO-tL) 5: 13.11 (s, 2H), 11.70 (s, 1H), 11.13 (s, 1H), 7.97 (d,7= 7.8 Hz, 2H), 7.47 (s, 1H), 7.41 (s, 1H), 7.38 (t, 7= 7.7 Hz, 1H) Scheme 4a. Synthesis of Monoamides la from KI-IBn General procedure from KI-IBn > Coupling via acyl chloride Model Reaction: synthesis of Ia-032a Benzyl 4-(2,5-bis(benzyloxy)-4-(benzyloxycarbonyl)benzoylamino)phenylacetate. To a solution of KI-IBn (233 mg, 84% purity) in DCM (10 mL) was added SOCh (1.8 mL, 60 eq) and the mixture was heated at 50°C for 3h. The solvents were evaporated and the residue co-evaporated with toluene (3x10 mL), to give the crude acyl chloride (237 mg, 99%). This material was dissolved in DCM (3 mL), and diisopropylethylamine (0.08 mL, 1.15 eq) was added, followed by a solution of benzyl 4-aminophenylacetate (92 mg, 0.95 eq) in DCM (3 mL). Final reaction volume was 10 mL. The reaction mixture was stirred at room temp, for 18h. The mixture was diluted with DCM (15 mL), washed with sat aqueous ammonium chloride (12 mL). The separated aqueous phase was extracted with DCM (2x2 mL), the organic phases were combined, dried (MgSO4), and concentrated. The crude product was submitted to column chromatography (Pet. Et. / DCM 1:1 then gradient to 100% DCM) to give a first fraction of pure KI-OBn, and second fraction containing the pure desired product (237 mg, 86%, corrected for the purity of KI-IBn). 1HNMR(400 MHz, CDCh): 5 10.10 (s, 1H), 8.08 (s, 1H), 7.65 (s, 1H), 7.53-7.30 (m, 20H), 7.22-7.13 (br AB, 4H), 5.39, 5.22, 5.21, 5.12 (4s, 4x2H), 3.61 (s, 2H). 4-(4-(Carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid (Ia-032a). To a solution of precursor prepared above (225 mg, 0.33 mmol) in DCM (20 mL) was added 5% Pd on charcoal (72 mg), followed by EtOH (20 mL). The flask was flushed with Ar (3x) then filled with hydrogen (atmospheric pressure) and the mixture stirred for 2h at room temperature. The catalyst was removed by filtration over a millipore filter, the filtrate was evaporated, and the residue dried to afford the product Ia-032a as a light yellow solid (107 mg, 99%). 1HNMR(250 MHz, DMSO-Jtf): 5 12.28 (br, 1H), 10.92 (s, 1H), 10.44 (s, 1H), 7.65 (br d, 2H), 7.41 (s, 1H), 7.38 (s, 1H), 7.25 (brd, 2H), 3.55 (s, 2H). la-002c la-003a la-003aTz la-003c COOH COOH HOOC la-013a la-014a COOH la-023a la-032 la-012a COOH 5 For conditions and yields: See Figures 4A-D 1) 4-(2-Carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-OOla UPLC-MS (acidic method, 2 min): r.t = 0.95 mins, m / z = 316 [M-H]", peak area > 97% XH NMR (400 MHz, DMSO-Jtf) 5 12.22 (s, 1H), 10.85 (s, 1H), 8.65 (d, 7= 8.4 Hz, 1H), 8.01 (dd, J = 8.0, 1.7 Hz, 1H), 7.71-7.56 (m, 1H), 7.41 (d, 7= 6.9 Hz, 2H), 7.22 (t, J= 7.6 Hz, 1H). 10 HRMS: [M+H]+, calc, for C15H12NO7: 318.06083, found: 318.06080. Biodata: la-OOla: FGF-1 IC50 [pM] = 41; FGF-2 IC50 [pM] = 39; VEGF-A1 IC50 [pM] = 7.3; VEGFR-Phosphorylation inhibition IC50 [pM] =2.25; PMN ROS [inhibition at 0.3 pM [%] = 48; PMN ROS inhibition IC50 [pM] = 0.355; Neutrophil adhesion inhibition [%] = 44.3; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 30.5; IL-Ip IC50 [pM] = 34.4; IL-2 IC50 [pM] = 15       94.3; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 1.24; IL-9 IC50 [pM] = 5.63; IL-10 IC50 [pM] = >100; IL-12p70 IC50 [pM] = 1.5; IL-13 IC50 [pM] = 26.4; IL-17A IC50 [pM] = 0.1; IL-17F IC50 [pM] = 14.7; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = >100; IL-33 IC50 [pM] = 19.3; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.02; TNFp IC50 [pM] = 13.2 Diethyl ester: UPLC-MS (acidic method, 2 min): r.t = 1.39 mins, m / z = 372.2 [M-H]", peak area > 98% 1HNMR(400 MHz, DMSO-J6) 5 11.96 (s, 1H), 11.05 (s, 1H), 9.87 (s, 1H), 8.57 (dd, J= 8.5, 1.2 Hz, 1H), 7.99 (dd, J= 7.9, 1.7 Hz, 1H), 7.65 (ddd, J= 8.7, 7.3, 1.7 Hz, 1H), 7.49 (s, 1H), 7.40 (s, 1H), 7.25 (td, J= 7.6, 1.2 Hz, 1H), 4.35 (m, 4H), 1.33 (m, 6H). HRMS: [M+H]+, calc, for C19H20NO7: 374.12342, found: 374.12354 Biodata: Ia-001a-E2: FGF-1 IC50 [pM] = 9.2; FGF-2 IC50 [pM] = 200; VEGF-A1 IC50 [pM] = 123; VEGFR-Phosphorylation inhibition IC50 [pM] =1.25; PMN ROS [inhibition at 0.3 pM [%] = 51.47; PMN ROS inhibition IC50 [pM] = 2.58; Neutrophil adhesion inhibition [%] = 50.5 2) 4-(2-(lH-Tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-001 aTz: UPLC-MS (acidic method, 4 min): rt = 1.17 min; m / z =342.0 [M+H]+, peak area >96% 1HNMR(400MHz, DMSO-JJ 5 11.60 (s, 1H), 10.90 (s, 2H), 8.47 (d, J =8.4 Hz, 1H), 7.93 (d, J = 7.9 Hz, 1H), 7.61 (t, J= 7.9 Hz, 1H), 7.50 - 7.32 (m, 3H). HRMS: [M+H]+, calc, for C15H12N5O5: 342.08329, found: 342.08318 Biodata: la-OOla-Tz: FGF-1 IC50 [pM] = 6.2; FGF-2 IC50 [pM] = 20; VEGF-A1IC50 [pM] = 17; VEGFR-Phosphorylation inhibition IC50 [pM] =0.23; PMN ROS [inhibition at 0.3 pM [%] = 54.33; PMN ROS inhibition IC50 [pM] = 1.54; Neutrophil adhesion inhibition [%] = 69.75; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = >100; IL-1 p IC50 [pM] = >100; IL-2 IC50 [pM] = 7.99; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.75; IL-9 IC50 [pM] = 8.63; IL-10 IC50 [pM] = 26.1; IL-12p70 IC50 [pM] = 32.4; IL-13 IC50 [pM] = 32.1; IL-17A IC50 [pM] = 0.11; IL-17F IC50 [pM] = 46.5; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = >100; IL-33 IC50 [pM] = 23.6; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.63; TNF p IC50 [pM] = 53 Ethyl ester: UPLC-MS (acidic method, 2 min): r.t = 1.08 mins, m / z = 370.1 [M+H]+, peak area > 97% 1HNMR(400MHz, DMSO-J6) 5 11.48 (s, 1H), 9.88 (s, 1H), 8.46 (d, J= 8.4 Hz, 1H), 7.89 (dd, J= 7.8, 1.6 Hz, 1H), 7.62 (ddd, J = 8.6, 7.4, 1.6 Hz, 1H), 7.47 (s, 1H), 7.42 - 7.34 (m, 2H), 4.37 (q, J= 7.1 Hz, 2H), 1.34 (t, J= 7.1 Hz, 3H). HRMS: [M+H]+, calc, for C17H16N5O5: 370.11460, found: 370.11458 Biodata: la-OOla-Tz-El: FGF-1IC50 [pM] = 200; FGF-2IC50 [pM] = 200; VEGF-A1IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =3.8; PMN ROS [inhibition at 0.3 pM [%] = 75.97; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 98.88 Ethyl ester Diacetate: UPLC-MS (acidic method, 4 min): r.t = 1.57 mins, m / z = 454.1 [M+H]+, peak area > 97% ‘HNMR (400 MHz, DMSO-J6) 5 11.23 (s, 1H), 8.23 (d, J = 8.6 Hz, 1H), 7.96 (dd, J = 7.9, 1.7 Hz, 1H), 7.84 (s, 1H), 7.73 (s, 1H), 7.64 (t, J= 7.5 Hz, 1H), 7.43 (td, J= 7.6, 1.2 Hz, 1H), 4.32 (q, J= 7.1 Hz, 2H), 2.34 (s, 3H), 2.18 (s, 3H), 1.32 (t, J= 7.1 Hz, 3H). HRMS: [M+H]+, calc, for C21H20N5O7: 454.13572, found: 454.13542 Biodata: Ia-001a-Tz-El-A2: FGF-1 IC50 [pM] = 60; FGF-2 IC50 [pM] = 200; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 49.85; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 98.2 3) 2,5-Dihydroxy-4-(2-sulfophenylaminocarbonyl)benzoic acid, compound la-OOlc: UPLC-MS (acidic method, 2 min): rt = 0.73 min; m / z =352.0 [M-H]", peak area >99% 1HNMR(400MHz, DMSO-Jtf) 5 11.54 (s, 1H), 10.99 (s, 1H), 8.34 (d, J = 8.2 Hz, 1H), 7.74 (dd, J = 7.7, 1.7 Hz, 1H), 7.42 - 7.28 (m, 3H), 7.12 (td, J = 7.5, 1.2 Hz, 1H). HRMS: [M+H]+, calc, for Ci4Hi2NO8S: 354.02781, found: 354.02754. Biodata: la-OOlc: FGF-1 IC50 [pM] = 21; FGF-2 IC50 [pM] = 13; VEGF-A1 IC50 [pM] = 100; VEGFR-Phosphorylation inhibition IC50 [pM] =3.31; PMN ROS [inhibition at 0.3 pM [%] = 40.36; PMN ROS inhibition IC50 [pM] = 2.4; Neutrophil adhesion inhibition [%] = 31.33; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 0.44; IL-1 p IC50 [pM] = >100; IL-2 IC50 [pM] = 12.8; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.95; IL-9 IC50 [pM] = 46.9; IL-10 IC50 [pM] = 1.9; IL-12p70 IC50 [pM] = 0.44; IL-13 IC50 [pM] = 86.1; IL-17A IC50 [pM] = 0.09; IL-17F IC50 [pM] = 89.7; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = >100; IL-33 IC50 [pM] = >100; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.05; TNF p IC50 [pM] = 29.7 4) 4-(3-Carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-002a: ‘H-NMR (250 MHZ, DMSO-tL) 5 ~13 (v br, 1H), 10.82 (br s, 1H), 10.60 (br s, 1H), 8.38 (s, 1H). 7.92 (d, 1H), 7.71 (d, 1H), 7.49 (t, 1H), 7.39 (s, 2H) Biodata: la-002a: FGF-1 IC50 [pM] = 20; FGF-2 IC50 [pM] = 59; VEGF-A1 IC50 [pM] = 71; VEGFR-Phosphorylation inhibition IC50 [pM] =5.7; PMN ROS [inhibition at 0.3 pM [%] = 42.1; PMN ROS inhibition IC50 [pM] = 0.312; Neutrophil adhesion inhibition [%] = 27.92 5) 4-(3-(lH-Tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-002aTz: UPLC-MS (acidic method, 4 min): rt = 1.13 min; m / z =342.0 [M+H]+, peak area >99% ‘HNMR (400 MHz, DMSO-tL) 5 10.81 (s, 1H), 10.67 (s, 1H), 8.54 (s, 1H), 7.91 - 7.84 (m, 1H), 7.79 (dt, J = 7.8, 1.4 Hz, 1H), 7.60 (t, J = 7.9 Hz, 1H), 7.41 (d, J = 2.2 Hz, 2H). HRMS: [M+H]+, calc, for C15H12N5O5: 342.08329, found: 342.08317 Biodata: Ia-002a-Tz: FGF-1IC50 [pM] = 10; FGF-2 IC50 [pM] = 53; VEGF-A1IC50 [pM] = 57; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 66.61; PMN ROS inhibition IC50 [pM] = 1.86; Neutrophil adhesion inhibition [%] = 38.5 6) 2,5-Dihydroxy-4-(3-sulfophenylaminocarbonyl)benzoic acid, compound Ia-002c: ‘H-NMR (250 MHZ, DMSO-J6) 5 11.04 (s, 1H), 10.53 (s, 1H), 7.96 (s, 1H), 7.69 (d, 1H), 7.43 (s, 2H) and 7.40-7.28 (m, 2H) Biodata: Ia-002c: FGF-1 IC50 [pM] = 14; FGF-2 IC50 [pM] = 150; VEGF-A1 IC50 [pM] = 150; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 38.9; PMN ROS inhibition IC50 [pM] = 0.405; Neutrophil adhesion inhibition [%] = 1.87 7) 4-(4-Carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-003a: ‘H-NMR (250 MHz, DMSO-J6) 5 12.8 (br, 1H), 10.73 (s, 1H), 10.68 (s, 1H), 7.94 (d of AB, 2H), 7.84 (d of AB, 2H), 7.39 (s, 1H), 7.34 (s, 1H) HRMS (AX033) Biodata: Ia-003a: FGF-1 IC50 [pM] = 12; FGF-2 IC50 [pM] = 34; VEGF-A1 IC50 [pM] = 150; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 44.4; PMN ROS inhibition IC50 [pM] = 0.414; Neutrophil adhesion inhibition [%] = 39.1 8) 4-(4-(lH-Tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-003aTz: UPLC-MS (acidic method, 2 min): rt = 0.79 min; m / z =342.0 [M+H]+, peak area >97% ‘HNMR (400 MHz, DMSO-J6) 5 10.77 (s, 1H), 10.70 (s, 1H), 8.04 (d, J = 8.7 Hz, 2H), 7.96 (d, J = 8.5 Hz, 2H), 7.41 (s, 1H), 7.37 (s, 1H). HRMS: [M+H]+, calc, for C15H12N5O5: 342.08329, found: 342.08326 Biodata: Ia-003a-Tz: FGF-1 IC50 [pM] = 6.7; FGF-2 IC50 [pM] = 45; VEGF-A1IC50 [pM] = 13; VEGFR-Phosphorylation inhibition IC50 [pM] =6.4; PMN ROS [inhibition at 0.3 pM [%] = 62.21; PMN ROS inhibition IC50 [pM] = 2.49; Neutrophil adhesion inhibition [%] = 30.33; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 2.95; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = 43; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 1.41; IL-9 IC50 [pM] = 3.62; IL-10 IC50 [pM] = 6.94; IL-12p70 IC50 [pM] = 1.26; IL-13 IC50 [pM] = 89.6; IL-17A IC50 [pM] = 0.07; IL-17F IC50 [pM] = 83.9; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 1.49; IL-33 IC50 [pM] = 72.2; TGF[3 IC50 [pM] = >100; TNF a IC50 [pM] = 0.18; TNF p IC50 [pM] = 55. 9) 2,5-Dihydroxy-4-(4-sulfophenylaminocarbonyl)benzoic acid, compound Ia-003c: ‘H-NMR (400 MHz, DMSO-J6) 5 10.90 (s, 1H), 10.51 (s, 1H), 7.66 (d of AB, 2H), 7.58 (d of AB, 2H), 7.40 (s, 1H), 7.39 (S, 1H) Biodata: Ia-003c: FGF-1 IC50 [pM] = 35; FGF-2 IC50 [pM] = 150; VEGF-A1 IC50 [pM] = 150; VEGFR-Phosphorylation inhibition IC50 [pM] =0.4; PMN ROS [inhibition at 0.3 pM [%] =N.D.; PMN ROS inhibition IC50 [pM]-; Neutrophil adhesion inhibition [%] = N.D. 10) 4-(3-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-004a: UPLC-MS (acidic method, 6.5 min): rt = 1.40 min; m / z =332.0 [M-H]", peak area >96% ‘HNMR (400 MHz, DMSO-J6) 5 10.94 (s, 1H), 10.37 (s, 1H), 8.20 (d, J = 2.7 Hz, 1H), 7.74 (dd, J = 8.9, 2.8 Hz, 1H), 7.39 (s, 1H), 7.34 (s, 1H), 6.93 (d, J = 8.9 Hz, 1H). HRMS: [M+H]+, calc, for Ci5Hi2NO8: 334.05574, found: 334.05572 Biodata: Ia-004a: FGF-1 IC50 [pM] = 32; FGF-2 IC50 [pM] = 15; VEGF-A1 IC50 [pM] = 28; VEGFR-Phosphorylation inhibition IC50 [pM] =7.7; PMN ROS [inhibition at 0.3 pM [%] = 64.61; PMN ROS inhibition IC50 [pM] = 0; Neutrophil adhesion inhibition [%] = 28.38 Ethyl Methyl ester: UPLC-MS (acidic method, 2 min): r.t = 1.16 mins, m / z = 376.1 [M+H]+, peak area > 95% 1HNMR(400 MHz, DMSO-d6) 5 10.90 (s, 1H), 10.50 (s, 1H), 10.36 (s, 1H), 9.91 (s, 1H), 8.26 (d, J= 2.7 Hz, 1H), 7.76 (dd, J= 8.9, 2.8 Hz, 1H), 7.43 (s, 1H), 7.36 (s, 1H), 7.01 (d, J= 8.9 Hz, 1H), 4.37 (q, J= 7.1 Hz, 2H), 3.91 (s, 3H), 1.34 (t, J= 7.1 Hz, 3H). HRMS: [M+H]+, calc, for Ci8Hi8NO8: 376.10269, found: 376.10259 Biodata: Ia-004a-E2: FGF-1 IC50 [pM] = 35; FGF-2 IC50 [pM] = 36; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =6.1; PMN ROS [inhibition at 0.3 pM [%] = 85.34; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 97.65 11) 4-(2-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-006a: UPLC-MS (acidic method, 2 min): rt = 0.81 min; m / z =334.0 [M+H]+, peak area >96% 1HNMR(400 MHz, DMSO-JJ 5 13.33 (s, 1H), 11.86 (s, 1H), 10.90 (s, 1H), 9.66 (s, 1H), 8.39 (d, J= 9.0 Hz, 1H), 7.40 (d, J= 6.8 Hz, 2H), 7.03 (dd, J= 9.0, 3.0 Hz, 1H). HRMS: [M+H]+, calc, for Ci5Hi2NO8: 334.05574, found: 334.05562. Biodata: Ia-006a: FGF-1 IC50 [pM] = 89; FGF-2 IC50 [pM] = 224; VEGF-A1 IC50 [pM] = 100; VEGFR-Phosphorylation inhibition IC50 [pM] =11.8; PMN ROS [inhibition at 0.3 pM [%] = 60.56; PMN ROS inhibition IC50 [pM] = 1.2; Neutrophil adhesion inhibition [%] = 25.33 12) 3-(4-Carboxy-2,5-dihydroxybenzamido)phthalic acid, compound la-Olla: UPLC-MS (acidic method, 2 min): rt = 0.69 min; m / z = 360.1 [M-H]", peak area >89% ‘H NMR (400 MHz, DMSO-Jtf) 5 13.46 (s, 2H), 11.37 (s, 1H), 10.97 (s, 1H), 8.33 (dd, J= 8.2, 1.3 Hz, 1H), 7.63 (dd, J= 7.7, 1.3 Hz, 1H), 7.57 (t, J= 7.9 Hz, 1H), 7.52 (s, 1H), 7.44 (s, 1H). HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05065, found: 362.05036 Biodata: la-Olla: FGF-1 IC50 [pM] = 35; FGF-2 IC50 [pM] = 110; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 57.71; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 42.32 13) 2-(4-Carboxy-2,5-dihydroxybenzamido)terephthalic acid, compound Ia-012a: UPLC-MS (acidic method, 4 min): rt = 1.12 min; m / z = 362.1 [M+H]+, peak area >96% ‘HNMR (400 MHz, DMSO-J6) 5 13.41 (brs, 2H), 12.29 (s, 1H), 10.94 (s, 1H), 9.26 (d, J= 1.7 Hz, 1H), 8.09 (d, J= 8.2 Hz, 1H), 7.73 (dd, J= 8.2, 1.7 Hz, 1H), 7.42 (s, 2H). HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05065, found: 362.05046. Biodata: Ia-012a: FGF-1 IC50 [pM] = 38; FGF-2 IC50 [pM] = 36; VEGF-A1 IC50 [pM] = 30; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 59.52; PMN ROS inhibition IC50 [pM] = 1.85; Neutrophil adhesion inhibition [%] = 28.5 14) 2-(4-Carboxy-2,5-dihydroxybenzamido)isophthalic acid, compound Ia-013a: UPLC-MS (acidic method, 4 min): rt = 0.91 min; m / z = 362.0 [M+H]+, peak area >98% ‘HNMR (400 MHz, DMSO-J6) 5 13.11 (s, 2H), 11.70 (s, 1H), 11.13 (s, 1H), 7.97 (d, J = 7.8 Hz, 2H), 7.47 (s, 1H), 7.41 (s, 1H), 7.38 (t, J = 7.7 Hz, 1H) HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05065, found: 362.05041 Biodata: Ia-013a: FGF-1 IC50 [pM] = 29; FGF-2 IC50 [pM] = 18; VEGF-A1 IC50 [pM] = 17; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 38.52; PMN ROS inhibition IC50 [pM] = 2.38; Neutrophil adhesion inhibition [%] = 27.67 15) 4-(4-Carboxy-2,5-dihydroxybenzamido)phthalic acid, compound Ia-014a: UPLC-MS (acidic method, 4 min): rt = 0.98 min; m / z = 362.1 [M+H]+, peak area >94% ‘HNMR (400 MHz, DMSO-J6) 5 10.76 (s, 1H), 10.70 (s, 1H), 8.14 (s, 1H), 7.94 - 7.84 (m, 2H), 7.38 (s, 1H), 7.30 (s, 1H). HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05065, found: 362.05047 Biodata: Ia-014a: FGF-1 IC50 [pM] = 20; FGF-2 IC50 [pM] = 20; VEGF-A1 IC50 [pM] = 88; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 61.3; PMN ROS inhibition IC50 [pM] = 1; Neutrophil adhesion inhibition [%] = 9.667 79 16) 5-(4-Carboxy-2,5-dihydroxybenzamido)isophthalic acid, compound Ia-015a: ‘HNMR (250 MHz, DMSO-J6) 5 10.74 (s, 1H), 8.56 (narrow d, 2H), 8.22 (narrow t, 1H), 7.41 (s, 1H) and 7.37 (s, 1H) Biodata: Ia-015a: FGF-1 IC50 [pM] = 20; FGF-2 IC50 [pM] = 9.3; VEGF-A1 IC50 [pM] = 19; VEGFR-Phosphorylation inhibition IC50 [pM] =0.15; PMN ROS [inhibition at 0.3 pM [%] = 43.8; PMN ROS inhibition IC50 [pM] = 0.387; Neutrophil adhesion inhibition [%] = 17.38; Whole Blood: GM-CSF IC50 [pM] = 2.76; IFNv IC50 [pM] = >100; IL-Ip IC50 [pM] = >100; IL-2 IC50 [pM] = 7.08; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.77; IL-9 IC50 [pM] = 1.47; IL-10 IC50 [pM] = 5.27; IL-12p70 IC50 [pM] = 0.12; IL-13 IC50 [pM] = 0.15; IL-17A IC50 [pM] = 0.05; IL-17F IC50 [pM] = 0.15; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 57.2; IL-33 IC50 [pM] = 0.24; TGF0 IC50 [pM] = >100; TNF a IC50 [pM] = 0.17; TNF p IC50 [pM] = 0.3. 17) 3-(4-carboxy-2,5-dihydroxybenzamido)isonicotinic acid, compound Ia-023a: UPLC-MS (acidic method, 4 min): rt = 0.63 min; m / z = 319.1 [M+H]+, peak area >93% ‘H NMR (400 MHz, DMSO-J6) 5 12.17 (s, 1H), 11.03 (s, 1H), 9.78 (s, 1H), 8.46 (d, J = 5.0 Hz, 1H), 7.82 (d, J= 5.0 Hz, 1H), 7.45 (s, 1H), 7.43 (s, 1H). HRMS: [M+H]+, calc, for C14H11N2O7: 319.05608, found: 319.05610 Biodata: Ia-023a: FGF-1 IC50 [pM] =N.D.; FGF-2 IC50 [pM] = 63; VEGF-A1IC50 [pM] = 143; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 61.95; PMN ROS inhibition IC50 [pM] = 0; Neutrophil adhesion inhibition [%] = 13.37 Diethyl ester: UPLC-MS (acidic method, 4 min): r.t = 1.87 mins, m / z = 375.1 [M+H]+, peak area > 98% ‘HNMR (400 MHz, DMSO-d6) 5 11.79 (s, 1H), 11.23 (s, 1H), 9.87 (s, 1H), 9.68 (s, 1H), 8.50 (d, J = 5.0 Hz, 1H), 7.81 (dd, J = 5.1, 0.7 Hz, 1H), 7.53 (s, 1H), 7.41 (s, 1H), 4.46 - 4.27 (m, 4H), 1.41 - 1.25 (m, 6H). HRMS: [M+H]+, calc, for Ci8Hi9N2O7: 375.11867, found: 375.11867 Biodata: Ia-023a-E2: FGF-1 IC50 [pM] =N.D.; FGF-2 IC50 [pM] = 76; VEGF-A1 IC50 [pM] = 141; VEGFR-Phosphorylation inhibition IC50 [pM] =6.6; PMN ROS [inhibition at 0.3 pM [%] = 69.47; PMN ROS inhibition IC50 [pM] = 0; Neutrophil adhesion inhibition [%] = 34 18) 4-(4-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-032a: ‘HNMR (250 MHz, DMSO-d6): 5 12.28 (br, 1H), 10.92 (s, 1H), 10.44 (s, 1H), 7.65 (br d, 2H), 7.41 (s, 1H), 7.38 (s, 1H), 7.25 (br d, 2H), 3.55 (s, 2H). Biodata: Ia-032a: FGF-1IC50 [pM] = N.D.; FGF-2IC50 [pM] = 91; VEGF-A1IC50 [pM] =N.D.; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = N.D.; PMN ROS inhibition IC50 [pM]-; Neutrophil adhesion inhibition [%] = N.D. 19) 4-(3-(Carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-033a: UPLC-MS (acidic method, 6.5 min): rt= 1.71 min; m / z = 332.1 [M+H]+, peak area>99% ‘HNMR (400 MHz, DMSO-J6) 5 10.89 (s, 1H), 10.46 (s, 1H), 7.65 (s, 1H), 7.59 (d, J = 8.1 Hz, 1H), 7.40 (s, 1H), 7.38 (s, 1H), 7.03 (d, J= 7.6 Hz, 1H), 3.57 (s, 2H). HRMS: [M+H]+, calc, for C16H14NO7: 332.07647, found: 332.07644 Biodata: Ia-033a: FGF-1 IC50 [pM] = 60; FGF-2 IC50 [pM] = 165; VEGF-A1 IC50 [pM] = 281; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 57.73; PMN ROS inhibition IC50 [pM] = 1.32; Neutrophil adhesion inhibition [%] = 38 20) 4-(2-(Carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-034a: UPLC-MS (acidic method, 2 min): rt = 0.82 min; m / z = 332.1 [M+H]+, peak area >98% ‘HNMR (400 MHz, DMSO-J6) 5 7.78 (d, J = 8.1 Hz, 1H), 7.31 (d, J = 3.0 Hz, 2H), 7.28 (d, J = 7.6 Hz, 2H), 7.15 (t, J= 7.4 Hz, 1H), 3.63 (s, 2H). HRMS: [M+H]+, calc, for C16H14NO7: 332.07648, found: 332.07641 Biodata: Ia-034a: FGF-1 IC50 [pM] = 79; FGF-2 IC50 [pM] = 14; VEGF-A1 IC50 [pM] = 102; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 49.07; PMN ROS inhibition IC50 [pM] = 2.28; Neutrophil adhesion inhibition [%] = 15 21) 4-(3,4-Dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-035a: UPLC-MS (acidic method, 2 min): rt = 1.02 min; m / z = 320.1 [M+H]+, peak area >91% ‘HNMR (400 MHz, DMSO- d6) 5 11.56 (s, 1H), 9.21 (t, J= 5.9 Hz, 1H), 8.91 (s, 1H), 8.79 (s, 1H), 7.46 (s, 1H), 7.28 (s, 1H), 6.72 (d, 7= 2.1 Hz, 1H), 6.67 (d, 7= 8.0 Hz, 1H), 6.57 (dd, J= 8.0, 2.1 Hz, 1H), 4.32 (d, J= 5.8 Hz, 2H). HRMS: [M+H]+, calc, for C15H14NO7: 320.07648, found: 320.07650 Biodata: Ia-035a: FGF-1 IC50 [pM] = 20; FGF-2 IC50 [pM] = 71; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =36; PMN ROS [inhibition at 0.3 pM [%] = 75.13; PMN ROS inhibition IC50 [pM] = 0.41; Neutrophil adhesion inhibition [%] = 27 22) 4-(2-(3,4-Dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-035a-2: UPLC-MS (acidic method, 2 min): rt = 0.77 min; m / z = 332.0 [M-H]", peak area >99% ‘HNMR (400 MHz, DMSO-r / e) 8 11.50 (s, 1H), 8.85 (t, J = 5.6 Hz, 1H), 8.76 (s, 1H), 8.66 (s, 1H), 7.41 (s, 1H), 7.28 (s, 1H), 6.67 - 6.60 (m, 2H), 6.48 (dd, J = 8.0, 2.1 Hz, 1H), 3.44 (q, J = 6.8 Hz, 2H), 2.67 (dd, J = 8.6, 6.0 Hz, 2H).8 11.56 (s, 1H), 9.21 (t, J = 5.9 Hz, 1H), 8.91 (s, 1H), 8.79 (s, 81 1H), 7.46 (s, 1H), 7.28 (s, 1H), 6.72 (d, J = 2.1 Hz, 1H), 6.67 (d, J = 8.0 Hz, 1H), 6.57 (dd, J = 8.0, 2.1 Hz, 1H), 4.32 (d, J = 5.8 Hz, 2H). HRMS: [M+H]+, calc, for Ci6Hi6NO7: 334.09213, found: 334.09242 Biodata: Ia-035a-2: FGF-1IC50 [pM] = 10; FGF-2 IC50 [pM] = 65; VEGF-A1IC50 [pM] = 109; VEGFR-Phosphorylation inhibition IC50 [pM] =10; PMN ROS [inhibition at 0.3 pM [%] = 58.81; PMN ROS inhibition IC50 [pM] = 1.1; Neutrophil adhesion inhibition [%] = 21.5 2 3) 4-(l-Carboxy-2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-035a-3: UPLC-MS (acidic method, 2 min): rt = 0.70 min; m / z = 376.0 [M-H]", peak area >99% ‘HNMR (400 MHz, DMSO-J6) 5 12.90 (s, 1H), 11.11 (s, 1H), 8.98 (d, J = 7.4 Hz, 1H), 8.73 (d, J = 13.1 Hz, 2H), 7.45 (s, 1H), 7.31 (s, 1H), 6.61 (dd, J = 5.1, 2.9 Hz, 2H), 6.47 (dd, J = 8.1, 2.1 Hz, 1H), 3.01 (dd, J = 13.9, 4.9 Hz, 1H), 2.96 - 2.84 (m, 1H). HRMS: [M+H]+, calc, for Ci7Hi6NO9: 378.08196, found: 378.08195 Biodata: Ia-035a-3: FGF-1 IC50 [pM] = 34; FGF-2 IC50 [pM] = 207; VEGF-A1IC50 [pM] = 198; VEGFR-Phosphorylation inhibition IC50 [pM] =10; PMN ROS [inhibition at 0.3 pM [%] = 79.62; PMN ROS inhibition IC50 [pM] = 0.66; Neutrophil adhesion inhibition [%] = 22 24) 4-(Carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-036a: UPLC-MS (acidic method, 2 min): rt = 0.62 min; m / z = 362.1 [M-H]", peak area >92% ‘HNMR (400 MHz, DMSO-J6) 5 11.00 (s, 1H), 9.32 (d, J= 6.7 Hz, 1H), 9.05 (s, 1H), 8.97 (s, 1H), 7.40 (s, 1H), 7.34 (s, 1H), 6.81 (d, 7= 2.1 Hz, 1H), 6.75 - 6.64 (m, 2H), 5.29 (d, 7= 6.6 Hz, 1H). HRMS: [M+H]+, calc, for Ci6Hi4NO9: 364.06630, found: 364.06615 Biodata: Ia-036a: FGF-1 IC50 [pM] =N.D.; FGF-2 IC50 [pM] = 37; VEGF-A1IC50 [pM] = 123; VEGFR-Phosphorylation inhibition IC50 [pM] =1.6; PMN ROS [inhibition at 0.3 pM [%] = 87.17; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 30.77 25) 4-(2-Carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ia-053a: UPLC-MS (acidic method, 4 min): rt = 1.08 min; m / z = 332.0 [M+H]+, peak area >97% ‘HNMR (400 MHz, DMSO-J6) 5 13.09 (s, 1H), 11.19 (s, 1H), 9.34 - 9.27 (m, 1H), 7.91 (dd, J = 7.8, 1.4 Hz, 1H), 7.55 (dd, J = 7.5, 1.5 Hz, 1H), 7.46 (d, J = 7.9 Hz, 2H), 7.39 (td, J = 7.5, 1.4 Hz, 1H), 7.32 (s, 1H), 4.82 (d, J = 5.9 Hz, 2H). HRMS: [M+H]+, calc, for Ci6Hi4NO7: 332.07648, found: 332.07622 Biodata: Ia-053a: FGF-1 IC50 [pM] = 150; FGF-2 IC50 [pM] = 124; VEGF-A1IC50 [pM] = 210; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 52.92; PMN ROS inhibition IC50 [pM] = 2.5; Neutrophil adhesion inhibition [%] = 18.67 Scheme 4b. Synthesis of ethyl 4-amino-2,5-dibenzyloxybenzoate (aniline A) OBn        Curtins                      OBn HO        / o rearrangement          >= /   ° \ / \ /   --------►  H2N— /  \— / CT \ / \>Et l.iBuOCOCl           \OEt Bno                 2- NaN3             BnO 3. Heat KI-1           4 H2O              Aniline A Protocole: synthesis of Aniline A Ethyl 4-amino-2,5-dibenzyl oxybenzoate (Aniline A). To a cooled solution (ice bath) of 2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid (KI-1) (2.0 g, 4.9 mmol) and EhN (1.6 mL, 11.3 mmol) in THF (25 mL) under inert atmosphere (N2), was slowly added DPPA (1.1 mL, 5.2 mmol). The mixture was slowly warmed up to r.t and stirred at this temperature for 3 h. Then water (8 mL) was added and the reaction mixture was heated to 70 °C for 2 h. The reaction mixture was poured into a saturated solution of sodium hydrogencarbonate (250 mL) and stirred for 5 min before being extracted with EtOAc (3 x 100 mL). The combined organic layers were dried over sodium sulphate, filtered, and concentrated under reduced pressure to give a colourless oil. The residue was purified by flash column chromatography (iso-Hexane / EtOAc 1:0 then gradient to 30% EtOAc) to yield the title compound Aniline A (1.0 g, 53%) as an off-white solid. UPLC-MS (acidic method, 2 min): rt = 1.26 min; m / z = 378.2 [M+H]+, peak area 94% ‘HNMR (400 MHz, DMSO-tL) 5 7.54 - 7.46 (m, 4H), 7.44 - 7.36 (m, 4H), 7.35 - 7.25 (m, 3H), 6.46 (s, 1H), 5.65 (s, NH2), 5.06 (s, 2H), 5.02 (s, 2H), 4.16 (q, J = 7.1 Hz, 2H), 1.22 (t, J = 7.1 Hz, 3H). 26) 4-(4-Carboxy-2,5-dihydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound la-056a: UPLC-MS (acidic method, 4 min): rt = 0.90 min; m / z = 348.0 [M-H]-, peak area 97% 1HNMR (400 MHz, DMSO-d6) 5 11.28 (brs, 1H), 11.26 (s, 1H), 9.97 (s, 1H), 8.09 (s, 1H), 7.48 (s, 1H), 7.42 (s, 1H), 7.26 (s, 1H). Diethyl ester : UPLC-MS (acidic method, 4 min): rt = 1.86 min; m / z = 404.2 [M-H]", peak area 92% 1HNMR(400 MHz, DMSO-t / U 6 11.48 (brs, 1H), 11.32 (brs, 1H), 10.28 (s, 1H), 10.07 (brs, 1H), 9.88 (s, 1H), 8.12 (s, 1H), 7.58 (s, 1H), 7.39 (s, 1H), 7.28 (s, 1H), 4.46 - 4.27 (m, 4H), 1.46-1.12 (m, 6H). Example 1.2 - Molecules of type lb: Diamides from diamines, 1 example 5 Scheme 5. Synthesis of Diamides of type lb Synthetic Procedures: see general procedures, steps [3], [4], [5] Example: For conditions and yields: See Figures 4A-D 27)3,5-Bis(2,5-dihydroxy-4-carboxybenzoylamino)benzoic acid, compound Ib-OlOa: UPLC-MS (acidic method, 4 min): rt = 0.98 min; m / z = 511.0 [M-H]", peak area >93% 1HNMR(400MHz, DMSO-JJ 5 10.81 (s, 2H), 10.65 (s, 2H), 8.38 (d, J =2.0 Hz, 1H), 8.12 (d, J 15        =2.0 Hz, 2H), 7.39 (d, J= 2.3 Hz, 4H). HRMS: [M+H]+, calc, for C23H17N2O12: 513.07760, found: 513.07736, Biodata: Ib-OlOa: FGF-1 IC50 [pM] = 14; FGF-2 IC50 [pM] = 3.8; VEGF-A1 IC50 [pM] = 15; VEGFR-Phosphorylation inhibition IC50 [pM] =1.6; PMN ROS [inhibition at 0.3 pM [%] = 71.84; PMN ROS inhibition IC50 [pM] = 1.06; Neutrophil adhesion inhibition [%] = 1.5; Whole Blood: 84 GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 2.22; IL-Ip IC50 [pM] = 33.3; IL-2 IC50 [pM] = 2.74; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 1.02; IL-9 IC50 [pM] = 11.58; IL-10 IC50 [pM] = >100; IL-12p70 IC50 [pM] = 0.27; IL-13 IC50 [pM] = >100; IL-17A IC50 [pM] = 0.42; IL-17F IC50 [pM] = >100; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 67.8; IL-33 IC50 [pM] = 31.3; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.31; TNF p IC50 [pM] = 49.3 Triethyl ester: UPLC-MS (acidic method, 2 min): r.t = 1.29 mins, m / z = 597.1 [M+H]+, peak area > 96% 'H NMR (400 MHz, DMSO-J6) 5 10.80 (s, 2H), 10.68 (s, 2H), 9.95 (s, 2H), 8.40 (t, J= 2.0 Hz, 1H), 8.15 (d, J= 2.0 Hz, 2H), 7.42 (s, 2H), 7.39 (s, 2H), 4.42 - 4.33 (m, 6H), 1.38 - 1.33 (m, 9H). HRMS: [M+H]+, calc, for C29H29N2O12: 597.17150, found: 597.17131 Biodata: Ib-010a-E3: FGF-1 IC50 [pM] = 26; FGF-2 IC50 [pM] = 226; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.09; PMN ROS [inhibition at 0.3 pM [%] = 36.41; PMN ROS inhibition IC50 [pM] = 6.52; Neutrophil adhesion inhibition [%] = 79.5; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 2.79; IL-1 p IC50 [pM] = >100; IL-2 IC50 [pM] = 36.2; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.24; IL-9 IC50 [pM] = 26.8; IL-10 IC50 [pM] = >100; IL-12p70 IC50 [pM] = 0.84; IL-13 IC50 [pM] = 33; IL-17A IC50 [pM] = 0.52; IL-17F IC50 [pM] = 34.2; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = >100; IL-33 IC50 [pM] = 20; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.98; TNF p IC50 [pM] = 38.2. Triethyl ester Tetraacetate: UPLC-MS (acidic method, 2 min): r.t = 1.19 mins, m / z = 782.1 [M+NH4]+, peak area 91% 'H NMR (400 MHz, DMSO-J6) 5 10.84 (s, 2H), 8.40 (m, 1H), 8.08 (d, J = 2.0 Hz, 2H), 7.80 (s, 2H), 7.63 (s, 2H), 4.45 - 4.22 (m, 6H), 2.32 (s, 6H), 2.23 (s, 6H), 1.38 - 1.27 (m, 9H). Biodata: Ib-010a-E3-A4: FGF-1 IC50 [pM] = 200; FGF-2 IC50 [pM] = 200; VEGF-A1IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.54; PMN ROS [inhibition at 0.3 pM [%] = 54.86; PMN ROS inhibition IC50 [pM] = 1.49; Neutrophil adhesion inhibition [%] = 96 Example 1.3. - Molecules of type Ic: Diamides from diacids, 4 examples O OH Procedures: see general procedures from KI-6 [3], [4], [5] Examples: For conditions and yields: See Figures 4A-D 28) Ni,N4-Bis(2-(lH-tetrazol-5-yl)phenyl)-2,5-dihydroxyterephthalamide, compound Ic-001aTz2: UPLC-MS (acidic method, 2 min): rt = 0.97 min; m / z = 485.1 [M+H]+, peak area >97% 1HNMR(400MHz, DMSO-Jtf) 5 11.53 (s, 1H), 10.98 (s, 1H), 8.49 (dd, J = 8.4, 1.2 Hz, 1H), 7.90 (dd, J = 7.8, 1.6 Hz, 1H), 7.62 (ddd, J = 8.7, 7.4, 1.6 Hz, 1H), 7.58 (s, 1H), 7.37 (td, J = 7.6, 1.2 Hz, 1H). HRMS: [M+H]+, calc, for C22H17N10O4: 485.14287, found: 485.17274 Biodata: Ic-001aTz2: FGF-1 IC50 [pM] = 200; FGF-2 IC50 [pM] = 70; VEGF-A1 IC50 [pM] = 45; VEGFR-Phosphorylation inhibition IC50 [pM] =2.2; PMN ROS [inhibition at 0.3 pM [%] = 60.64; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 97.15; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 1.38; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = 9.45; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.52; IL-9 IC50 [pM] = 9.13; IL-10 IC50 [pM] = >100; IL-12p70 IC50 [pM] = 29.1; IL-13 IC50 [pM] = 0.12; IL- 17AIC50 [pM] = 0.31; IL-17FIC50 [pM] = 0.15; IL-18 IC50 [pM] = 33.9; IL-21 IC50 [pM] = 32; IL-33 IC50 [pM] = 0.23; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.1; TNF p IC50 [pM] = 0.41. 29) 5-(4-(3-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid, compound Ic-007a: UPLC-MS (acidic method, 2 min): rt = 0.80 min; m / z = 469.1 [M+H]+, peak area >91% 1HNMR(400 MHz, DMSO-J6) 5 8.08 (s, 2H), 7.65 (s, 2H), 7.59 (s, 2H), 7.30 - 6.89 (m, 5H), 6.79 (d, 7=8.8 Hz, 2H). 13C NMR (100 MHz, DMSO-^) 8 172.1, 165.2, 158.3, 150.1, 130.2, 129.2 (CH), 122.8, 122.6 (CH), 117.7 (CH), 117.3 (CH), 113.3. HRMS: [M+H]+, calc, for C22H17N2O10: 469.08777, found: 469.08739 Biodata: Ic-007a: FGF-1 IC50 [pM] = 13; FGF-2 IC50 [pM] = 5.4; VEGF-A1 IC50 [pM] = 3.2; VEGFR-Phosphorylation inhibition IC50 [pM] =0.09; PMN ROS [inhibition at 0.3 pM [%] = 57.99; PMN ROS inhibition IC50 [pM] = 2.7; Neutrophil adhesion inhibition [%] = 57.5; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 1.44; IL-lp IC50 [pM] = >100; IL-2 IC50 [pM] = >100; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.09; IL-9 IC50 [pM] = 27.1; IL-10 IC50 [pM] = 12.5; IL-12p70 IC50 [pM] = 0.49; IL-13 IC50 [pM] = 30.1; IL-17A IC50 [pM] = 0.04; IL-17F IC50 [pM] = 22.9; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 1.9; IL-33 IC50 [pM] = 18.4; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.27; TNF p IC50 [pM] = 6.52 Dimethyl ester: UPLC-MS (acidic method, 2 min): r.t = 1.13 mins, m / z = 497.0 [M+H]+, peak area > 95% 1HNMR(400 MHz, DMSO-d6) 5 11.08 (s, 2H), 10.48 (s, 2H), 10.38 (s, 2H), 8.27 (d, J= 2.8 Hz, 2H), 7.89 - 7.74 (m, 2H), 7.56 (s, 2H), 7.03 (d, J= 8.9 Hz, 2H), 3.93 (s, 6H). HRMS: [M+H]+, calc, for C24H21N2O10: 497.11907, found: 497.11874. Biodata: Ic-007a-E2: FGF-1 IC50 [pM] = 23; FGF-2 IC50 [pM] = 49; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.25; PMN ROS [inhibition at 0.3 pM [%] = 21.33; PMN ROS inhibition IC50 [pM] = 7.9; Neutrophil adhesion inhibition [%] = 2 Alternative, Large-scale synthesis of Ic-007a a) 5-(4-(3-Methoxycarbonyl-4-hydroxyphenylaminocarbonyl)-2,5-dibenzyloxybenzamido)-2-hydroxybenzoic acid methyl ester A 5 L flange flask was charged with 2,5-bis(benzyloxy)terephthalic acid (KI-6, 141.00 g, 0.373 mol), benzyltriethylammonium chloride (850 mg, 3.73 mmol, 0.01 eq) and chloroform (2.5 L). Then it was fitted with a nitrogen inlet, thermometer, pressure-equalizing dropping funnel, outlet to blank Dreschel bottle and sodium hydroxide bubbler. The stirred solution was warmed to 55°C, and thionyl chloride (59 mL, 0.802 mol, 2.15 eq) was added dropwise over a period of 40 min. The solution was held at 5 5 °C for 6h, then allowed to cool to room temperature overnight. An aliquot was sonicated in ethanol for 5 min., then analysed by LCMS analysis, which showed only diethylester. The mixture was transferred to two round bottom flasks and the volatiles were removed in vacuo; the acid chloride was azeotroped with toluene (800 mL in each flask). A 10 L jacketed vessel was charged with methyl 5-amino-2-hydroxybenzoate (137.00 g, 0.819 mol, 2.2 eq), and dichloromethane (2.5 L, 18 vol); the solution was cooled to 15°C. The acid chloride was taken up in dichloromethane (2.5 L, 18 vol) and added to the stirred reaction. The reaction immediately forms large amounts of solid and stirring becomes difficult; also the reaction exotherms to 30°C. However, on protracted stirring the mixture becomes a pink / purple fine suspension. The mixture was stirred at 25°C over 72h. The suspension was filtered, washed with dichloromethane (2 L, 14 vol) and the resulting solid dried in a vacuum oven to give 240.00 g of product (94% yield). b) 5-(4-(3-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxy benzoic acid, Ic-007a Saponification: A 5L 3-neck round bottom flask was charged with freshly ground 5-(4-(3-methoxycarbonyl-4-hydroxyphenylaminocarbonyl)-2,5-dibenzyloxybenzamido)-2-hydroxy-benzoic acid methyl ester (150.00 g, 0.22 mol) and isopropanol (1.5L, 10 vol). The mixture was warmed up to 50°C and tetrabutylammonium hydroxide (444 mL, 0.67 mol, 3 eq) and water (1.1 L, 7 vol) were added. After Ih some solids remained, so a further 60 mL of tetrabutylammonium hydroxide solution was added together with water (120 mL), the mixture stirred at 50°C for 6h, then allowed to cool to room temperature overnight. Additional tetrabutylammonium hydroxide (80 mL) was added and the mixture was further stirred at 60°C for Ih until no solid remained. Hydrogenolysis: The reaction was degassed (3 cycles with N2), then the catalyst (30.00 g, 10% Pd on C) was added as a slurry in water (100 mL). The reaction was further degassed (3 cycles with N2, 2 with H2) and placed under H2 (balloon pressure) at 50°C overnight. The reaction was recharged with hydrogen and held at 50°C for a further 4h after which time LCMS analysis showed complete reaction. The reaction mixture was degassed (3 cycles with N2), filtered through a pad of celite and washed with warm water / isopropanol (1 L, 1:1, 60°C). The volume was reduced to ~1.2 L in vacuo. The mixture was transferred to a 5 L flange flask with water (-3 L). The flask was fitted with an overhead stirrer (large anchor-type) and acidified with hydrochloric acid (35%). During the addition a heavy precipitate formed. The mixture was heated at 55°C for 6h, then allowed to cool to room temperature over 72h. The mixture was filtered and the solid slurried in IM aq HC1 (3L) and heated to 50°C for 3h, before allowing to cool to r.t. overnight. The mixture was filtered, washed with IM aq HC1 (2 L), water (1.5 L) and acetone (1 L). The solid was dried in the vacuum oven to give 100.00 g of product still contaminated by ~5 mol% of tetrabutylammonium salt (NMR). This solid was stirred in IM aq hydrochloric acid (3 L) at 70°C for 8h, then allowed to cool to r.t. overnight. The solid was filtered, washed with water and dried in the vacuum oven. The amount of tetrabutylammonium was reduced to -0.62 mol%. (85.90 g, 82% yield) (brown powder). 30) 2-(2,5-Dihydroxy-4-(4-hydroxy-2-carboxyphenylaminocarbonyl)benzamido)-5-hydroxybenzoic acid, compound Ic-009a: UPLC-MS (acidic method, 2 min): rt = 0.85 min; m / z = 469.0 [M+H]+, peak area >98% XHNMR (400 MHz, DMSO-J6) 5 13.31 (s, 2H), 11.93 (s, 2H), 10.85 (s, 2H), 9.64 (s, 2H), 8.41 (d, J= 9.0 Hz, 2H), 7.55 (s, 2H), 7.39 (d, J= 3.0 Hz, 2H), 7.03 (dd, J= 9.0, 3.0 Hz, 2H). HRMS: calc, for C22H17N2O10: 469.08777, found: 469.08755 Biodata: Ic-009a: FGF-1 IC50 [pM] = 32; FGF-2 IC50 [pM] = 202; VEGF-A1 IC50 [pM] = 208; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 72.85; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 72.21 Dimethyl ester: UPLC-MS (acidic method, 2 min): r.t = 1.03 mins, m / z = 497.1 [M+H]+, peak area > 92% ‘HNMR (400 MHz, DMSO-d6) 5 11.69 (s, 2H), 11.01 (s, 2H), 9.75 (s, 2H), 8.36 (d, J= 9.0 Hz, 2H), 7.62 (s, 2H), 7.37 (d, J= 3.0 Hz, 2H), 7.07 (dd, J= 9.0, 3.0 Hz, 2H), 3.87 (s, 6H). HRMS: calc, for C24H21N2O10: 497.11907, found: 497.11913 Biodata: Ic-009a-E2: FGF-1 IC50 [pM] = 23; FGF-2 IC50 [pM] = 30; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.02; PMN ROS [inhibition at 0.3 pM [%] = 24.12; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 41.05 Scheme 7. Synthesis of Amides of type Ic with R R’ Synthetic Procedures: See general procedure from KI-1. Example: O OH lc-001aTz / 004a For conditions and yields: See Figures 4A-D 31) 5-(4-(2-(lH-Tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid, compound Ic-001aTz / 004a: UPLC-MS (acidic method, 4 min): rt = 1.40 min; m / z = 477.2 [M-H]", peak area >99% 10 ^NMR (400 MHz, DMSO-r / tf) 5 10.92 (s, 1H), 10.42 (s, 1H), 8.47 (dd, J = 8.4, 1.2 Hz, 1H), 8.25 (d, J = 2.7 Hz, 1H), 7.98 - 7.88 (m, 1H), 7.76 (dd, J = 8.9, 2.8 Hz, 1H), 7.63 - 7.56 (m, 2H), 7.51 (s, 1H), 7.37 (td, J = 7.6, 1.2 Hz, 1H), 6.97 (d, J = 8.9 Hz, 1H). HRMS: [M+H]+, calc, for C22H17N6O7: 477.11532, found: 477.11475 Biodata: Ic-001a-Tz / 004a: FGF-1IC50 [pM] = 19; FGF-2 IC50 [pM] = 87; VEGF-A1IC50 [pM] 15       = 25; VEGFR-Phosphorylation inhibition IC50 [pM] =2.6; PMN ROS [inhibition at 0.3 pM [%] = 82.83; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 96.99; Whole Blood: GM-CSF IC50 [pM] = 3.4; IFNy IC50 [pM] = 0.61; IL-1 p IC50 [pM] = >100; IL-2 IC50 [pM] = 4.91; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 3.04; IL-9 IC50 [pM] = 8.48; IL-10 IC50 [pM] = 19.5; IL-12p70 IC50 [pM] = 12.2; IL-13 IC50 [pM] = 1.5; IL- 17A IC50 [pM] = 0.02; IL-17F IC50 [pM] = 2.4; IL-18 IC50 [pM] = 46.6; IL-21 IC50 [pM] = 0.3; IL-33 IC50 [pM] = 1.67; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.002; TNF p IC50 [pM] = 3.02 Methyl ester: UPLC-MS (acidic method, 2 min): r.t = 1.06 mins, m / z = 491.1 [M+H]+, peak area > 89% ‘HNMR (400 MHz, DMSO-d6) 5 11.55 (s, 1H), 10.90 (s, 1H), 10.45 (s, 1H), 10.37 (s, 1H), 8.47 (dd, J = 8.4, 1.2 Hz, 1H), 8.30 (d, J = 2.7 Hz, 1H), 7.91 (dd, J = 7.8, 1.6 Hz, 1H), 7.76 (dd, J = 8.9, 2.7 Hz, 1H), 7.63 (ddd, J = 8.7, 7.4, 1.6 Hz, 1H), 7.58 (s, 1H), 7.51 (s, 1H), 7.38 (td, J = 7.6, 1.2 Hz, 1H), 7.02 (d, J = 8.8 Hz, 1H), 3.93 (s, 4H). HRMS: [M+H]+, calc, for C23H19N6O7: 491.13097, found: 491.13071 Biodata: Ic-001a-Tz / 004a-El: FGF-1IC50 [pM] = 104; FGF-2IC50 [pM] = 200; VEGF-A1IC50 [pM] = 35; VEGFR-Phosphorylation inhibition IC50 [pM] =0.1; PMN ROS [inhibition at 0.3 pM [%] = 73.97; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 97.56 Example 1.4. Molecules of type Id: Benzimidazole-linked, 1 example OH HOOC 1 || 1 H 1        11      / / ----.COOH OH       X Scheme 8. Synthesis of compounds of type Id OBn                        OBn EtOOC^ / L               EtOOC^J^        COOEt n 1  —- %^X;OOH   [3]           I’lZ       J     161 OBn                        OBn H2NZ KI-1 OH hooc^L       cooh HI. [sf    LAxnxAx X LjQ Synthetic procedure: see general procedure from KI-1 [3], [4], [5] Cyclization step: see Figures 4A-D Example: OBn EtooCx / L        COOEt 32) 2-(4-Carboxy-2,5-dihydroxyphenyl)-lH-benzo[d]imidazole-4-carboxylic acid, compound Id-030a: UPLC-MS (acidic method, 4 min): rt = 0.99 min; m / z = 313.1 [M-H]", peak area >97% ‘HNMR (400 MHz, DMSO-JJ 5 8.10 (d, J = 8.2 Hz, 1H), 8.05 (d, J = 7.7 Hz, 1H), 7.80 (s, 1H), 7.68 (t, J = 8.0 Hz, 1H), 7.62 (s, 1H) Biodata - unstable in DMSO Ethyl Methyl ester: UPLC-MS (acidic method, 4 min): r.t = 2.09 mins, m / z = 357.1 [M+H]+, peak area > 89% 'H NMR (400 MHz, DMSO-Jtf+D2O 10%) 5 7.97 (d, J= 8.0 Hz, 1H), 7.90 - 7.83 (m, 2H), 7.44 -7.36 (m, 2H), 4.35 (q, J= 7.1 Hz, 2H), 3.94 (s, 3H), 1.33 (t, J= 7.1 Hz, 3H). HRMS: [M+H]+, calc, for Ci8Hi7N2O6: 357.10811, found: 357.10827 Biodata: Id-030a-E2: FGF-1 IC50 [pM] = 115; FGF-2 IC50 [pM] = 200; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.33; PMN ROS [inhibition at 0.3 pM [%] = 0; PMN ROS inhibition IC50 [pM] = 0; Neutrophil adhesion inhibition [%] = 43 Example 1.5: Molecules of type Ila: Monoamides, 16 examples SYNTHESIS OF PRECURSORS Scheme 9a. Synthesis of Intermediates KI-2 and KI-7 KI-2                      KI-7 Procedures'. Synthesis of KI-2 an KI-7 2,6-Di(ethoxycarbonyl)cyclohexane-l,4-dione [Step l][Ref: Rodriguez et al. Synth. Comm. 28 (1998) 2259-69]: 1,3-Dichloroacetone (12.5 g, 0.1 mol) in THF (500 mL) was added dropwise, over a period of 30 min, to a suspension of diethyl 1,3-acetonedicarboxylate (18 mL, 0.1 mol) and potassium carbonate-325 mesh (21.5 g, 0.15 mol) in THF (1 L) at reflux temperature. After 2 h, the reaction was complete and the mixture was cooled down to room temperature then filtered thought Celite®; the solid residue was washed with THF (200 mL), the solvent was then removed under reduced pressure. The crude product was purified by flash column chromatography (Hexanes / EtOAc 0 to 20%) to give the title compound (9.3 g, 37% yield). UPLC-MS (acidic method, 2 min): rt = 1.01 min; m / z = 257.1 [M+H]", peak area >74% ’H NMR (400 MHz, DMSO-r / tf) Complex mixture of enol and cis / trans isomers 5 12.10 (s), 4.23 (q, J = 7.1 Hz), 4.11 (m), 3.85 - 3.77 (m), 3.70 (s), 3.10 - 2.89 (m), 2.89 - 2.80 (m), 2.62 - 2.58 (m), 1.25 (t, J = 7.1 Hz), 1.22-1.15 (m, 9H). Diethyl 2,5-dihydroxyisophthalate [Step 2]: [Protocole taken from Zhong et al.: Chern Eur. J. 25 (2019) 8177-8169]: To a stirred solution of 2,6-di(ethoxycarbonyl)-cyclohexane-1,4-dione (5.0 g, 20 mmol) in AcOH (17 mL) at room temperature was added NBS (3.5 g, 20 mmol) in portions over 30 min. After 20 additional min, the reaction was quenched by the addition of water (100 ml). The desired product separated as a solid. After filtration and drying, the title compound was isolated as a white solid (4.6 g, 93% yield). UPLC-MS (acidic method, 2 min): rt = 1.00 min; m / z = 253.1 [M-H]", peak area >90% 1HNMR(400 MHz, DMSO-tL) 5 10.85 (s, 1H), 9.57 (s, 1H), 7.39 (s, 2H), 4.32 (q, J= 7.1 Hz, 4H), 1.31 (t, J=1A Hz, 6H). Diethyl 2,5-bis(benzyloxy)isophthalate [Step 3]: To a suspension of diethyl 2,5-dihydroxyisophthalate (19.0 g, 75 mmol) and potassium carbonate-325 mesh (82.6 g, 598 mmol) in DMF (83 mL) was added dropwise benzyl bromide (43.0 mL, 362 mmol) over 10 min. The reaction mixture was heated at 100 °C during 2 h. After cooling down to room temperature the solvent was removed under reduced pressure. Water (500 mL) was then added to the residue. The mixture was extracted with EtOAc (3 x 250 mL), the gathered organic layers were washed with brine (300 mL), dried over Na2SO4, filtered then concentrated under reduced pressure. The crude material was purified by flash column chromatography (Hexanes / EtOAc 0 to 15%) to give the title compound (29.4 g, 90% yield). UPLC-MS (acidic method, 2 min): rt = 1.38 min; m / z = 435.2 [M+H]+, peak area >90% 'H NMR (400 MHz, DMSO-d6) 5 7.50 (s, 2H), 7.49 - 7.45 (m, 2H), 7.44 - 7.37 (m, 5H), 7.37 - 7.29 (m, 3H), 5.17 (s, 2H), 4.95 (s, 2H), 4.26 (q, J= 7.1 Hz, 4H), 1.22 (t, J = 7.1 Hz, 6H). 2,5-bis(benzyloxy)-3-(ethoxycarbonyl)benzoic acid (KI-2) [Step 4]: A solution of potassium hydroxide (4.4 g, 79 mmol) in water (66 mL) was rapidly added to a solution of diethyl 2,5-bis(benzyloxy)isophthalate (31.3 g, 72 mmol) in 1,4-dioxane (430 mL). The reaction mixture was stirred at room temperature for 1.5 h. 1,4-Dioxane was removed under reduced pressure, an aqueous saturated solution of Na2CO3 (IL) was then added, the aqueous layer was extracted with EtOAc (3x 500 mL), dried over Na2SO4, filtered and the solvent was removed in vacuo. The residue was purified by filtration over a Silica Pad using Hexanes / EtOAc (1 / 1) then EtOAc (1 % v / v AcOH) as eluent to yield two different fractions: The starting material: Diethyl 2,5-bis(benzyloxy)isophthalate (20.4 g, 65% yield). UPLC-MS (acidic method, 2 min): rt = 1.38 min; m / z = 435.2 [M+H]+, peak area >78% 'H NMR (400 MHz, DMSO-d6) 5 7.50 (s, 2H), 7.49 - 7.45 (m, 2H), 7.44 - 7.37 (m, 5H), 7.37 - 7.29 (m, 3H), 5.17 (s, 2H), 4.95 (s, 2H), 4.26 (q, J= 7.1 Hz, 4H), 1.22 (t, J= 7.1 Hz, 6H). The desired product, 2,5-bis(benzyloxy)-3-(ethoxycarbonyl)benzoic acid as a white fluffy solid, (KI-2) (3.5 g, 12% yield). UPLC-MS (acidic method, 2 min): rt = 1.22 min; m / z = 405.1 [M-H]", peak area >90% 'H NMR (400 MHz, DMSO-J6) 5 13.30 (s, 1H), 7.48 (t, J= 3.0 Hz, 2H), 7.46 - 7.42 (m, 5H), 7.39 (m, 3H), 7.37-7.31 (m, 2H), 5.17 (s, 2H), 4.96 (s, 2H), 4.25 (q, J= 7.1 Hz, 2H), 1.22 (t, J= 7.1 Hz, 3H). The original saturated aqueous solution of Na2CO3 was then acidified to pH~7 using concentrated hydrochloric acid. Then extracted with EtOAc (2 x 500 mL), dried over sodium sulfate, filtered and concentrated under reduced pressure to give a mixture of KI-2 and KI-7 (3.0 g, 11% yield). UPLC-MS (acidic method, 2 min): rt = 1.00 min; m / z = 377.1 [M-H]", peak area 25%, rt = 1.22 min; m / z = 405.1 [M-H]", peak area 56% ‘HNMR (400 MHz, DMSO-J6) 5 13.23 (s, 2H), 7.52 - 7.29 (m, 12H), 5.17 (s, 2H), 4.97 (s, 2H). Scheme 9b: Alternative Synthesis of KI-7 OH Ac2O, pyr 95% [Step 1] NBS, AIBN 70% [Step 2] Formic Acid 78% [Step 3] KI-7 2,6-Dimethyl-l,4-phenylene diacetate [Step 1]: To a stirred solution of 2,6-dimethylhydroquinone (5.0 g, 36 mmol) in pyridine (10 mL) was rapidly added acetic anhydride (10 mL). The solution was stirred at room temperature for 18 h. The solvent was then removed under reduced pressure and the residue was dissolved with EtOAc (250 mL) and subsequently washed with an aqueous solution of hydrochloric acid (1 M, 250 mL), a saturated aqueous solution of NaHCCL (250 mL) and water (250 mL), dried over Na2SC>4, filtered and the solvent was removed in vacuo, to afford the title compound (7.4 g, 92%) as a white solid. UPLC-MS (acidic method, 2 min): rt = 1.07 min; m / z = 240.2 [M+NH4]+, peak area >90% ‘HNMR (400 MHz, DMSO-J6) 5 6.88 (HAr, 2H), 2.37 - 2.30 (m, 3H), 2.27 - 2.21 (m, 3H), 2.12 - 2.02 (m, 6H). 2,6-Bis(dibromomethyl)-l,4-phenylene diacetate [Step 2]: To a stirred solution of 2,6-dimethyl-l,4-phenylene diacetate (6.34 g, 29 mmol) in 1,2-Dichloroethane (130 mL) was sequentially added 2,2'-Azobis(2-methylpropionitrile) (AIBN) (0.93 g, 6 mmol) and / V-Bromosuccinimide (NBS) (25.39 g, 143 mmol). The solution was stirred under reflux for 24 h. Additional 2,2'-Azobis(2-methylpropionitrile) (AIBN) (0.93 g, 6 mmol) and A-Bromosuccinimide (NBS) (5.08 g, 28.6 mmol) were added and the reaction mixture was stirred under reflux for another 24 h. The reaction was cooled down to room temperature and the residual solid was removed by filtration and washed with DCM (250 mL). The filtrate was washed with an aqueous saturated solution of sodium hydrogen carbonate (250 mL), an aqueous solution of hydrochloric acid (1 M, 250 mL) and brine (250 mL). The organic layer was then dried with sodium sulfate, filtered and concentrated under reduced pressure to afford the title compound (9.38 g, 61%) as an orange oil. UPLC-MS (acidic method, 2 min): rt = 1.23 min; m / z = 553.1 [M+NH4]+, peak area >88% ^NMR (400 MHz, DMSO-J6) 5 7.69 (s, 2H), 7.31 (s, 2H), 2.49 (s, 3H), 2.32 (s, 3H). 2,5-Dihydroxyisophthalaldehyde [Step 3]: To a stirred suspension of 2,6-bis(dibromomethyl)-l,4-phenylene diacetate (3.89 g, 7.23 mmol) in formic acid (50 mL) was added water (5 mL). The mixture was stirred under reflux for 18 h. The reaction mixture was then slowly poured into aqueous saturated sodium hydrogen carbonate (300 mL). The formed precipitate was then isolated by filtration to give the title compound (0.94 g, 78%) as a brown solid. UPLC-MS (acidic method, 2 min): rt = 0.74 min; m / z = 165.0 [M-H]", peak area >98% 2,5-Bis(benzyloxy)isophthalaldehyde [Step 4]: Potassium carbonate-325 mesh (2.34 g, 17.0 mmol) was added to a stirred solution of 2,5-dihydroxyisophthalaldehyde (0.94 g, 5.7 mmol) in DMF (6 mL) at ambient temperature. Benzyl bromide (2.0 mL, 17.0 mmol) was then added to the reaction flask, and the resulting mixture was heated at 100 °C for 18 h. The reaction mixture was cooled down to ambient temperature and treated with a solution of saturated aqueous ammonium chloride (100 mL). The resulting suspension was stirred for 30 min, then filtered. The solid material was washed with a solution of saturated aqueous ammonium chloride (2x50 mL). The solid was then triturated with ethanol (5 mL), dried by suction to give the desired product as a brown solid (1.58 g, 68%) UPLC-MS (acidic method, 2 min): rt = 1.28 min, no ionization observed, peak area 78% ‘HNMR (400 MHz, DMSO-J6) 5 10.14 (s, 2H), 7.63 (s, 2H), 7.53 - 7.28 (m, 10H), 5.23 (s, 2H), 5.21 (s, 2H). 2,5-Bis(benzyloxy)isophthalic acid (KI-7) [Step 5]: 2,5-bis(benzyloxy)isophthalaldehyde (1.58 g, 4.5 mmol) was dissolved in a 2-methyl-2-butene solution in THF (2.0 M, 25 mL). A solution of sodium chlorite (5.1 g, 45.0 mmol) and potassium dihydrogen phosphate (4.6 g, 33.8 mmol) in water (25 mL) was then added and the reaction mixture was stirred at room temperature for 18 h. The reaction mixture was then poured into a saturated aqueous solution of NaHCCL (400 mL). The aqueous layer was washed with EtOAc (3 x 100 mL) followed by acidification with cone, hydrochloric acid (pH~l). The aqueous layer was then extracted with DCM (2x150 mL) and Et2O (2 x 200 mL), the gathered organic layer was dried with sodium sulfate, filtered and concentrated under reduced pressure. The residue was then triturated with w-pentane (3 x 50 mL) to give the title compound KI-7 as a white solid (0.98 g, 58%). UPLC-MS (acidic method, 2 min): rt = 1.03 min, m / z = 379.1 [M+H]+, peak area >96% ‘HNMR (400 MHz, DMSO-JJ 5 13.23 (s, 2H), 7.57 - 7.28 (m, 12H), 5.17 (s, 2H), 4.97 (s, 2H). Scheme 9c: Synthesis of KI-2Ac2 KI-2Ac2 Methyl 2,5-diacetoxy-3-methylbenzoate. 3-Methylsalicylic acid was oxidized with persulfate as reported by Nudenberg et al (J. Org. Chem. 1943, 8, 500-508). 3-Methylsalicylic acid (15.0 g, 98.6 mmol) was dissolved in a solution of sodium hydroxide (15.0 g, 375 mmol, 3.8 eq.) in water (37.5 mL). The light brown solution was cooled to 20 °C and treated, while stirring, with 7.75 mL portions of 40% sodium hydroxide and 33.8 mL portions of 10% potassium persulfate solutions, beginning with the hydroxide, at such a rate that a temperature of 30-35 °C was maintained and until ten portions of each were added. After the addition was completed, stirring was continued for 1 h, the mixture was allowed to stand at room temperature for 16-20 h, and cone HC1 was then added until blue to Congo. Unreacted 3-methylsalicylic acid separated at this point as a solid and was removed by filtration. The filtrate was extracted with ether several times (5x50 mL) to recover the remainder of 3-methylsalicylic acid. The aqueous solution was then treated with cone HC1 (100 mL) and then refluxed for 2 h to decompose the intermediate monosulfate. The warm solution was allowed to cool to r.t. and the almost black crystalline solid which precipitated was filtered, washed with water, and dried. Extraction of the aqueous filtrate with ether gave an additional batch of 2,5-dihydroxy-3-methylbenzoic acid as a brown solid (total: 7.71 g, 47%). Mp 212-214 °C;‘HNMR (250 MHz, DMSO): 8 10.94 (br. s., 1H), 7.00 (dd, J= 3.0 and 0.75, IHar), 6.86 (dd, J= 3.0 and 0.75, lHar), 2.12 (s, 3H). Esterification. Concentrated sulfuric acid (0.7 mL) was carefully added at 0 °C and under nitrogen to a solution of 2,5-dihydroxy-3-methylbenzoic acid (2.05 g, 12.2 mmol) in MeOH (7 mL). The reaction mixture was then stirred for 6 h at 100 °C. After cooling down to r.t., the solvent was removed under reduced pressure. The crude product obtained was dissolved in ethyl acetate (50 mL) and the solution washed with water (20 mL), 10% aq.NaHCCL (20 mL), 5% aq. HC1 (20 mL), and brine (20 mL), and was then dried (MgSO4). After filtering, the organic layer was concentrated in vacuo to give the residue which was purified by flash chromatography on silica gel (petroleum ether / ethyl acetate = 9 / 1) to afford methyl 2,5-dihydroxy-3-methylbenzoate as a white solid (370 mg, 75%). Mp 101-103 °C; 'HNMR (250 MHz, CDCh): 8 10.56 (d, J= 0.50 Hz, 1H), 7.12 (dd, J= 3.25 and 0.50 Hz, lHar), 6.90 (dt, J= 3.00 and 0.50 Hz, lHar), 4.45 (s, 3H),, 2.24 (s, 3H); HRMS (ESI+): m / z calcd for C9H11O4 [M+H]+: 183.0652; found 183.0651. Acetylation. Excess acetic anhydride (10 mL) was added to a solution of methyl 2,5-dihydroxy-3 -methyl-benzoate (4.43 g, 24.3 mmol) in pyridine (10 mL) under argon. After 12 h of stirring at r.t., pyridine and acetic anhydride were eliminated by co-evaporation with toluene (25 mL) under reduced pressure. The crude product was then dissolved in ethyl acetate (15 mL) and the solution washed successively with a 2% aq HC1 (5 mL), saturated aq NaHCCL (5 mL) and brine (5 mL). The organic phase was dried (MgSO4) and the solvent was evaporated under reduced pressure. The colorless oil obtained was purified by flash chromatography on silica gel (petroleum ether / ethyl acetate = 8 / 2) to afford the acetylated title product (2,5-acetoxy-3-methyl-benzoate) as a white solid (6.25 g, 97%). Mp 69-71 °C; ’H NMR (250 MHz, CDCh): 8 7.58 (dd, J= 3.00 and 0.50 Hz, lHar), 7.18 (dd, J= 3.00 and 0.75 Hz, lHar), 3.85 (s, 3H), 2.37 (s, 3H), 2.30 (s, 3H), 2.22 (s, 3H); HRMS (ESI+): m / z calcd for Ci3Hi8NO6 [M+NH4]+: 284.1129; found 284.1128. Methyl 2,5-diacetoxy-3-dibromomethylbenzoate. A solution of methyl 2,5-acetoxy-3-methyl-benzoate (2.15 g, 8.08 mmol), A-bromosuccinimide (2.87 mg, 16.2 mmol, 2.0 eq.) and azobisisobutyronitrile (AIBN, 27.0 mg, 0.162 mmol, 0.02 eq.) in carbon tetrachloride (45 mL) was refluxed for about 12 h until a white solid was floating on the surface. After cooling down, the mixture was filtered, and the filtrate was then concentrated under reduced pressure. The colorless oil obtained was purified by flash chromatography on silica gel (petroleum ether / ethyl acetate = 9 / 1) to afford the dibrominated product as a white solid (3.29 g, 84%). Mp 117-119 °C; ’H NMR (250 MHz, CDCI3): 8 7.86 (d, J= 2.75 Hz, lHar), 7.78 (d, J= 2.75 Hz, lHar), 6.81 (s, 1H), 3.86 (s, 3H), 2.42 (s, 3H), 2.33 (s, 3H);HRMS (ESI+): m / z calcd for CnHnB^NaOe [M+Na]+: 444.8893; found 444.8896. Methyl 2,5-diacetoxy-3-formylbenzoate. A solution of methyl 2,5 -diacetoxy-3 -dibromomethylbenzoate (2.30 g, 5.42 mmol) and silver nitrate (2.29 g, 13.5 mmol, 2.5 eq.) in a mixture acetone - H2O (4.7: 1, 40 mL) was stirred at r.t. and in the dark during 12 h. The mixture was then filtered, and the filtrate was extracted with ethyl acetate (2 x 20 mL). The combined organic phases were washed with brine (5 mL), dried (MgSO4) and concentrated under reduced pressure. The colorless oil thus obtained was purified by flash chromatography on silica gel (petroleum ether / ethyl acetate = 9 / 1) to afford the aldehyde as a yellow solid (1.14 g, 75%). Mp 102-104 °C; 1H NMR (250 MHz, CDCH): □ 10.17 (s, 1H), 8.00 (d, J = 3.00 Hz, lHar), 7.82 (d, J = 3.00 Hz, lHar), 3.90 (s, 3H), 2.44 (s, 3H), 2.34 (s, 3H). 2,5-Diacetoxyisophthalic acid monomethyl ester (KI-2AC2). A solution of sodium hydrogen phosphate (1.35 g, 9.81 mmol, 2.5 eq.) in water (3.5 mL) was added dropwise to a solution of methyl 2,5-diacetoxy-3-formylbenzoate (1.10 g, 3.93 mmol) in DMSO (14 mL). The mixture was then cooled to 0 °C and a solution of sodium chlorite (1.06 g, 9.34 mmol, 2.4 eq.) in water (3.5 mL) was slowly 98 added. After 72 h of stirring at r.t., the mixture was quenched with aqueous saturated NaHCOs (10 mL) and extracted with ethyl acetate (2x30 mL). The aqueous phase was then acidified with IM HC1 to pH = 1 and extracted ethyl acetate (2 x 30 mL). The combined organic phases were washed with brine (5 mL), dried (MgSO4) and concentrated under reduced pressure. The orange oil obtained was used in the 5 next step without any purification. SYNTHESIS OF MONOAMIDES Scheme 10. Synthesis of Monoamides Ila Protocoles: Synthesis of Monoamides Amide Coupling and Deprotection Procedures See General Procedures from KI-1 and KI-6 steps [3], [4], [5], same procedures from KI-2, KI-2Ac2 and KI-7 15 Examples Ila-001 a Ila-001 aTz Ila-001 c lla-002a COOH lla-003a Ila-012a For conditions and yields: See Table 2 (Figures 5A-C) 33) 3-(2-Carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ila-OOla: 5 UPLC-MS (acidic method, 2 min): rt = 0.86 min; m / z = 318.0 [M+H]+, peak area >92% 1HNMR(400 MHz, DMSO-d6) 5 13.49 (s, 1H), 12.16 (s, 1H), 9.54 (s, 1H), 8.70 (dd, J= 8.5, 1.2 Hz, 1H), 7.99 (dd, 7=7.9, 1.7 Hz, 1H), 7.70 - 7.51 (m, 2H), 7.42 (d, 7= 3.3 Hz, 1H), 7.20 (td, 7= 7.6, 1.2 Hz, 1H). HRMS: [M+H]+, calc, for C15H12NO7: 318.06083, found: 318.06082 10 Biodata: Ila-OOla: FGF-1IC50 [pM] = 8.6; FGF-2 IC50 [pM] = 11; VEGF-A1IC50 [pM] = 150; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 30.5; PMN ROS inhibition IC50 [pM] = 0.408; Neutrophil adhesion inhibition [%] = 36.24 34)3-(2-(lH-Tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ila-001 aTz: 15 UPLC-MS (acidic method, 2 min): rt = 0.71 min; m / z = 342.1 [M+H]+, peak area >99% ‘HNMR(400 MHz, DMS0-7O 5 11.40 (s, 1H), 9.49 (s, 1H), 8.51 (d, J = 8.3 Hz, 1H), 7.87 (d, J = 7.7 Hz, 1H), 7.72 - 7.51 (m, 2H), 7.51 - 7.26 (m, 2H) HRMS: [M+H]+, calc, for C15H12N5O5: 342.08329, found: 342.08317 Biodata: Ila-OOla-Tz: FGF-1 IC50 [pM] =N.D.; FGF-2 IC50 [pM] = 9.8; VEGF-A1 IC50 [pM] = 187; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 74.15; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 24.18 Ethyl ester UPLC-MS (acidic method, 4 min): rt = 1.46 min; m / z = 370.1 [M+H]+, peak area >92% ‘HNMR (400 MHz, DMSO-J6) 5 11.51 (s, 1H), 11.37 (s, 1H), 9.63 (s, 1H), 8.47 (d, J= 8.3 Hz, 1H), 7.92 (dd,J=7.8, 1.6 Hz, 1H), 7.66 - 7.57 (m, 2H), 7.43 (d, 7= 3.2 Hz, 1H), 7.38 (td, J= 7.6, 1.2 Hz, 1H), 4.40 (q, J= 7.1 Hz, 2H), 1.36 (t, J= 7.1 Hz, 3H), HRMS: [M+H]+, calc, for C17H16N5O5: 370.11460, found: 370.11444 Biodata: Ila-OOlaTz-El: FGF-1 IC50 [pM] = 200; FGF-2 IC50 [pM] = 42; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 68.86; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 81.94 35)2,5-Dihydroxy-3-(2-sulfophenylaminocarbonyl)benzoic acid, compound Ila-OOlc: UPLC-MS (acidic method, 2 min): rt = 0.63 min; m / z = 354.0 [M+H]+, peak area >80% 1HNMR(400MHz, DMSO-Jtf) 5 11.18 (s, 1H), 9.48 (s, 1H), 8.34 - 8.27 (m, 1H), 7.72 (dd,J = 7.7, 1.7 Hz, 1H), 7.52 (d, J = 3.2 Hz, 1H), 7.41 - 7.31 (m, 2H), 7.08 (td, J = 7.5, 1.2 Hz, 1H). HRMS: [M+H]+, calc, for Ci4Hi2NO8S: 354.02781, found: 354.02781 Biodata: Ila-OOlc: FGF-1 IC50 [pM] =N.D.; FGF-2 IC50 [pM] = 71; VEGF-A1IC50 [pM] = 283; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 72.62; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 43.53 36) 3-(3-Carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound IIa-002a: 'H NMR (250 MHz, CD3OD): 5 8.37 (t, 1H), 7.93 (br d, 1H), 7.81 (br d, 1), 7.76 (d, 1H), 7.52 (d, 1H), 7.48 (t, 1H). HRMS (ESI-): [M-H]’, calc, for C15H10NO7: 316.0461, found: 318.0463 Biodata: IIa-002a: FGF-1 IC50 [pM] = 19; FGF-2 IC50 [pM] = 131; VEGF-A1 IC50 [pM] = 150; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 43.3; PMN ROS inhibition IC50 [pM] = 0.299; Neutrophil adhesion inhibition [%] = 17.39 37)3-(4-Carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid)amide, compound IIa-003a: 1HNMR(250 MHz, CD3OD): □ 8.06 (BB’ of AA’BB’, 2H), 7.85 (AA’ of AA’BB’, 2H), 7.75 (d, 1H), 7.58 (d, 1H) HRMS (ESI-): calcd for C15H10NO7 [M-H]': 316.0461; found 316.0462 Biodata: IIa-003a: FGF-1 IC50 [pM] = 22; FGF-2 IC50 [pM] = 13; VEGF-A1 IC50 [pM] = 150; VEGFR-Phosphorylation inhibition IC50 [pM] =2.5; PMN ROS [inhibition at 0.3 pM [%] = 59.3; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 35.27 38)3-(3-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ila-004a: UPLC-MS (acidic method, 2 min): rt = 0.76 min; m / z = 334.0 [M+H]+, peak area >99% ‘HNMR (400 MHz, DMSO-J6) 5 14.02 (brs, 1H), 11.07 (brs, 1H), 10.32 (s, 1H), 9.47 (brs, 1H), 8.27 (d, J= 2.7 Hz, 1H), 7.76 (dd, J= 8.9, 2.7 Hz, 1H), 7.42 (d, J= 3.2 Hz, 1H), 7.36 (d, J= 3.2 Hz, 1H), 6.96 (d, J= 8.9 Hz, 1H). HRMS: [M+H]+, calc, for Ci5Hi2NO8: 334.05574, found: 334.05571 Biodata: IIa-004a: FGF-1 IC50 [pM] = 47; FGF-2 IC50 [pM] = 33; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 63.5; PMN ROS inhibition IC50 [pM] = 1.002; Neutrophil adhesion inhibition [%] = 36 39)3-(2-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ila-006a: UPLC-MS (acidic method, 2 min): rt = 0.65 min; m / z = 334.0 [M+H]+, peak area >99% ‘H NMR (400 MHz, DMSO-tL) 5 13.36 (s, 1H), 11.83 (s, 1H), 9.62 (s, 1H), 9.47 (s, 1H), 8.47 (d, J= 9.1 Hz, 1H), 7.64 (d, J= 3.3 Hz, 1H), 7.41 (d, J= 3.2 Hz, 1H), 7.37 (d, J= 3.0 Hz, 1H), 7.03 (dd, 7= 9.1, 3.0 Hz, 1H). HRMS: [M+H]+, calc, for Ci5Hi2NO8: 334.05574, found: 334.05548 Biodata: IIa-006a: FGF-1 IC50 [pM] = N.D.; FGF-2 IC50 [pM] = 43; VEGF-A1IC50 [pM] = 121; VEGFR-Phosphorylation inhibition IC50 [pM] =2.9; PMN ROS [inhibition at 0.3 pM [%] = 84.29; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 20.29 40) 3-(3-Carboxy-2,5-dihydroxybenzamido)phthalic acid, compound Ila-Olla: UPLC-MS (acidic method, 2 min): rt = 0.72 min; m / z = 360.1 [M-H]", peak area >77% ‘HNMR (400 MHz, DMSO-JJ 5 10.83 (s, 1H), 9.55 (s, 1H), 8.43 (dd, J= 7.9, 1.5 Hz, 1H), 7.73 (d, J= 3.3 Hz, 1H), 7.63 - 7.53 (m, 2H), 7.46 (d, J= 3.3 Hz, 1H), HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05066, found: 362.05045, Biodata: Ila-Olla: FGF-1 IC50 [pM] = 141; FGF-2 IC50 [pM] = 123; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 58.1; PMN ROS inhibition IC50 [pM] = 1.18; Neutrophil adhesion inhibition [%] = 26 41) 2-(3-Carboxy-2,5-dihydroxybenzamido)terephthalic acid, compound IIa-012a: UPLC-MS (acidic method, 2 min): rt = 0.73 min; m / z = 362.0 [M+H], peak area >97% ‘HNMR (DMSO-J6) 5: 13.81 (s, 1H), 13.34 (s, 1H), 12.23 (s, 1H), 9.50 (s, 1H), 9.30 (d, J= 1.6 Hz, 1H), 8.06 (d, . / = 8.2 Hz, 1H), 7.71 (dd, . / = 8.2, 1.7 Hz, 1H), 7.64 (d, 7= 3.3 Hz, 1H), 7.43 (d, J =3.3 Hz, 1H), HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05066, found: 362.05046, Biodata: IIa-012a: FGF-1IC50 [pM] = 150; FGF-2 IC50 [pM] = 150; VEGF-A1IC50 [pM] = 32; VEGFR-Phosphorylation inhibition IC50 [pM] =3.31; PMN ROS [inhibition at 0.3 pM [%] = 44.8; PMN ROS inhibition IC50 [pM] = 0.313; Neutrophil adhesion inhibition [%] = 7.5 42)2-(3-Carboxy-2,5-dihydroxybenzamido)isophthalic acid, compound IIa-013a: UPLC-MS (acidic method, 2 min): rt = 1.68 min; m / z = 362.0 [M+H]+, peak area >96% ‘HNMR (400 MHz, DMSO-J6) 5 13.12 (brs, 3H), 11.71 (s, 1H), 9.47 (s, 1H), 7.96 (s, 1H), 7.94 (s, 1H), 7.66 (d, J= 3.3 Hz, 1H), 7.44 (d, J= 3.3 Hz, 1H), 7.35 (t, J= 7.8 Hz, 1H). HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05066, found: 362.05047 Biodata: IIa-013a: FGF-1 IC50 [pM] = 137; FGF-2 IC50 [pM] = 12; VEGF-A1 IC50 [pM] = 34; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 57.68; PMN ROS inhibition IC50 [pM] = 2.54; Neutrophil adhesion inhibition [%] = 15.75 43)4-(3-Carboxy-2,5-dihydroxybenzamido)phthalic acid, compound IIa-014a: UPLC-MS (acidic method, 2 min): rt = 0.63 min; m / z = 362.1 [M+H]+, peak area >88% ‘HNMR (400 MHz, DMSO-d6) 5 10.80 (s, 1H), 9.45 (s, 1H), 8.01 (d, J= 22 Hz, 1H), 7.86 (dd, J= 8.5, 2.2 Hz, 1H), 7.74 (d, J= 8.5 Hz, 1H), 7.45 - 7.33 (m, 2H), HRMS: [M+H]+, calc, for Ci6Hi2NO9: 362.05066, found: 362.05048 Biodata: IIa-014a: FGF-1 IC50 [pM] = 40; FGF-2 IC50 [pM] = 61; VEGF-A1 IC50 [pM] = 91; VEGFR-Phosphorylation inhibition IC50 [pM] =17.6; PMN ROS [inhibition at 0.3 pM [%] = 73.94; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 21.5 44) 5-(3-Carboxy-2,5-dihydroxybenzamido)isophthalic acid, compound IIa-015a: ‘HNMR (250 MHz, CD3OD): 5 8.60 (d, J= 1.5 Hz, 2H), 8.44 (t, J= 1.5 Hz, 1H), 7.75 (d, J= 3.2 Hz, 1H), 7.56 (d, J = 3.2 Hz, 1) HRMS (ESI+): m / z calcd for C16H12NO9 [M+H]+: 362.0507; found 362.0505 [LM-163] Biodata: IIa-015a: FGF-1 IC50 [pM] = N.D.; FGF-2 IC50 [pM] = 125; VEGF-A1 IC50 [pM] = N.D.; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = N.D.; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = N.D. 45) (3-(3-(Carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ila-033a: UPLC-MS (acidic method, 2 min): rt = 0.78 min; m / z = 330.1 [M-H]", peak area >98% ‘HNMR (400 MHz, DMSO-JU 5 10.40 (s, 1H), 9.45 (s, 1H), 7.66 (t, J = 1.9 Hz, 1H), 7.63 - 7.57 (m, 1H), 7.45 (d, J = 3.3 Hz, 1H), 7.38 (d, J = 3.2 Hz, 1H), 7.29 (t, J = 7.8 Hz, 1H), 7.05 - 6.95 (m, 1H), 3.56 (s, 2H). HRMS: [M+H]+, calc, for C16H14NO7: 332.07648, found: 332.07644, Biodata: IIa-033a: FGF-1 IC50 [pM] = 35; FGF-2 IC50 [pM] = 32; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =4.9; PMN ROS [inhibition at 0.3 pM [%] = 50.64; PMN ROS inhibition IC50 [pM] = 0.914; Neutrophil adhesion inhibition [%] = 11.75 46)3-(2-(Carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound IIa-034a: UPLC-MS (acidic method, 2 min): rt = 0.74 min; m / z = 332.0 [M+H]+, peak area >95% ‘HNMR (400 MHz, DMSO-JU 5 12.48 (s, 1H), 10.65 (s, 1H), 9.30 (s, 1H), 7.97 (d, J= 8.3 Hz, 1H), 7.64 (d, J= 3.2 Hz, 1H), 7.40 (d, J= 3.3 Hz, 1H), 7.33 - 7.26 (m, 2H), 7.13 (td, J= 7.5, 1.3 Hz, 1H), 3.70 (s, 2H). HRMS: [M+H]+, calc, for C16H14NO7: 332.07648, found: 332.07653 Biodata: IIa-034a: FGF-1 IC50 [pM] = 22; FGF-2 IC50 [pM] = 5.7; VEGF-A1 IC50 [pM] = 86; VEGFR-Phosphorylation inhibition IC50 [pM] =100; PMN ROS [inhibition at 0.3 pM [%] = 69.2; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 26.58 Diethyl ester UPLC-MS (acidic method, 2 min): rt = 1.12 min; m / z = 388.1 [M+H]+, peak area >99% ‘HNMR (400 MHz, DMSO-JJ 5 11.81 (s, 1H), 9.58 (s, 1H), 7.77 (t, J= 8.5 Hz, 1H), 7.65 (d, J= 3.4Hz, 1H), 7.42 (d,7=3.4 Hz, 1H), 7.36 - 7.31 (m, 2H), 7.20 (t, J= 7.4 Hz, 1H), 4.39 (q, J= 7.1 Hz, 2H), 4.05 (q, J= 7.1 Hz, 2H), 3.77 (s, 2H), 1.36 (t, J= 7.1 Hz, 3H), 1.13 (t, J= 7.1 Hz, 3H). HRMS: [M+H]+, calc, for C20H22NO7: 388.13907, found: 388.13887 Biodata: IIa-034a-E2: FGF-1 IC50 [pM] =N.D.; FGF-2 IC50 [pM] = 164; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 68.73; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 11.86 47)3-(3,4-Dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound Ila-035a: UPLC-MS (acidic method, 2 min): rt = 0.69 min; m / z = 318.0 [M-H]", peak area >99% ‘HNMR (400 MHz, DMSO-JU 5 9.38 (s, 1H), 8.84 (s, 1H), 8.75 (s, 1H), 7.55 (d, J = 3.2 Hz, 1H), 7.34 (d, J = 3.2 Hz, 1H), 6.74 (d, J = 2.1 Hz, 1H), 6.67 (d, J = 8.0 Hz, 1H), 6.58 (dd, J = 8.1, 2.1 Hz, 1H), 4.34 (d, J = 5.7 Hz, 2H). HRMS: [M+H]+, calc, for C15H14NO7: 320.07647, found: 320.07625. Biodata: IIa-035a: FGF-1 IC50 [pM] = 16; FGF-2 IC50 [pM] = 61; VEGF-A1 IC50 [pM] = 45; VEGFR-Phosphorylation inhibition IC50 [pM] =0.52; PMN ROS [inhibition at 0.3 pM [%] = 76.99; PMN ROS inhibition IC50 [pM] = 1; Neutrophil adhesion inhibition [%] = 36.67 48)3-(2-Carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid, compound IIa-053a: UPLC-MS (acidic method, 4 min): rt = 1.08 min; m / z = 332.0 [M+H]+, peak area >97% ‘HNMR (DMSO-J6) 5: 13.13 (brs, 1H), 12.73 (brs, 1H), 9.40 (s, 1H), 9.05 (s, 1H), 7.91 (dd, J = 7.8, 1.4 Hz, 1H), 7.65 - 7.29 (m, 5H), 4.80 (d, J = 6.1 Hz, 2H). HRMS: [M+H]+, calc, for C16H14NO7: 332.07648, found: 332.07626 Biodata: IIa-053a: FGF-1 IC50 [pM] = 84; FGF-2 IC50 [pM] = 18; VEGF-A1 IC50 [pM] = 37; VEGFR-Phosphorylation inhibition IC50 [pM] =0.27; PMN ROS [inhibition at 0.3 pM [%] = 63.13; PMN ROS inhibition IC50 [pM] = 0.62; Neutrophil adhesion inhibition [%] = 20; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 1.04; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = 1.67; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 2.2; IL-9 IC50 [pM] = 1.41; IL-10 IC50 [pM] = >100; IL-12p70 IC50 [pM] = 0.27; IL-13 IC50 [pM] = 29.9; IL-17A IC50 [pM] = >100; IL-17F IC50 [pM] = 28.8; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = >100; IL-33 IC50 [pM] = 12.1; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.02; TNF p IC50 [pM] = 91.5. Example 1.6. Molecules of type lib: Diamides from diamines, 1 example Scheme 11. Synthesis of Diamides of type lib Procedure: see general procedure from KI-1 [3], [4], [5] For example: COOH llb-010a For conditions and yields: See Table 2 (Figures 5A-C) 49)3,5-Bis(2,5-dihydroxy-3-carboxybenzoylamino)benzoic acid, compound Ilb-OlOa: UPLC-MS (acidic method, 4 min): rt = 0.98 min; m / z = 511.1 [M-H]", peak area >93% 5 ’H NMR (400 MHz, DMSO-J6) 5 10.81 (s, 2H), 10.65 (s, 2H), 8.38 (m, 1H), 8.12 (d, J = 2.0 Hz, 2H), 7.39 (d, J = 2.3 Hz, 4H). HRMS: [M+H]+, calc, for C23H17N2O12: 513.07760, found: 513.07774 Biodata: Ilb-OlOa: FGF-1IC50 [pM] = 200; FGF-2 IC50 [pM] = 102; VEGF-A1IC50 [pM] = 28; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 81.87; 10 PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 59.84 Example 1.7. Molecules of type lie: Diamides from diacids, 2 examples O OH O OH Scheme 12. Synthesis of Amides of type lie with R = R’ Procedure: see general procedure from KI-6 [3], [4], [5] For examples O OH O R, R' = COOH llc-007a                llc-009a For conditions and yields: See Table 2 (Figures 5A-C) 50)5-(3-(3-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2- hydroxybenzoic acid, compound IIc-007a: UPLC-MS (acidic method, 4 min): rt = 1.20 min; m / z = 469.1 [M+H]+, peak area >91% ‘HNMR (400 MHz, DMSO-d6) 5 10.41 (s, 2H), 9.51 (s, 1H), 8.22 (d, J = 2.7 Hz, 2H), 7.79 (dd, J = 9.0, 2.7 Hz, 2H), 7.58 (s, 2H), 6.98 (d, J = 8.9 Hz, 2H), 13C NMR (100 MHz, DMSO-JJ 5 172.1, 166.1, 158.3, 152.0, 149.4, 130.2, 129.5 (CH), 122.8 (CH), 120.3, 119.8 (CH), 117.7 (CH). 113.0. HRMS: [M+H]+, calc, for C22H17N2O10: 469.08777, found: 469.08803 Biodata: IIc-007a: FGF-1 IC50 [pM] = 11; FGF-2 IC50 [pM] = 91; VEGF-A1 IC50 [pM] = 8.2; VEGFR-Phosphorylation inhibition IC50 [pM] =0.44; PMN ROS [inhibition at 0.3 pM [%] = 93.04; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 64.61 ; Whole Blood: GM-CSF IC50 [pM] = 26; IFNyIC50 [pM] = 0.11; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = 12.8; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.05; IL-9 IC50 [pM] = 2.14; IL-10 IC50 [pM] = 17.9; IL-12p70 IC50 [pM] = 3.37; IL-13 IC50 [pM] = 0.25; IL-17A IC50 [pM] = 0.01; IL-17F IC50 [pM] = 0.26; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 9.41; IL-33 IC50 [pM] = 0.18; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.03; TNF p IC50 [pM] = 0.29 Alternative Large Scale Synthesis of IIc-007a 2,5-Dibenzyloxyisophthalic acid (KI-7) To a 5L jacketed vessel was charged 2,5-dibenzyloxyisophthalaldehyde (Scheme 9b)(300g, 866 mmol), resorcinol (286g, 2.60mol), KH2PO4 (354g, 2.60mol), acetone (1.5L) and water (516ml). The slurry was stirred at 15-25°C. A solution of 80% NaC102 (294g, 2.60mol) in water (IL) was charged at 15-30°C over 90 mins (exotherm). After the addition was complete, the reaction was stirred at 15-25°C for Ihr. A solution of 85%H3PO4 (85ml, 1.24mol) in water (1175ml) [~1M] was charged over 10 mins atT<30°C (exotherm) affording a precipitate. The batch was cooled to 0-5°C and filtered. The solids were washed with water (3xl.2L) and oven dried (50°C) to afford 325.6g diacid KI-7. HPLC: 98.9%; NMR >95%. Corrected yield (90.6%). 5-(3-(3-Methoxycarbonyl-4-hydroxyphenylaminocarbonyl)-2,5-dibenzyloxybenzamido)-2-hydroxybenzoic acid methyl ester. To a 2L jacketed vessel was charged diacid KI-7 (80g, 21 Immol), HBTU (2-(IH-benzotriazol-l-yl)-1,1,3,3-tetramethyluronium hexafluorophosphate) (176.8g, 466mmol) and THF (560ml). The batch was stirred at 15-25°C and N-methylimidazole (50.6ml, 635mmol) was charged. After 30min, methyl 5-amino-2-hydroxybenzoate (77.8g, 466mmol) was charged and the reaction stirred at 25°C overnight. Water (1.2L) was charged and the batch stirred at 20°C for 30min. The batch was filtered, washed with water (2x480ml) then MeCN (320ml). The resulting solid (236g) was charged back to the vessel along with MeCN (800ml). The slurry was heated to 50°C for 40min then cooled to 20°C. The batch was filtered and washed with MeCN (320ml). NMR analysis of the solid (156g) indicated no TMU, HOBt, NMI or HBTU. The material was dried at 50°C overnight to afford 125g diamide. HPLC: 98.2%. NMR: >97%. Yield: 88%. 5-(3-(3-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dibenzyloxybenzamido)-2-hydroxybenzoic acid. To a 2L jacketed vessel was charged the previous diamide (110g, 163mmol), THF (550ml) and water (1100ml). The batch was stirred at 15-25°C and 85% KOH (32.2g, 488mmol) charged (minor exotherm). The solution was heated to 50°C for 4h then cooled to 20°C and stirred out overnight. 6M aq. AcOH (550ml, 3.3mol) was then charged over 30min at 15-25°C. After the addition was complete, the batch was stirred for 30mins and then filtered. The solids were washed with water (3x550ml) then oven dried at 50°C. This afforded 102g free diacid. HPLC: 98.9% (0.3% mono-amide, 0.19% monoacid). NMR: >97%. Yield: 97%. 5-(3-(3-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid IIc-007a. To a 2L jacketed vessel under N2 was charged 10% Pd / C (10g, 50% wet, type 87L) followed by the previous diacid (100g, 154mmol), AcOH (5ml, 88mmol) and THF (1200ml). The batch was stirred then sparged with H2 and heated to 40°C for 2hr. The batch was sparged with N2 and then filtered (GF / F). The vessel was rinsed with THF (300ml) and the rinse used to wash the catalyst on the filter. The filtrate was charged to the vessel and the volume adjusted to 2L with THF (400ml). The solution was warmed to 30°C, SPM32 (10g) charged, and the batch stirred at 30°C overnight. The SPM32 was filtered off and washed with THF (200ml). The solvent was removed in vacuo to afford a light yellow solid (110g). NMR analysis indicated 28% THF. The material was slurried in EtOH (IL) at 20°C for 2hr and then filtered off. The solids were washed with EtOH (400ml) and oven dried at 60°C overnight. NMR indicated 8.7% EtOH, no THF. The material was further dried at 80°C for 4 nights to afford 66.5g IIc-007a as an off-white solid in a 92% yield. HPLC: 99.5% (0.31% monoamide). NMR: 4.6% EtOH, no THF. Pd by ICP-OES: <2ppm. IIc-007a-THF solvate: Concentration of the THF filtrate gives a yellow solid, typically containing 2530% THF by NMR, which could not be removed through drying, indicating a non-stoichiometric solvate. A small sample of the THF solvate (1.45g) was heated to 50°C in THF (10ml) for Ihr, cooled to RT and isolated, washing with 3ml THF. This afforded 1.13g IIc-007a-THF. NMR: 27% THF. HPLC: 99.6% (0.1% monoamide). The isolation of the THF solvate by filtration leads to an increase in purity and an effective purge of the major impurity (monoamide, IIa-004a) from 0.7% to 0.1%. Recovery yield: 78%. THF solvate solubility in THF calculated as ~25mg / ml at 20°C. Desolvation trials were performed on the material in acetone, EtOH and EtOAc. Each batch was heated for Ihr at 50°C in 20vols of solvent, then isolated at RT and oven dried (60°C). Ethanol was chosen as the desolvation solvent due to the low level of EtOH incorporated in the product after drying and excellent purge of THF from the system. The desolvation step was performed on 12.1g product (25% THF). To the material was charged EtOH (20vols) and the batch was stirred at RT overnight. A sample was filtered off and this indicated successful desolvation at RT. Overall yield: 8.67g. HPLC: 99.4%. NMR: >97% (0.8% EtOH). XRPD indicated a high degree of crystallinity of the isolated product. The product IIc-007a also forms a DMSO solvates (DMSO:product in 3:2 ratio). 51)2-(3-(2-Carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-5- hydroxylbenzoic acid, compound IIc-009a: UPLC-MS (acidic method, 2 min): rt = 0.79 min; m / z = 469.1 [M+H]+, peak area >95% 1HNMR(400 MHz, DMF-d7) 5 10.11 (s,lH), 10.01 (s,2H), 8.71 (d, J= 9.0 Hz, 2H), 8.01 (s, 2H), 7.82 (d, J= 3.0 Hz, 2H), 7.46 (d, J= 8.9 Hz, 2H). HRMS: [M+H]+, calc, for C22H17N2O10: 469.08777, found: 469.08714 Biodata: IIc-009a: FGF-1IC50 [pM] = 30; FGF-2IC50 [pM] =N.D.; VEGF-A1IC50 [pM] = 182; VEGFR-PhosphorylationinhibitionIC50 [pM] =1.7;PMNROS [inhibitionat0.3 pM [%] = 75.31; PMN ROS inhibition IC50 [pM] =N.D.; Neutrophil adhesion inhibition [%] = 53.15; Whole Blood: GM-CSF IC50 [pM] = >100; IFNyIC50 [pM] = 0.54; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = 19.6; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.27; IL-9 IC50 [pM] = 18.9; IL-10 IC50 [pM] = 11.31; IL-12p70 IC50 [pM] = >100; IL-13 IC50 [pM] = 0.13; IL-17A IC50 [pM] = 0.001; IL-17F IC50 [pM] = 0.13; IL-18 IC50 [pM] = 2.95; IL-21 IC50 [pM] = 8.01; IL-33 IC50 [pM] = 0.29; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.11; TNF p IC50 [pM] = 6.94. Example 1.8: Molecules of type Illa: Monoamides, 4 examples HOOC OH Synthesis of Precursors Scheme 13. Synthetic Intermediates: KI-8 and KI-9 from KI-1 Synthetic Protocoles Intermediates KI-8 and KI-9 (by way of KI-10 and KI-11) Ethyl 2,5-bis(benzyloxy)-4-(hydroxymethyl)benzoate (KI-10) [Step 1]: To a cooled solution at -20 °C of KI-1 (62.3 g, 153 mmol) in THF (700 mL) under positive flow of inert gas (N2) was slowly added a pre-cooled solution of BH3.THF (615.0 mL, 615 mmol) (at -10 °C). The addition was done in such a way that the internal temperature of the reaction never exceeded -15 °C. The reaction was slightly warmed , the internal temperature being not allowed to exceed -7 °C. The mixture was maintained at this temperature for 2.5 h. The reaction mixture was then poured into ice / water (8 L). The blurry white mixtures obtained were left to stir at room temp, for 2 h and the residual white suspension was filtered through a fritted funnel (Porosity 3). The white solid thus obtained was further dried into vaccum oven at 40 °C overnight, to afford ethyl 2,5-bis(benzyloxy)-4-(hydroxymethyl)benzoate (KI-10) (60.5 g, 97% yield) as a white solid. UPLC-MS (acidic method, 2 min): rt = 1.25 min; m / z = 391.2 [M-H]", peak area >68% 1H NMR (400 MHz, DMSO-Jft 5 7.54 - 7.48 (m, 2H), 7.48 - 7.43 (m, 2H), 7.43 - 7.35 (m, 4H), 7.35 -7.27 (m, 4H), 5.28 (t, 7= 5.4 Hz, 1H), 5.13 (s, 2H), 5.11 (s, 2H), 4.58 (d, 7= 5.4 Hz, 2H), 4.25 (q,7 = 7.1 Hz, 2H), 1.26 ( / , J = 7.1 Hz, 3H). Alternatively intermediate KI-10 can be obtained from KI-1 by way of a mixed anhydride (treatment of KI-1 with isobutylchloroformate in THF in the presence of triethylamine) followed by reduction of the mixed anhydride with sodium borohydride in THF (yields 85-90%, 150g-scale). Ethyl 2,5-bis(benzyloxy)-4-(chloromethyl)benzoate (KI-11) [Step 2]: Tosyl chloride (17.0 g, 70 mmol) was added slowly to a cooled solution (ice bath) of KI-10 (25.0 g, 64 mmol), DIPEA (12.2 mL, 70 mmol) and DMAP (0.778 g, 6 mmol) in DCM (260 mL). The reaction mixture was stirred at 60 °C for 30 h, whereupon the reaction was judged complete. DCM (100 mL) was added and the organic layer was separated, washed with saturated aqueous sodium hydrogen carbonate (4 x 50 mL), water (2 x 50 mL) and brine (50 mL), dried over sodium sulphate and concentrated. The crude product was submitted to column chromatography (Hexanes / EtOAc 0-20%) to give ethyl 2,5-bis(benzyloxy)-4-(chloromethyl)benzoate (KI-11) (23.5 g, 75%). UPLC-MS (acidic method, 2 min): rt = 1.39 min; m / z = no ion, peak area >84%. ‘HNMR (400 MHz, DMSO-tL) 5 7.54 - 7.44 (m, 4H), 7.43 - 7.36 (m, 6H), 7.36 - 7.28 (m, 2H), 5.18 (s, 2H), 5.13 (s, 2H), 4.76 (s, 2H), 4.26 (q, J = 7.1 Hz, 2H), 1.25 (t, J = 7.1 Hz, 3H). Alternatively intermediate KI-11 can be obtained by treating KI-10 with thionyl chloride (1.14 equiv) in dichloromethane at -10°C, then evaporation of the solvent and precipitation from heptane (yield 90%, 300g-scale) Ethyl 2,5-bis(benzyloxy)-4-(cyanomethyl)benzoate [Step 3]: A suspension of KI-11 (7.5 g, 18.2 mmol) in a mixture of EtOH (90 mL) and H2O (45 mL) was treated with potassium cyanide (1.8 g, 27.4 mmol). The reaction mixture was heated to 75 °C and stirred at this temperature for 16 h. The reaction mixture was diluted with water (500 mL) and extracted with EtOAc (2 x 200 mL), the combined organic phases were then washed with brine (200 mL), dried over sodium sulfate, fdtered and concentrated in vacuo. The crude product was isolated as a mixture of ethyl 2,5-bis(benzyloxy)-4-(cyanomethyl)benzoate and 2,5-bis(benzyloxy)-4-(cyanomethyl)benzoic acid (7.1 g), the product was used in the next step without further purification. UPLC-MS (acidic method, 2 min): rt = 1.30 min; m / z = 402.2 [M+H]+, peak area >65% and rt = 1.15 min; m / z = 374.1 [M+H]+, peak area >8%. ‘HNMR (400 MHz, DMSO-^) 5 7.56 - 7.27 (m, 12H), 5.19 (s, 2H), 5.14 (s, 2H), 4.26 (q, J = 7.1 Hz, 2H), 3.95 (s, 2H), 1.25 (t, J = 7.1 Hz, 3H). 2,5-Bis(benzyloxy)-4-(carboxymethyl)benzoic acid (KI-9) [Step 4]: To a suspension of ethyl 2,5-bis(benzyloxy)-4-(cyanomethyl)benzoate (7.1 g, 13.2 mmol) in EtOH (20 mL) was added a solution of sodium hydroxide (8.5 g, 212.5 mmol) in water (50 mL) and the reaction mixture was stirred under reflux for 18 h. The reaction mixture was diluted with water (100 mL) and the resulting solution was washed with EtOAc (2 x 100 mL), the thus obtained organic layer was extracted with water (100 mL) and all aqueous layers were gathered. Then the aqueous layer was acidified to pH ~ 3 with a saturated aqueous solution of citric acid, the formed precipitate was filtered and dried under reduced pressure. The solid was further dried in the vac. oven at 40 °C overnight to give 2,5-bis(benzyloxy)-4-(carboxymethyl)benzoic acid (KI-9) (6.4 g, 92% yield) as a yellowish solid. UPLC-MS (acidic method, 2 min): rt = 1.07 min; m / z = 393.2 [M+H]+, peak area >74%. ‘HNMR (400 MHz, DMSO-d6) 5 12.46 (s, 2H), 7.55 - 7.27 (m, 11H), 7.19 (s, 1H), 5.11 (s, 2H), 5.09 (s, 2H), 3.61 (s, 2H). 2,5-Bis(benzyloxy)-4-(2-ethoxycarbonylmethyl)benzoicacid (KI-8) [Step 5]: KI-9 (5.5 g, 14.0mmol) was suspended in EtOH (30 mL)and the suspension was treated with thionyl chloride (0.52 mL, 7.1 mmol) and the reaction mixture was stirred at room temperature for 24 h. Then, the reaction mixture was poured into a saturated solution of sodium bicarbonate (1 L), leading to a white suspension. The solid was isolated by fdtration and further triturated with Et2O (2 x 20 mL). The solid was further dried in the vac. oven overnight to give 2,5-bis(benzyloxy)-4-(2- ethoxycarbonylmethyl)benzoic acid (KI-8) (4.2 g, 64%) as a white solid. UPLC-MS (acidic method, 2 min): rt = 1.23 min; m / z = 419.3 [M-H]", peak area >79%. 1HNMR(400 MHz, DMSO-JJ 5 12.68 (brs, 1H), 7.58 - 7.27 (m, 11H), 7.19 (s, 1H), 5.11 (s, 2H), 5.08 (s, 2H), 4.01 (q, J = 7.1 Hz, 2H), 3.66 (s, 2H), 1.11 (t, J = 7.1 Hz, 3H). Synthesis of Monoamides Scheme 14. Synthesis of Monoamides Illa Synthetic Protocoles Amide Coupling and Deprotection Procedures: See General Procedures from KI-1 and KI-6 steps [3], [4], [5] Examples HOOC OH For conditions and yields: See Table 3 (Figure 6) 52) 2-(4-(Carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid, compound Illa-OOla: UPLC-MS (acidic method, 2 min): rt = 0.89 min; m / z = 332.1 [M+H]+, peak area >98% ‘HNMR (400 MHz, DMSO-d6) 5 13.38 (s, 1H), 12.17 (s, 1H), 10.67 (s, 1H), 9.23 (s, 1H), 8.64 (dd, J= 8.5, 1.2 Hz, 1H), 8.00 (dd, J= 7.9, 1.7 Hz, 1H), 7.62 (ddd, J= 8.7, 7.3, 1.7 Hz, 1H), 7.33 (s, 1H), 7.19 (td, 7= 7.6, 1.2 Hz, 1H), 6.80 (s, 1H), 3.49 (s, 2H). HRMS: [M+H]+, calc, for C16H14NO7: 332.07648, found: 332.07666 Biodata: Illa-OOla: FGF-1 IC50 [pM] = 62; FGF-2 IC50 [pM] = 10; VEGF-A1 IC50 [pM] = 32; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 74.79; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 30.4 Ethyl methyl ester UPLC-MS (acidic method, 2 min): rt = 1.14 min; m / z = 374.2 [M+H]+, peak area >96%. XH NMR (400 MHz, DMSO-d6) 8 11.91 (s, 1H), 10.78 (s, 1H), 9.25 (s, 1H), 8.60 (dd, J = 8.5, 1.2 Hz, 1H), 7.97 (dd, J = 8.0, 1.7 Hz, 1H), 7.64 (ddd, J = 8.7, 7.3, 1.7 Hz, 1H), 7.38 (s, 1H), 7.26 -7.18 (m, 1H), 6.81 (s, 1H), 4.08 (q,7=7.1 Hz, 2H), 3.88 (s, 3H), 3.56 (s, 2H), 1.19 (t,7=7.1 Hz, 3H). HRMS: [M+H]+, calc, for C19H20NO7: 374.12342, found: 374.12333 Biodata: IIIa-001a-E2: FGF-1 IC50 [pM] = 200; FGF-2 IC50 [pM] = 33; VEGF-A1IC50 [pM] = 43; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 69.66; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 44.46 53) (2-(lH-Tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid, compound Illa-001 aTz: UPLC-MS (acidic method, 2 min): rt = 0.87 min; m / z = 356.1 [M+H], peak area >95%. 1HNMR(400 MHz, DMS0-7O 8 12.22 (s, 1H), 11.43 (s, 1H), 10.74 (s, 1H), 9.21 (s, 1H), 8.46 (dd, 7=8.5, 1.2 Hz, 1H), 7.87 (d, 7= 8.1 Hz, 1H), 7.60 (td, 7= 8.6, 7.9, 1.6 Hz, 1H), 7.39 - 7.30 (m, 2H), 6.80 (s, 1H), 3.48 (s, 2H). HRMS: [M+H]+, calc, for C16H14N5O5: 356.09894, found: 356.09889 Biodata: IIIa-OOlaTz: FGF-1 IC50 [pM] = 51; FGF-2 IC50 [pM] = 14; VEGF-A1 IC50 [pM] = 12; VEGFR-Phosphorylation inhibition IC50 [pM] =0.71; PMN ROS [inhibition at 0.3 pM [%] = 69.35; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 39.74; Whole Blood: GM-CSF IC50 [pM] = >100; IFNyIC50 [pM] = 18.9; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = >100; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 1.98; IL-9 IC50 [pM] = 3.01; IL-10 IC50 [pM] = 7.78; IL-12p70 IC50 [pM] = 0.48; IL-13 IC50 [pM] = 0.15; IL-17A IC50 [pM] = 0.17; IL-17F IC50 [pM] = 0.16; IL-18 IC50 [pM] =27.7; IL-21 IC50 [pM] = 3; IL-33 IC50 [pM] = 0.14; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.31; TNF p IC50 [pM] = 0.23. Ethyl ester: UPLC-MS (acidic method, 4 min): rt = 1.56 min; m / z = 384.2 [M+H]+, peak area >95%. 1HNMR(400 MHz, DMSO-JJ 5 11.34 (s, 1H), 10.73 (s, 1H), 9.25 (s, 1H), 8.45 (dd, J= 8.5, 1.2 Hz, 1H), 7.85 (dd, J= 7.8, 1.6 Hz, 1H), 7.61 (ddd, J= 8.7, 7.4, 1.6 Hz, 1H), 7.39 - 7.30 (m, 2H), 6.80 (s, 1H), 4.08 (q, J= 7.1 Hz, 2H), 3.56 (s, 2H), 1.19 (t, J = 7.1 Hz, 3H). HRMS: [M+H]+, calc, for Ci8Hi8N5O5: 384.13024, found: 384.12999 Biodata: IIIa-OOlaTz-El: FGF-1 IC50 [pM] = 200; FGF-2 IC50 [pM] = 200; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.32; PMN ROS [inhibition at 0.3 pM [%] = 70.03; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 91.76 54) 2-(4-(Carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid, compound IIIa-013a: UPLC-MS (acidic method, 4 min): rt = 0.82 min; m / z = 376.0 [M+H]+, peak area >89%. XH NMR (400 MHz, DMSO-d6) 5 13.67 - 11.48 (m, 3H), 10.82 (s, 1H), 9.19 (s, 1H), 7.95 (d,J = 7.8 Hz, 2H), 7.36 (s, 1H), 7.33 (t, J= 7.8 Hz, 1H), 6.79 (s, 1H), 3.48 (s, 2H). HRMS: [M+H]+, calc, for C17H14NO9: 376.06630, found: 376.06638 Biodata: IIIa-013a: FGF-1 IC50 [pM] = 17; FGF-2 IC50 [pM] = 31; VEGF-A1 IC50 [pM] = 43; VEGFR-Phosphorylation inhibition IC50 [pM] =1.3; PMN ROS [inhibition at 0.3 pM [%] = 76.55; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 30.667; Whole Blood: GM-CSF IC50 [pM] = 27.8; IFNy IC50 [pM] = 0.15; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = 57.1; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 3.55; IL-9 IC50 [pM] = 11.9; IL-10 IC50 [pM] = 37.3; IL-12p70 IC50 [pM] = 0.5; IL-13 IC50 [pM] = 0.37; IL-17A IC50 [pM] = 0.15; IL-17F IC50 [pM] = 0.41; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 1.63; IL-33 IC50 [pM] = 1.11; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.51; TNF p IC50 [pM] = 0.89. 55) 5-(4-(Carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid, compound IIIa-015a: UPLC-MS (acidic method, 4 min): rt = 0.93 min; m / z = 376.0 [M+H]+, peak area >96%. ‘HNMR (400 MHz, DMSO-d6+10% D2O) 5 8.34 (s, 2H), 8.18 (s, 1H), 7.38 (s, 1H), 6.71 (s, 1H), 3.39 (s, 2H). HRMS: [M+H]+, calc, for C17H14NO9: 376.06630, found: 376.06665 Biodata: IIIa-015a: FGF-1IC50 [pM] = 16; FGF-2IC50 [pM] = 114; VEGF-A1IC50 [pM] = 202; VEGFR-Phosphorylation inhibition IC50 [pM] =0.89; PMN ROS [inhibition at 0.3 pM [%] = 78.76; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 12.13 Ethyl dimethyl ester UPLC-MS (acidic method, 4 min): rt = 1.69 min; m / z = 432.1 [M+H]+, peak area >97%. 1HNMR(400 MHz, DMSO-d6) 5 9.23 (s, 1H), 8.58 (s, 1H), 8.58 (s, 1H), 8.23 - 8.21 (m, 1H), 7.31 (s, 1H), 6.81 (s, 1H), 4.08 (q, J = 7.0 Hz, 2H), 3.91 (s, 6H), 3.58 (s, 2H), 1.19 (t, J = 7.1 Hz, 3H), HRMS: [M+H]+, calc, for C21H22NO9: 432.12891, found: 432.02903 Biodata: IIIa-015a-E3: FGF-1 IC50 [pM] =N.D.; FGF-2 IC50 [pM] = 191; VEGF-A1IC50 [pM] = 87; VEGFR-Phosphorylation inhibition IC50 [pM] =7.2; PMN ROS [inhibition at 0.3 pM [%] = 91.37; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 61.22 Example 1.9. Molecules of type Illb: Diamides from diamines, 1 example Scheme 15. Synthesis of Diamides of type Illb Procedure: see general procedure from KI-1 steps [3], [4], [5] For example: COOH Illb-OlOa For conditions and yields: See Table 3 (Figure 6) 56)3,5-Bis(2,5-dihydroxy-4-carboxymethylbenzoylamino)benzoic acid, compound Illb-OlOa: UPLC-MS (acidic method, 4 min): rt = 1.08 min; m / z = 539.2.1 [M-H]", peak area 80%. ‘HNMR (400 MHz, DMSO-J6) 5 10.85 (brs, 2H), 10.57 (brs, 2H), 9.20 (s, 2H), 8.26 (m, 1H), 8.09 (d, J= 2.0 Hz, 2H), 7.36 (s, 2H), 6.82 (s, 2H), 3.50 (s, 4H). HRMS: [M+H]+, calc, for C23H17N2O12: 513.07760, found: 513.07774 Triethyl ester UPLC-MS (acidic method, 4 min): rt = 1.81 min; m / z = 623.3 [M-H]", peak area 94%. ‘HNMR (400 MHz, DMSO-tL) 5 10.87 (s, 2H), 10.65 (s, 2H), 9.23 (s, 2H), 8.31 - 8.28 (m, 1H), 8.10 (d, J = 2.0 Hz, 2H), 7.35 (s, 2H), 6.81 (s, 2H), 4.35 (q, J = 7.1 Hz, 2H), 4.08 (q, J = 7.1 Hz, 4H), 3.58 (s, 4H), 1.35 (t, J = 7.1 Hz, 3H), 1.19 (t, J = 7.1 Hz, 6H). Biodata: IIIb-010a-E3: FGF-1 IC50 [pM] = 200; FGF-2 IC50 [pM] = 200; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.65; PMN ROS [inhibition at 0.3 pM [%] = N.D.; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 0 Example 1.10: MOLECULES OF TYPE IIIc. Dimers, 6 examples Synthetic Schemes and Procedures Scheme 16: X=O Synthetic procedures Formation of ether linkage from KI-10 and KI-11 Ethyl     2,5-dibenzyloxy-4- [(2,5-dibenzyloxy-4-ethoxycarbonyphenyl)methoxymethyl] benzoate [Step 1]: To a solution of KI-11 (340 mg, 0.83 mmol) and KI-10 (250 mg, 0.64 mmol) in DMF (6 mL), cooled down in an ice bath, was added portionwise sodium hydride (76 mg, 1.9 mmol). After 1 h, the reaction mixture was poured into a saturated aqueous solution of ammonium chloride (50 mL) and the material was extracted with EtOAc (3x30 mL), the organic phase was further washed with water (2 x 50 mL) and brine (50 mL), dried with sodium sulfate and concentrated under reduced pressure. The crude product was purified by flash column chromatography (Hexane s / EtO Ac 0 to 20%) to give th title compound (161 mg, 33% yield) as a brown solid. Deprotection procedures: See General procedures [4], [5] For examples IIIb-060a For conditions and yields: See Table 4 (deprotections) (Figure 7) 57) 4-((2,5-Dihydroxy-4-carboxyphenyl)methoxymethyl)-2,5-dihydroxybenzoic acid, compound IIIc-060a: UPLC-MS (acidic method, 4 min): rt = 0.94 min; m / z = 349.1 [M-H]", peak area >90%. ‘HNMR (400 MHz, DMSO-d6) 5 7.20 (s, 2H), 6.92 (s, 2H), 4.56 (s, 4H), Biodata: IIIc-060a: FGF-1IC50 [pM] = 200; FGF-2IC50 [pM] = 51; VEGF-A1IC50 [pM] = 114; VEGFR-Phosphorylation inhibition IC50 [pM] =1.3; PMN ROS [inhibition at 0.3 pM [%] = 86.84; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 41.38 Scheme 17: X = NH O OBn KI-13 O OBn        OBn O Synthetic procedures Formation of amine linkage from KI-12 and KI-13 via KI-10 and KI-11 Ethyl 2,5-Bis(benzyloxy)-4-formylbenzoate (KI-12): To a solution of KI-10 (3.4 g, 8.6 mmol) in dichloromethane (50 mL) was added manganese dioxide (4.5 g, 51.9 mmol). The resulting suspension was stirred under reflux for 4 h. The reaction was filtered through a pad of Celite® and the solid washed with dichloromethane (300 mL), the solvent was then removed under reduced pressure to give the title compound (3.2 g, 94% yield) as a yellowish solid. UPLC-MS (acidic method, 2 min): rt = 1.33 min; m / z = no ion, peak area >93% ‘HNMR (400 MHz, DMSO-J6) 5 10.39 (s, 1H), 7.56 (s, 1H), 7.54 - 7.26 (m, 11H), 5.28 (s, 2H), 5.20 (s, 2H), 4.30 (q, J= 7.1 Hz, 2H), 1.27 (t, J= 7.1 Hz, 3H). Ethyl 4-(azidomethyl)-2,5-bis(benzyloxy)benzoate: To a suspension of KI-10 (3.0 g, 7.6 mmol) and l,8-Diazabicyclo[5.4.0]undec-7-ene (DBU) (1.5 mL. 9.9 mmol) in toluene (30 mL) was added diphenyl phosphoryl azide (DPPA) (2 mL, 9.1 mmol). The resulting mixture was stirred at room temperature for 18 h. An aqueous solution of IM hydrogen chloride (200 mL) was added and the product was extracted with EtOAc (3 x 100 mL), the combined organic layers were washed with water (2x50 mL), dried over sodium sulfate and concentrated under reduced pressure. The residue was purified by flash column chromatography (Hexanes / EtOAc 0 to 20%) to yield the title compound (3.1g, 98%) as a colourless oil that became a white solid overtime. UPLC-MS (acidic method, 2 min): rt = 1.37 min; m / z = 390.2, [M+H-N2]+, peak area >93% ‘HNMR (400 MHz, DMSO-tL) 5 7.53 - 7.46 (m, 4H), 7.44 - 7.26 (m, 8H), 5.16 (s, 2H), 5.14 (s, 2H), 4.48 (s, 2H), 4.26 (q, J = 7.1 Hz, 2H), 1.25 (t, J = 7.1 Hz, 3H). Ethyl 4-(aminomethyl)-2,5-bis(benzyloxy)benzoate (KI-13): To a solution of ethyl 4-(azidomethyl)-2,5-bis(benzyloxy)benzoate (2.8 g, 6.7 mmol) in THF (60 mL) and water (6 mL) was added polymerbound triphenylphosphine (4.7 g, ~3mmol / g loading) and the resulting mixture was left to stir at room 118 temperature for 18 h. The resin was removed by filtration and washed with water (100 mL) and EtOAc (2 x 100 mL). The phases were separated, and the aqueous layer was further extracted with EtOAc (100 mL), the gathered organic layers were washed with brine (200 mL), dried over sodium sulfate and concentrated to give the title compound (KI-13) (1.8 g, 70% yield) as a white solid. UPLC-MS (basic method, 2 min): rt = 1.20 min; m / z = 392.2, [M+H]+, peak area >93% ‘HNMR (400 MHz, DMSO-JJ 5 7.60 - 7.22 (m, 12H), 5.14 (s, 2H), 5.10 (s, 2H), 4.24 (q, J = 7.1 Hz, 2H), 3.75 (s, 2H), 1.25 (t, J = 7.1 Hz, 3H). Ethyl 2,5-dibenzyloxy-4-[(2,5-dibenzyloxy-4-ethoxycarbonylphenyl)methylaminomethyl] benzoate: KI-12 (500 mg, 1.3 mmol) and KI-13 (641 mg, 1.6 mmol) were dissolved in DCM (35 mL) followed by addition of activated molecular sieves (10 beads). The resulting mixture was stirred at room temperature for 5 h. Sodium triacetoxyborohydride (654 mg, 3.1 mmol) was then added and the resulting mixture was stirred at room temperature for 18 h. DCM (25 mL) was added, the reaction mixture was decanted into a separating funnel and washed with water (50 mL), dried with sodium sulfate and concentrated under reduced pressure. The residue was purified by flash column chromatography ((Hexanes / EtOAc 0 to 50%) to yield the titled compound (631 mg, 64% yield) as a colourless oil that became solid overtime. UPLC-MS (acidic method, 2 min): rt = 1.37 min; m / z = 766.3, [M+H]+, peak area >92% ‘HNMR (400 MHz, DMSO-JJ 5 7.47 - 7.42 (m, 4H), 7.38 - 7.25 (m, 20H), 5.08 (s, 4H), 5.04 (s, 4H), 4.25 (q, J= 7.1 Hz, 4H), 3.76 (s, 4H), 1.25 (t, J= 7.1 Hz, 6H). Deprotection procedures: See General procedures [4], [5] For conditions and yields: See Figure 7. For examples OH            OH HOOC / L                COOH Y 1 H M Il JI OH            OH 58)Bis(4-carboxy-2,5-dihydroxyphenylmethyl)amine, compound IIIc-056a: UPLC-MS (acidic method, 4 min): rt = 0.57 min; m / z = 350.0 [M+H]+, peak area >96%. ‘HNMR (400 MHz, DMSO-d6) 5 9.97 (s, 2H), 9.08 (s, 2H), 7.31 (s, 2H), 7.02 (s, 2H), 4.11 (s, 4H). HRMS: [M+H]+, calc, for Ci6Hi6NO8: 350.08704, found: 350.08706 Biodata: IIIc-056a: FGF-1IC50 [pM] = 200; FGF-2IC50 [pM] = 35; VEGF-A1IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 90.07; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 35 Scheme 18: X = NAc O OBn        OBn O Synthetic procedures N,N-Bis-[2,5-dibenzyloxy-4-ethoxycarbonylphenyhnethyl]acetamide: To a solution ofN,N-bis-[2,5-dibenzyloxy-4-ethoxycarbonylphenylmethyl]amine (300 mg, 0.39 mmol) and pyridine (0.2 mL, 2.4 mmol) in DCM (6 mL), under an atmosphere of nitrogen, was added acetic anhydride (0.2 mL, 2.1 mmol). The reaction mixture was stirred at room temperature for 1 h and concentrated under reduced pressure. The residue was purified by flash column chromatography (Hexanes / EtOAc, 0 to 50 %) to give the title compound (316 mg, 92% yield) as a colourless oil. UPLC-MS (acidic method, 2 min): rt = 1.44 min; m / z = 808.2 [M+H]+, peak area >95%. ‘HNMR (400 MHz, DMSO-d6) 5 7.49 - 7.17 (m, 22H), 6.92 (s, 1H), 6.72 (s, 1H), 5.03 (s, 2H), 5.00 (s, 2H), 4.96 (s, 2H), 4.94 (s, 2H), 4.46 (s, 4H), 4.31 - 4.16 (m, 4H), 1.96 (s, 3H), 1.28 - 1.20 (m, 6H). Deprotection procedures: See General procedures [4], [5] For examples For conditions and yields: See Figure 7 (deprotections) 59)N,N-Bis(4-carboxy-2,5-dihydroxyphenylmethyl)acetamide, compound IIIc-057a: UPLC-MS (acidic method, 4 min): rt = 0.84 min; m / z = 392.1 [M+H]+, peak area >99%. 1HNMR(400MHz, DMSO-d6) 5 9.50 (s, 1H), 9.34 (s, 1H), 7.22 (s, lH),7.17(s, 1H), 6.63 (s, 1H), 6.53 (s, 1H), 4.48 (s, 2H), 4.39 (s, 2H), 2.11 (s, 3H). HRMS: [M+H]+, calc, for Ci8Hi8NO9: 392.09761, found: 392.09766 Biodata: IIIc-057a: FGF-1 IC50 [pM] = 87; FGF-2 IC50 [pM] = 77; VEGF-A1 IC50 [pM] = 38; VEGFR-Phosphorylation inhibition IC50 [pM] =0.2; PMN ROS [inhibition at 0.3 pM [%] = 90.34; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 40.04; Whole Blood: GM-CSF IC50 [pM] = >100; IFNyIC50 [pM] = 0.9; IL-ip IC50 [pM] = 16.2; IL-2 IC50 [pM] = 24.2; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.19; IL-9 IC50 [pM] = 11.1; IL-10 IC50 [pM] = >100; IL-12p70 IC50 [pM] = 0.73; IL-13 IC50 [pM] = 4.73; IL-17A IC50 [pM] = 1.32; IL-17F IC50 [pM] = 5.06; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 1.56; IL-33 IC50 [pM] = 2.93; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.15; TNF p IC50 [pM] = 1.58. Scheme 19: X = NCH2C6H3(OH)2COOH Synthetic procedures Formation of tertiary amine from KI-11 and NHs Tris(4-ethoxycarbony-2,5-dibenzyloxyphenylmethyl)amine : A sealed tube was charged with KI-11 (32.5 g, 79 mmol), sodium iodide (0.79 g, 5 mmol), a solution of ammonia in MeOH (7 N) (38 mL, 264 mmol) and EtOAc (80 mL). The tube was then sealed and the reaction mixture was heated at 60 °C for 24 h. After 24 h, the starting material (KI-11) was consumed and the reaction mixture contained the desired product but also monomeric and dimeric structures. Water (100 mL) was added and the resulting mixture was extracted with EtOAc (3 x 100 mL), the gathered organic layer was dried over Na2SO4, fdtered and concentrated under reduced pressure. The residue obtained was dissolved in EtOAc (165 mL) and KI-11 (2.5 g, 6 mmol), sodium iodide (0.79 g, 5 mmol), DIPEA (10 mL, 58 mmol) were added and the resulting solution was heated at 60 °C. After 18h, water (100 mL) was added and the resulting mixture was extracted with EtOAc (3 x 100 mL), the gathered organic layer was dried over Na2SO4, filtered and concentrated under reduced pressure. The residue was purified by recrystallisation using EtOH / EtOAc 95 / 5 (20 mL) as solvent to yield to the title compound (15.0 g, 50%) as white crystals. UPLC-MS (basic method, 2 min): rt = 1.71 min; m / z = 1140.3 [M+H]+, peak area >99%. 1HNMR(400 MHz, DMSO-tL) 5 6.56 - 6.49 (m, 12H), 6.48 - 6.38 (m, 24H), 4.22 (s, 6H), 4.04 (s, 6H), 3.42 (q, J = 7.1 Hz, 6H), 3.00 (s, 6H), 0.42 (t, J = 7.1 Hz, 9H). Alternatively, the product can be purified via silica gel flash column chromatography: scale, up to 270g; Instrument: Combi / Za^ / ? Torrent; cartridge: RediSep Column, Silica 3kg; loading type: Crude dissolved into IL of heptane: toluene (1:1). Elution with ethyl acetate / heptane. Detection: UV - 240 nm Deprotection procedures: See General procedures [4], [5] For conditions and yields: See Figure 7 (deprotections) Alternative, Large scale deprotection procedures: Saponification. Tris(4-ethoxycarbony-2,5-dibenzyloxyphenylmethyl)amine (95.00 g, 0.083 mol), sodium hydroxide (40.00 g, 0.99 mol), water (570 mL) and tetrahydrofuran (1.9 L) were added to a 5 L round bottom flask. The reaction mixture was heated, using a temperature block, at 80°C (reflux temperature was 65°C) for 48h then stirred at room temperature for 24h. The solvents were then removed in vacuo. The crude material was collected and further diluted with water (2.85 L). In another 10 L flask, a mixture of acetic acid (180 mL) and water (950 mL) was stirred at rt. The mixture of the crude product in water was added to the acetic acid mixture over a period of 30 min. while stirring with an overhead stirrer, and a cream solid precipitated. The reaction mixture was stirred for an additional Ih and the solid was isolated upon filtration; the mother liquor pH was 4,2. The solid isolated was stirred with water (1425 mL) for Ih then filtered. The mother liquor pH was 4,5. The solid recovered was stirred with more water (1425 mL) for Ih then filtered; the mother liquor pH was 4,5. The above solid was stirred with acetone (950 mL) for Ih and filtered. The cream colour solid was dried in the vacuum oven at 50°C for 48h prior to analysis (82.00 g, 93% yield) (yields vary between 90-95%). Note: The pH is a critical parameter during the washings in order to keep the product in the free acid form and removing the excess acetic acid from the product. Ideal pH: 4.2 to 4.5 (final sodium content vary between 2ppm-20ppm). Hydrogenolysis and Isolation. Tris(4-carboxy-2,5-dibenzyloxyphenylmethyl)amine (58.00 g, 54.00 mmol, leq) and tetrahydrofuran (1160 mL) were charged in a 2 L round bottom flask. The mixture was degassed with nitrogen, then flushed with hydrogen / vacuum cycle 4-5 times. Palladium on carbon (JM 10% 424 Pd / C, 70 g, 15% loading) was added to the reaction mixture and stirred at 25°C for 5-6h. The reaction was then degassed and the catalyst removed by filtration through a pad of celite, which was washed with tetrahydrofuran (3x1160 mL). Finally, the filtrates were concentrated under reduce pressure. The crude solid was collected, stirred with heptane (1160 mL) and filtered in order to give a grey solid, which was dried in the vacuum oven at 50°C overnight (32.50 g, >100 % yield on crude basis). The crude material collected was dissolved in ethanol (325 mL) and heated to 60°C (clear solution). Then, water was slowly added (325 mL) at 60°C (keeping the temperature at least at 50°C during addition) over a period of 15-20 min. At this stage a hazy liquid was observed. The hazy reaction mixture was stirred at reflux temperature for 30 min. After this time, the reaction mixture was allowed to cool to room temperature for another 30 min. The precipitated solid was isolated upon filtration and washed with a 1:1 mixture of ethanohwater (66 mL). The solid was dried in the vacuum oven at 50°C for at least 72h prior to analysis, in order to afford the desired product IIIc-061a (22.00 g, 76% yield) (yield vary between 65-75%). LCMS: >95%, NMR: >95% purity. .COOH HOOC. IH HO. Tris(4-carboxy-2,5-dihydroxyphenylmethyl)amine, compound IIIc-061a: UPLC-MS (acidic method, 4 min): rt = 0.74 min; m / z = 516.0 [M+H]+, peak area >86%. ‘HNMR (400 MHz, DMSO-d6) 5 7.27 (s, 3H), 6.83 (s, 3H), 4.33 (s, 6H). 13C NMR (100 MHz, DMSO-Jtf) 5 172.0, 154.3, 148.3, 134, 117.8 (CH), 114.9 (CH), 112.4,53.6 (CH2). HRMS: [M+H]+, calc, for C24H22NO12: 516.11365, found: 516.11389 Biodata: IIIc-061a: FGF-1 IC50 [pM] = 9; FGF-2 IC50 [pM] = 7.6; VEGF-A1 IC50 [pM] = 21; VEGFR-Phosphorylation inhibition IC50 [pM] =4.3; PMN ROS [inhibition at 0.3 pM [%] = 92.5; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 58.69; Whole Blood: GM-CSF IC50 [pM] = 31.2; IFNyIC50 [pM] = 2.48; IL-ip IC50 [pM] = >100; IL-2 IC50 [pM] = >100; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.18; IL-9 IC50 [pM] = 8.85; IL-10 IC50 [pM] = 17.9; IL-12p70 IC50 [pM] = 37.2; IL-13 IC50 [pM] = 0.31; IL-17A IC50 [pM] = 0.04; IL-17F IC50 [pM] = 0.32; IL-18 IC50 [pM] = 32.4; IL-21 IC50 [pM] = 6.38; IL-33 IC50 [pM] = 0.31; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.03; TNF p IC50 [pM] = 0.81 Triethyl ester UPLC-MS (acidic method, 2 min): rt = 1.05 min; m / z = 600.2 [M+H]+, peak area >82%. 3H NMR (400 MHz, DMSO-d6) 5 10.02 (s, 3H), 9.54 (s, 3H), 7.17 (s, 3H), 7.00 (s, 3H), 4.33 (q, J = 7.1 Hz, 6H), 3.59 (s, 6H), 1.31 (t, J = 7.1 Hz, 9H). HRMS: [M+H]+, calc, for C30H34NO12: 600.20755, found: 600.20790 Biodata: IIIc-061a-E3: FGF-1 IC50 [pM] = 200; FGF-2 IC50 [pM] = 200; VEGF-A1IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =0.34; PMN ROS [inhibition at 0.3 pM [%] = N.D.; PMN ROS inhibition IC50 [pM] = N.D.; Neutrophil adhesion inhibition [%] = 10.4 Scheme 20: X = S Synthetic procedures Formation of thioether linkage from KI-11 See Scheme 21. Same conditions to create the thioether linkage. Deprotection procedures: see General procedures [4], [5] For examples For conditions and yields: See Figure 7 (deprotections) 60)4-((2,5-Dihydroxy-4-carboxyphenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid, compound IIIc-058a: UPLC-MS (acidic method, 2 min): rt = 0.84 min; m / z = 365.1 [M-H]", peak area >79% ‘HNMR (400 MHz, Methanol-^) 5 7.25 (s, 2H), 6.83 (s, 2H), 3.69 (s, 4H). HRMS: [M+H]+, calc, for CieHisOsS: 367.04822, found: 367.04768, Biodata: IIIc-058a: FGF-1IC50 [pM] = 12; FGF-2 IC50 [pM] = 12; VEGF-A1IC50 [pM] = 124; VEGFR-Phosphorylation inhibition IC50 [pM] =0.29; PMN ROS [inhibition at 0.3 pM [%] = 61.22; PMN ROS inhibition IC50 [pM] = 1.17; Neutrophil adhesion inhibition [%] = 23 Scheme 21: X = SO2 Synthetic procedures Oxidation of thioether linkage See preparation of IVc-059a: same conditions of oxidation. Deprotection procedures: see General procedures [4], [5] For examples For conditions and yields: See Figure 7 (deprotections) 61) 4-((2,5-Dihydroxy-4-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic      acid, compound IIIc-059a: UPLC-MS (acidic method, 2 min): rt = 0.72 min; m / z = 397.1 [M-H]", peak area >97% ‘HNMR (400 MHz, DMSO-J6) 5 13.94 (brs, 2H), 10.63 (brs, 2H), 9.71 (s, 2H), 7.27 (s, 2H), 6.91 (s, 2H), 4.44 (s, 4H). HRMS: [M+H]+, calc, for Ci6Hi5OioS: 399.03804, found: 399.03768 Biodata: IIIc-059a: FGF-1IC50 [pM] = 47; FGF-2 IC50 [pM] = 50; VEGF-A1IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =3.61; PMN ROS [inhibition at 0.3 pM [%] = 66.39; PMN ROS inhibition IC50 [pM] = 1; Neutrophil adhesion inhibition [%] = 14.67 Example 1.11: Compounds of type IVc Scheme 22: X=S Synthesis via dimethyl ether O OH Duff reaction Mel,K2CO3 DMF 2. DTT, DMF 1. NaOMe, MeOH Synthetic procedures Synthesis from 5-O-methyl gentisic acid 3-Formyl-2-hydroxy-5-methoxybenzoic acid. Hexamethylenetetramine (40.019 g, 0.285 mol) was added to the mixture of 2-hydroxy-5-methoxybenzoic acid (24.0 g, 0.143 mol) in trifluoroacetic acid (190.0 mL). The reaction was refluxed for 18 h. After completion, the reaction was cooled down to ambient temperature and a solution of 2M hydrochloric acid (700 mL) was added to the mixture which was stirred at ambient temperature for 24 h. The precipitate was filtered, washed with water (500 mL) and dried in the vacuum oven to give 3-formyl-2-hydroxy-5-methoxybenzoic acid as a pale yellow solid (21.30 g, 0.11 mol, 77.0%) UPLC-MS (acidic method, 2 min): rt = 0.69 min; m / z = 195.1 [M-H]", peak area >98% ‘HNMR (400 MHz, DMSO-J6) 5 10.36 (s, 1H), 7.62 (d, J= 3.4 Hz, 1H), 7.44 (d, J= 3.4 Hz, 1H), 3.78 (s, 3H). Methyl 3-formyl-2,5-dimethoxybenzoate. Methyl iodide (6.7 mL, 0.107 mol) was added to a mixture of 3-formyl-2-hydroxy-5-methoxybenzoic acid (10.0 g, 0.05 mol) and potassium carbonate-325 mesh (28.18 g, 0.20 mol) in DMF (100.0 mL). The resulting mixture was stirred at ambient temperature for 18 h. The reaction was cooled down to ambient temperature and treated with cold water (400 mL) resulting in the formation of a precipitate. The resulting suspension was stirred for 10 min, then filtered and dried in the vacuum oven to give methyl 3-formyl-2,5-dimethoxybenzoate as a yellow solid (8.90 g, 0.04 mol, 78.0%). UPLC-MS (acidic method, 2 min): rt = 0.95 min; m / z = 225.1 [M+H]+, peak area >98% 1HNMR(400MHz, DMSO-Jtf) 5 10.27 (s, 1H), 7.55 (d, J = 3.4 Hz, 1H), 7.41 (d, J = 3.4 Hz, 1H), 3.88 (s, 3H), 3.87 (s, 3H), 3.83 (s, 3H). Methyl 3-(hydroxymethyl)-2,5-dimethoxybenzoate. Sodium borohydride (16.198 g, 0.428 mol) was added slowly to a solution of methyl 3-formyl-2,5-dimethoxybenzoate (48.0 g, 0.214 mol) in MeOH (900 mL) at 0 °C and the resulting mixture was stirred at ambient temperature for 15 min. The solvent was removed in vacuo and the residue was dissolved in DCM (200 mL) then washed with water (200 5 mL). The organic layer was dried over Na2SC>4, filtered, and concentrated to dryness to give methyl 3-(hydroxymethyl)-2,5-dimethoxybenzoate as white solid (45.6 g, 0.20 mol, 95.0%) UPLC-MS (acidic method, 2 min): rt = 0.84 min; no ionization, peak area >98% ‘HNMR (400 MHz, DMSO-tL) 5 7.20 (d, J = 3.2 Hz, 1H), 7.08 (d, J = 3.3 Hz, 1H), 5.24 (t, J = 5.7 Hz, 1H), 4.54 (d, J = 5.6 Hz, 2H), 3.83 (s, 3H), 3.76 (s, 3H), 3.68 (s, 3H). 10 Methyl 3-(chloromethyl)-2,5-dimethoxybenzoate. Thionyl chloride (17.2 mL, 0.235 mol) was added dropwise to a solution of methyl 3-(hydroxymethyl)-2,5-dimethoxybenzoate (45.60 g, 0.20 mol) over 30 min at ambient temperature. The resulting mixture was stirred for 18 h at ambient temperature. After completion, the reaction mixture was washed with a saturated solution of aqueous sodium carbonate (3 x 500 mL) and brine (500 mL). The organic layer was dried over Na2SO4, filtered and concentrated to 15 dryness to give methyl 3-(chloromethyl)-2,5-dimethoxybenzoate as a brown solid (49.1 g, 0.18 mol, 90%,) UPLC-MS (acidic method, 2 min): rt = 1.10 min; no ionization, peak area >92% 'H NMR (400 MHz, DMSO-J6) 5 7.29 (d, J = 3.2 Hz, 1H), 7.22 (d, J = 3.3 Hz, 1H), 4.74 (s, 2H), 3.85 (s, 3H), 3.77 (s, 3H), 3.76 (s, 3H). 20 Methyl 3-(acetylthiomethyl)-2,5-dimethoxybenzoate. Potassium thioacetate (15.54 g, 0.136 mol) was added to the solution of methyl 3-(chloromethyl)-2,5-dimethoxybenzoate (22.20 g, 0.091 mol) in THF (500.0 mL) at ambient temperature. The reaction mixture was stirred a 75 °C for 18 h. After completion, the solvent was removed under reduced pressure to give a red oily residue which was treated with a saturated brine solution (500 mL), then extracted with diethyl ether (2 x 250 mL). The organic phases 25 were combined, dried over Na2SO4, filtered and concentrated to dryness to yield methyl 3-(acetylthiomethyl)-2,5-dimethoxybenzoate as a brown solid (25.50 g, 0.09 mol, 99%). UPLC-MS (acidic method, 2 min): rt = 1.10 min; no ionization, peak area >92% 'H NMR (400 MHz, DMSO-JJ 5 7.12 (d, J = 3.3 Hz, 1H), 7.10 (d, J = 3.2 Hz, 1H), 4.10 (s, 2H), 3.84 (s, 3H), 3.74 (s, 3H), 3.70 (s, 3H), 2.35 (s, 3H). 30 Methyl 3-(mercaptomethyl)-2,5-dimethoxybenzoate. To a solution of methyl 3-(acetylthiomethyl)-2,5-dimethoxybenzoate (25.5 g, 89.68 mmol) in dry methanol (800 mL) was added in a dropwise manner at 0 °C, a solution of sodium methanolate (5.81 g, 107.62 mmol) under a nitrogen atmosphere. The mixture was stirred at room temperature for 45 min before being quenched with Dowex X8(H+) ionexchange resin and stirred for 15 min. After filtration, the solvent was evaporated under reduced pressure 35 to give the crude product as a brown oil (which contained the desired product and the corresponding 127 disulphide compound in a 2:1 ratio). The residue was dissolved in DMF (400.0 mL) and treated with dithiothreitol (DTT) (33.95 g, 0.26 mol) under a nitrogen atmosphere. The reaction mixture was stirred at 75 °C for 18 h. After completion of the disulphide to thiol conversion, the solvent was evaporated. The resulting residue was dissolved in DCM (1 L), washed with brine (7 x 500 mL), dried over Na2SC>4, filtered and concentrated to dryness to yield homogeneous methyl 3-(mercaptomethyl)-2,5-dimethoxybenzoate as a brown oil (21.40 g, 88.32 mmol, 99%) UPLC-MS (acidic method, 2 min): rt = 1.05 min; m / z = 243.1 [M+H]+, peak area >95% 'H NMR (400 MHz, DMSO-JJ 5 7.19 (d, J = 3.2 Hz, 1H), 7.09 (d, J = 3.3 Hz, 1H), 3.83 (s, 3H), 3.76 (s, 3H), 3.73 (s, 3H), 3.71 (d, J = 8.0 Hz, 2H), 2.93 (t, J = 8.0 Hz, 1H). Dimethyl 3,3'-(thiobis(methylene))bis(2,5-dimethoxybenzoate). Triethylamine (19.0 mL, 136.61 mmol) was added to a solution of methyl 3-(mercaptomethyl)-2,5-dimethoxybenzoate (21.40 g, 88.32 mmol) and methyl 3-(chloromethyl)-2,5-dimethoxybenzoate (22.69 g, 92.74 mmol) under a nitrogen atmosphere. The reaction was stirred at ambient temperature for 18 h. After completion, the solvent was removed under vacuum to give a brown oil residue which was treated with water (1 L), then extracted with diethyl ether (3 x 500 mL). The organic phases were combined, washed with brine (5 x 250 mL), dried over Na2SO, filtered and concentrated to dryness to yield the crude product as a brown oil, which was purified by silica gel chromatography: elution was made with a gradient of ethyl acetate (0 to 20%) in iso-hexane to yield dimethyl 3,3'-(thiobis(methylene))bis(2,5-dimethoxybenzoate) as a brown solid (29.9 g, 66.37 mmol, 76%) UPLC-MS (acidic method, 2 min): rt = 1.22 min; m / z = 451.2 [M+H]+, peak area >92% 'H NMR (400 MHz, DMSO-J6) 5 7.12- 7.08 (m, 4H), 3.83 (s, 6H), 3.76 (s, 4H), 3.73 (s, 6H), 3.67 (s, 6H). 3,3'-(thiobis(methylene))bis(2,5-dimethoxybenzoic acid). A solution of Lithium hydroxide monohydrate (1.0 g, 23.83 mmol) in water (30.0 mL) was added to the solution of dimethyl 3,3'-(thiobis(methylene))bis(2,5-dimethoxybenzoate) (2.0 g, 4.44 mmol) in THF (100.0 mL). The reaction was stirred at ambient temperature for 48 h. After completion, water (100 mL) was added to the reaction and the mixture was washed with ethyl acetate (100 mL). The aqueous layer was acidified with a 1 M aqueous hydrochloric acid to pH=2 and extracted with ethyl acetate (3 X 100 mL). The organic layers were collected, dried (Na2SC>4), filtered and concentrated to give 3,3'-(thiobis(methylene))bis(2,5-dimethoxybenzoic acid) as abrown solid (1.91 g, 4.11 mmol, 93%) UPLC-MS (acidic method, 2 min): rt = 0.93 min; m / z = 421.1 [M-H]", peak area >95% 'HNMR (400 MHz, DMSO-J6) 5 12.96 (s, 2H), 7.10 (d, J = 3.3 Hz, 2H), 7.08 (d, J = 3.2 Hz, 2H), 3.76 (s, 4H), 3.73 (s, 6H), 3.69 (s, 6H). 3-[(2,5-Dihydroxy-3-carboxyphenyl)methylthiomethyl]-2,5-dihydroxybenzoic acid. To a solution of preceding thioether (5.0 g, 0.01 mol) in DCM (200.0 mL) was added slowly a IM solution of tribromoborane in DCM (100.7 mL, 0.101 mol) at 0 °C and the reaction mixture was refluxed for 48 h. After this time, the solid was filtered, washed with DCM (500 mL) and then suspended in a solution of IM hydrochloric acid (50 mL). The resulting mixture was refluxed for 2 h. The resulting brown suspension was filtered and dried to give the crude product, which was purified by reverse phase column chromatography (25 g, MeCN:H2O 5% to 95% over 12 CV) to yield 2,5-dihydroxy-3-[(2,5-dihydroxy-3-carboxyphenyl)methylthiomethyl]benzoic acid as white solid (1.1g, 0.003 mol, 26%). UPLC-MS (acidic method, 2 min): rt = 0.70 min; m / z = 365.1 [M-H]", peak area >95% ‘HNMR (400 MHz, DMSO-tL) 5 13.86 (s, 2H), 11.09 (s, 2H), 9.14 (s, 2H), 7.08 (d, J = 3.1 Hz, 2H), 7.02 (d, J= 3.1 Hz, 2H), 3.65 (s, 4H). Example: 62)3-((2,5-Dihydroxy-3-carboxyphenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid, compound IVc-058a: UPLC-MS (acidic method, 2 min): rt = 0.70 min; m / z = 365.1 [M-H]", peak area >95% 1HNMR(400 MHz, DMSO-JJ 5 13.86 (s, 2H), 11.09 (s, 2H), 9.14 (s, 2H), 7.08 (d, J= 3.1 Hz, 2H), 7.02 (d, J= 3.1 Hz, 2H), 3.65 (s, 4H). HRMS: [M+H]+, calc, for CieHisOsS: 367.04822, found: 367.04734 Biodata: IVc-058a: FGF-1 IC50 [pM] = 36; FGF-2 IC50 [pM] = 4.9; VEGF-A1 IC50 [pM] = 83; VEGFR-Phosphorylation inhibition IC50 [pM] =0.53; PMN ROS [inhibition at 0.3 pM [%] = 77.04; PMN ROS inhibition IC50 [pM] = 0.29; Neutrophil adhesion inhibition [%] = 43.5; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 10.6; IL-1 p IC50 [pM] = 27.5; IL-2 IC50 [pM] = 3.82; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.21; IL-9 IC50 [pM] = 31.1; IL-10 IC50 [pM] = 16.4; IL-12p70 IC50 [pM] = 4.23; IL-13 IC50 [pM] = 55.9; IL-17A IC50 [pM] = 0.1; IL-17F IC50 [pM] = 86.8; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 3.2; IL-33 IC50 [pM] = 33.9; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.18; TNF p IC50 [pM] = 59.3. Scheme 23: X = SO2 O OH        OH O                       O OH        OH O Synthesis from compound IVc-058a 3-((2,5-Dihydroxy-3-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid. To a solution of thioether IVc-058a (4.25 g, 9.28 mmol) in DMF (20.0 mL) was added slowly a solution of 3-chlorobenzene-1-carboperoxy acid (mCPBA purity grade <77%, 5.80 g, 25.88 mmol) in DMF (20.0 129 mL). The reaction mixture was stirred for 18 h at ambient temperature. The crude product was submitted for HPLC purification (see general conditions) to give a white solid (3.20 g) which was triturated with IM HC1 (50 mL) to yield the desired product as white solid (2.55 g, 6.40 mmol, 56%) UPLC-MS (acidic method, 4 min): rt = 0.68 min; m / z = 397.1 [M-H]", peak area >95% 63)3-((2,5-Dihydroxy-3-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid, compound IVc-059a: UPLC-MS (acidic method, 4 min): rt = 0.68 min; m / z = 397.1 [M-H]", peak area >95% 1HNMR(400 MHz, DMSO-tL) 5 11.24 (s, 1H), 9.32 (s, 1H), 7.21 (d, J = 3.1 Hz, 1H), 7.09 (d, J= 3.1 Hz, 1H),4.44 (s, 2H). 13CNMR(100MHz, DMSO-r / tf) 5 172.4, 153.4, 149.2, 117.4, 116.1 (CH), 113.3 (CH), 53.6 (CH2). HRMS: [M+H]+, calc, for Ci6Hi5OioS: 399.03804, found: 399.03775 Biodata: IVc-059a: FGF-1 IC50 [pM] = 6.7; FGF-2 IC50 [pM] = 2.7; VEGF-A1 IC50 [pM] = 12; VEGFR-Phosphorylation inhibition IC50 [pM] =4.8; PMN ROS [inhibition at 0.3 pM [%] = 74; PMN ROS inhibition IC50 [pM] = 0.147; Neutrophil adhesion inhibition [%] = 10; Whole Blood: GM-CSF IC50 [pM] = >100; IFNy IC50 [pM] = 4.34; IL-ip IC50 [pM] = 38.6; IL-2 IC50 [pM] = 21.2; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.11; IL-9 IC50 [pM] = 0.4; IL-10 IC50 [pM] = 1.31; IL-12p70 IC50 [pM] = 42; IL-13 IC50 [pM] = >100; IL-17A IC50 [pM] = 0.16; IL-17F IC50 [pM] = >100; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = 1.87; IL-33 IC50 [pM] = 27.5; TGFp IC50 [pM] = >100; TNF a IC50 [pM] = 0.16; TNF p IC50 [pM] = 0.33 Dimethyl ester UPLC-MS (acidic method, 2 min): rt = 0.94 min; m / z = 427.1 [M+H]+, peak area >95% 1HNMR(400 MHz, DMSO-J6) 5 10.28 (s, 2H), 9.43 (s, 2H), 7.21 (d, J= 3.1 Hz, 2H), 7.13 (d, J= 3.1 Hz, 2H), 4.47 (s, 4H), 3.91 (s, 6H). HRMS: [M+H]+, calc, for Ci8Hi9Oi0S: 427.06934, found: 427.06942 Biodata: IVc-059a-E2: FGF-1 IC50 [pM] = 78; FGF-2 IC50 [pM] = 94; VEGF-A1 IC50 [pM] = 200; VEGFR-Phosphorylation inhibition IC50 [pM] =2.7; PMN ROS [inhibition at 0.3 pM [%] = 45.67; PMN ROS inhibition IC50 [pM] = 2.64; Neutrophil adhesion inhibition [%] = 50.5 Dimethyl ester tetraacetate UPLC-MS (acidic method, 2 min): rt = 1.05 min; m / z = 593.1 [M-H]", peak area >95% 'H NMR (400 MHz, DMSO-J9) 5 7.75 (d, J= 2.8 Hz, 2H), 7.53 (d, J= 2.9 Hz, 2H), 4.65 (s, 4H), 3.81 (s, 6H), 2.31 (s, 6H), 2.23 (s, 6H). HRMS: [M+H]+, calc, for C26H27O14S: 595.11160, found: 595.11149 Biodata: IVc-059a-E2-A4: FGF-1IC50 [pM] = 54; FGF-2 IC50 [pM] = 200; VEGF-A1IC50 [pM] = 25; VEGFR-Phosphorylation inhibition IC50 [pM] =ND; PMN ROS [inhibition at 0.3 pM [%] = 29.17; PMN ROS inhibition IC50 [pM] = 4.13; Neutrophil adhesion inhibition [%] = 87.5; Whole Blood: GM-CSF IC50 [pM] = 1.83; IFNyIC50 [pM] = 3.5; IL-ip IC50 [pM] = 14.1; IL-2 IC50 [pM] = 10.4; IL-4 IC50 [pM] = >100; IL-5 IC50 [pM] = >100; IL-6 IC50 [pM] = 0.99; IL-9 IC50 [pM] = 2.9; IL-10 IC50 [pM] = 16.8; IL-12p70 IC50 [pM] = 51.4; IL-13 IC50 [pM] = 18.7; IL-17A IC50 [pM] = 0.02; IL-17F IC50 [pM] = 25.8; IL-18 IC50 [pM] = >100; IL-21 IC50 [pM] = >100; IL-33 IC50 [pM] = 23.2; TGFp IC50 [pM] = >100; TNFa IC50 [pM] = 0.3; TNF p IC50 [pM] = 19.4 Alternative, scalable synthesis of IVc-059a Scheme 24: synthesis of IVc-059a from 2,5-dibenzyloxyphthalaldehyde 2,5-Bis(benzyloxy)-3-(hydroxymethyl)benzaldehyde [Step 1]: 2,5-Bis(benzyloxy)-isophthalaldehyde (25.0 g, 72.1 mmol) (see Scheme 9b) was dissolved in THF (150 mL) and EtOH (15 mL) was added. The brown solution was kept under positive flow of nitrogen and stirred at r.t for 10 min then solid NaBH4 (695 mg, 18.37 mmol) was added portion-wise over 20 min, the internal temperature of the reaction was not allowed to exceed 25 °C (water bath used). The reaction mixture was left to stir at r.t for 30 min then every 15 min additional NaBH4 was added until complete conversion of the starting material (total: 107 mg, in two portions). The reaction mixture was then poured into water (1.2 L) and stirred for 20 min. The thus formed brown precipitate was isolated by filtration and the solid obtained was further dried in the vacuum oven at 40 °C until constant mass to afford the title compound (22.9 g, 76% corrected yield) as a brown oil. NMR profile showed 83% of desired product, 15% of over-reduced diol, 2% of starting material, the material was carried over to the next step without further purification. UPLC-MS (acidic method, 2 min): r.t = 1.19 min, 86%, m / z = 347.2 [M-H]- 1HNMR (400 MHz, DMSO-d6) 5 10.11 (s, 1H), 7.52 - 7.28 (m, 11H), 7.19 (d, J = 3.3 Hz, 1H), 5.34 (t, J = 5.6 Hz, 1H), 5.15 (s, 2H), 4.99 (s, 2H), 4.60 (d, J = 5.6 Hz, 2H). 2,5-Bis(benzyloxy)-3-(hydroxymethyl)benzoic acid [Step 2]: 2,5-Bis(benzyloxy)-3-(hydroxy-methyl)benzaldehyde (44.3 g, 103 mmol, 81% purity) and KH2PO4 (25.9 g, 190 mmol) were dissolved in acetone (440 mL) and water (130 mL). Resorcinol (21.0 g, 191 mmol) was added and the reaction mixture was stirred at r.t for 10 min. A solution of sodium chlorite (21.5 g, 191 mmol) in water (60 mL) was added slowly over 30 min, not allowing the internal temperature to go above 25 °C. The reaction mixture was stirred at r.t for 3 h and a 2 M aqueous solution of H3PO4 (95 mL) was added. The mixture was stirred for 20 min and cooled down to 6 °C with an ice bath before being filtered. The solid was further washed with water until the pH of the filtrate was ~6. The solid obtained was suspended in water (c.a. 300 mL) and a pre-cooled (5 - 10 °C) solution of NaOH (17 g, 412 mmol) in water (200 mL) was added. The suspension was stirred at r.t for 30 min before being filtered on a sinter funnel. The isolated solid was further washed with 1 M aqueous NaOH (2x50 mL) and water (50 mL). The alkaline liquor was then acidified using a 6N HC1 aqueous solution pre-cooled (5-10 °C) until pH ~1. The resulting suspension was magnetically stirred for 20 min before being filtered, the solid obtained that was further dried in the vacuum oven at 40 °C until constant mass to yield the title compound as a light beige solid (34.8 g, 88%). UPLC-MS (acidic method, 2 min): rt = 1.06 min, 99%, m / z = 363.2 [M-H]". 1HNMR (400 MHz, DMSO-d6) 5 13.02 (s, 1H), 7.51 - 7.31 (m, 10H), 7.28 (d, J = 3.2 Hz, 1H), 7.22 (d, J = 3.3 Hz, 1H), 5.21 (s, 1H), 5.12 (s, 2H), 4.88 (s, 2H), 4.53 (s, 2H). Ethyl 2,5-bis(benzyloxy)-3-(hydroxymethyl)benzoate [Step 3]: 2,5-Bis(benzyloxy)-3-(hydroxy-methyl)benzoic acid (32.5 g, 89.3 mmol) and CS2CO3 (32.3 g, 99.2 mmol) were suspended in DMF (200 mL) and ethyl iodide (9.0 mL, 112 mmol) was added to the reaction mixture. After stirring at r.t for 3 h the reaction mixture was poured into a saturated aqueous solution of NH4C1 (IL) and solid NaCl (~30 g) was added. After stirring for 10 min, the material was extracted with EtOAc (2 x 500 mL). The gathered organic layer was washed with brine (2 x 500 mL), dried with sodium sulfate, filtered and concentrated under reduced pressure to give a brown oil residue (42.0 g, crude, 89.3 mmol). The crude material was carried over to the next step without further purification. UPLC-MS (acidic method, 2 min): rt = 1.24 min, 93%, m / z = weak ionisation. 1HNMR (400 MHz, DMSO-d6) 5 7.51 - 7.32 (m, 10H), 7.31 (d, J = 3.3 Hz, 1H), 7.22 (d, J = 3.3 Hz, 1H), 5.24 (t, J = 5.6 Hz, 1H), 5.13 (s, 2H), 4.87 (s, 2H), 4.54 (d, J = 5.6 Hz, 2H), 4.26 (q, J = 7.1 Hz, 2H), 1.24 (t, J = 7.1 Hz, 3H) Ethyl 2,5-bis(benzyloxy)-3-(chloromethyl)benzoate (KI-14) [Step 4]: Ethyl 2,5-bis(benzyloxy)-3-(hydroxymethyl)benzoate (42 g crude material from previous step, 89.3 mmol) was dissolved in DCM (200 mL) under inert atmosphere (N2), then SOCI2 (9.8 mL, 133.9 mmol) was added at 0 °C (ice bath) and the reaction mixture was allowed to warm up to r.t.. After 2 h the volatiles were removed under reduced pressure followed by azeotrope distillation using toluene (3 x 100 mL) leading to a semi solid brown oil (38.0 g, crude, 89.3 mmol). UPLC-MS (acidic method, 2 min): rt = 1.40 min, 91%, m / z = weak ionisation. 1HNMR (400 MHz, DMSO-d6) 5 7.54 - 7.26 (m, 12H), 5.14 (s, 2H), 4.95 (s, 2H), 4.71 (s, 2H), 4.28 (q, J = 7.1 Hz, 2H), 1.28 - 1.22 (t, J = 7.1 Hz, 3H). Bis(2,5-dibenzyloxy-3-ethoxycarbonylphenylmethyl)sulfide [Step 5]:To a solution of KI-14 (38.0 g, crude material, 89.3 mmol) in DMF (420 mL) was added thioacetamide (8.4 g, 111.8 mmol) followed by the addition of K2CO3 - 325 Mesh (16.7 g, 120.8 mmol). The reaction was heated at 45 °C for 48 h. The reaction was cooled down to room temperature followed by addition of thioacetamide (2.5 g, 33.3 mmol) and K2CO3 - 325 Mesh (5.0 g, 36.1 mmol) and further stirring at 45 °C for 18 h to complete the reaction. The reaction mixture was poured into water (4 L). The reaction mixture was stirred for 20 min before addition of EtOAc (2 L) followed by solid NaCl (~60 g). The phases were separated followed by additional extraction using EtOAc (1.5 L). The gathered organic layer was washed with Brine (1.5 L), dried over Na2SO4, fdtered and concentrated under reduced pressure to give the crude title compound (39.8 g, 44.6 mmol) as a brown oil which was used in the following step without purification. UPLCMS (acidic method, 2min): rt = 1.57 min, m / z = 800.5 [M+NH4]+, peak area 77%. 1HNMR(4OO MHz, DMSO-d6) 5 7.46-7.17 (m, 24H), 5.05 (s, 4H), 4.83 (s, 4H), 4.23 (q, J = 7.1 Hz, 4H), 3.73 (s, 4H), 1.20 (t, J = 7.1 Hz, 6H). Bis(2,5-dibenzyloxy-3-ethoxycarbonylphenylmethyl)sulfone [Step 6]: To a solution of Bis(2,5-dibenzyloxy-3-ethoxycarbonylphenylmethyl)sulfide (39.8 g crude, 44.6 mmol) in acetic acid (850 mL) was added slowly a 30% wt. solution of hydrogen peroxide (50 mL, 490 mmol). The reaction was stirred at r.t for 18 h. The reaction mixture was poured into ice / water (5 L) and stirred at room temperature for 30 min followed by addition of EtOAc (2 L) and solid NaCl (~40 g). After separation of the phases, the aqueous layer was extracted one more time with EtOAc (IL). The gathered organic layer was washed with Brine (1.5 L), dried over Na2SO4, filtered and concentrated under reduced pressure to give a brown solid. The solid was suspended in MTBE (250 mL) and magnetically stirred for 30 min followed by filtration and further trituration with MTBE (150 mL) to yield the title compound (23.56 g, 28.9 mmol, 64% yield over 4 steps). UPLC-MS (acidic method, 2 min): rt = 1.48 min; m / z = 832.5 [M+NH4]+, peak area 96% 1H NMR (400 MHz, DMSO-d6) 5 7.50 - 7.24 (m, 24H), 5.08 (s, 4H), 4.85 (s, 4H), 4.50 (s, 4H), 4.26 (q, J = 7.1 Hz, 4H), 1.25-1.17 (m, 6H). Bis(2,5-dibenzyloxy-3-carboxyphenylmethyl)sulfone [Step 7]: A solution of lithium hydroxide (9.7 g, 233 mmol) in water (100 mL) was added to a solution of bis(2,5-dibenzyloxy-3-ethoxycarbonylphenylmethyl)sulfone (33.3 g, 38.8 mmol) in THF (350 mL) and the resulting mixture was stirred at reflux for 18 h. After this time, most of the THF was removed under reduced pressure 133 leading to a white suspension. Upon addition of water (3 L) and aqueous solution of sodium hydroxide (1 M, 1 L) the mixture remains a suspension. The suspension was stirred at r.t for 18 h and the aqueous layer was acidified to pH~l by addition of 6 M aqueous hydrochloric acid solution and the resultant solid was collected by filtration and washed with water, until the liquors were neutral, the thus obtained white solid was further dried in the vacuum oven at 40 °C until constant mass to give the title compound as a white solid (29.4 g, 38.7 mmol, 99%). UPLC-MS (acidic method, 2 min): rt = 1.39 min; m / z = 757.1 [M-H]-, peak area 100% 1H NMR (400 MHz, DMSO-d6) 5 13.23 (s, 2H), 7.47 - 7.25 (m, 24H), 5.08 (s, 4H), 4.88 (s, 4H), 4.48 (s, 4H). Bis(2,5-dihydroxy-3-carboxyphenylmethyl)sulfone [Step 8], IVc-059a: To a suspension of bis(2,5-dibenzyloxy-3-carboxyphenylmethyl)sulfone (10.08 g, 13.28 mmol) in EtOH (140 mL) and THF (140 mL) was added palladium on charcoal (20% wt., 2 g) as a suspension in water (20 mL). After several vacuum / hydrogen cycles the mixture was maintained under an atmosphere of H2 at 25 °C and stirred for 20 h. After completion, the mixture was filtered through Celite® using THF. The filtrate was concentrated under reduced pressure to give an off-white solid. The residue was then suspended in acetonitrile (100 mL) and heated to reflux under magnetic stirring, the mixture was then cooled down to - 5 °C before being filtered and further washed cold acetonitrile. The product was further dried in the vacuum oven at 40 °C until constant mass to afford the desired product as a white solid (5.35 g, 12.78 mmol, 96%). UPLC-MS (acidic method, 4 min): rt = 0.67 min; m / z = 397.1 [M-H]-, peak area 100% NMR Data: see above. Example 1.12 - Molecules of type V: Reference compounds Diamides derived from 5-hydroxyisophthalic acid 2 examples O        O Ar\ JL     JL / Ar V Synthetic Schemes and Procedures Scheme 25: synthesis of V-OOla OBn Formation of amide Linkage See General procedure B for Amide Coupling [3B] using aniline A (2 moles) or methyl 5-aminosalicylate Deprotection procedures: See General procedures [4], [5] For details see Figure 8 For examples OH                     OH V-OOla 64) 5-Hydroxyisophthalic acid bis-N-(4-carboxy-2,5-dihydroxyphenyl)amide (V-OOla) UPLC-MS (acidic method, 2 min): rt = 0.72 min; m / z = 483.0 [M+H]+, peak area >95% 1HNMR(400 MHz, DMSO-d6) 5 10.28 (s, 1H), 9.83 (s, 2H), 9.48 (s, 2H), 7.92 (s, 1H), 7.68 (s, 2H), 7.52 (d, J = 1.5 Hz, 2H), 7.30 (s, 2H). Diethyl ester UPLC-MS (acidic method, 2 min): rt = 1.09 min; m / z = 539.2 [M-H]", peak area 94% ’H NMR (400 MHz, DMSO-d6) 5 10.23 (s, 2H), 9.92 (s, 2H), 9.49 (s, 2H), 7.91 (s, 1H), 7.73 (s, 2H), 7.51 (d, J = 1.5 Hz, 2H), 7.32 (s, 2H), 4.35 (q, J = 7.1 Hz, 4H), 1.34 (t, J = 7.1 Hz, 6H). COOH                  COOH V-002a 65]5-Hydroxyisophthalic acid bis-N-(3-carboxy-4-hydroxyphenyl)amide (V-002a) UPLC-MS (acidic method, 4 min): rt = 1.00 min; m / z = 451.1 [M-H]", peak area 97% ‘HNMR (400 MHz, DMSO-d6) 5 10.31 (s, 2H), 10.11 (s, 1H), 8.28 (d, J = 2.7 Hz, 2H), 7.98 (m, 1H), 5    7.89 (dd, J = 9.0, 2.7 Hz, 2H), 7.50 (d, J = 1.5 Hz, 2H), 6.97 (d, J = 9.0 Hz, 2H). Urea-linked Gentisic Acid Units 1 example Synthetic Scheme and Procedures Scheme 26: synthesis of V-003a Formation of urea Linkage Procedure from KI-1: 15 N,N’-Bis(2,5-dibenzyloxy-4-ethoxycarbonylphenyl)urea. To a cooled solution (ice bath) of 2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid (KI-1) (2.0 g, 4.9 mmol) and ELN (1.6 mL, 11.3 mmol) in THF (25 mL) under inert atmosphere (N2), was slowly added DPPA (1.1 mL, 5.2 mmol). The mixture was slowly warmed up to r.t and stirred at this temperature for 3 h. Then tBuOH (8 mL) was added and the reaction mixture was stirred at r.t for 18 h. The reaction profile showed a majority of urea linkage product instead of the desired Boc-aniline. The mixture was poured into a saturated solution of sodium hydrogencarbonate (250 mL) and stirred for 5 min before being extracted with EtOAc (3x50 mL). The combined organic layers were dried over sodium sulfate, filtered, and concentrated under reduced pressure to give a colourless oil. The residue was purified by flash column chromatography (iso-Hexane / EtOAc 1:0 then gradient to 30% EtOAc) to yield the title compound (1.1 g, 56%) as an off-white solid. UPLC-MS (basic method, 2 min): rt = 1.50 min; m / z = 781.2 [M+H]+, peak area 85% ’HNMR (400 MHz, DMSO-tL) 5 9.49 (s, 2H), 8.18 (s, 2H), 7.58 - 7.45 (m, 8H), 7.43 - 7.35 (m, 8H), 7.35 - 7.28 (m, 6H), 5.27 (s, 4H), 5.11 (s, 4H), 4.22 (q, J = 7.1 Hz, 4H), 1.24 (t, J = 7.1 Hz, 6H). Deprotection procedures: See General procedures [4], [5] For details see Figure 8 For example 66)N,N’-Bis(2,5-dihydroxy-4-carboxyphenyl)urea (V-003a) V-003a UPLC-MS (acidic method, 4 min): rt = 0.90 min; m / z = 363.1 [M-H]", peak area 93% 1HNMR(400 MHz, DMSO-d6) 5 13.36 (s, 2H), 10.86 (s, 2H), 9.64 (s, 2H), 9.48 (s, 2H), 7.77 (s, 2H), 7.17 (s, 2H). Diethyl ester UPLC-MS (acidic method, 4 min): rt = 1.79 min; m / z = 419.2 [M-H]", peak area 97% 'H NMR (400 MHz, DMSO-d6) 5 10.26 (s, 2H), 9.74 (s, 2H), 9.53 (s, 2H), 7.81 (s, 2H), 7.20 (s, 2H), 4.32 (q, J = 7.1 Hz, 4H), 1.33 (t, J = 7.1 Hz, 6H). Example 1.13: Formation of salts a) Solids. General protocole: salts were obtained as solids by adding the appropriate number of equivalent of base to solutions or suspensions of the desired compounds in water, sonicating until full dissolution, adjusting if needed the pH to values between 7.0 and 7.4 by addition of aqueous HC1 or excess base, then lyophilizing the solution. Atermatively certains salts could be obtained by dissolution in DMSO followed by precipitation with EtOH (IIc-007a). Solids were generated from the following bases: sodium hydroxide, diethylamine (DEA), lysine (Lys), meglumine (Meg), triethanolamine (TEA). For examples: Sodium and diethylammonium (DEA) salts of Ic-007a, IIc-007a, IIIc-061a as solids were obtained according to the general protocole without adjusting the pH. - Approximate solubilities in water: Ic-007a-DEA2: < 10 mg / mL Ic-007a-DEA3: > 20 mg / mL IIc-007a-DEAl: >10 mg / mL IIc-007a-DEA2: > 20 mg / mL IIIc-061a-DEA3: > 25 mg / mL - Stability of free acids and salts as solids: The free acids Ic-007a, IIc-007a, IIIc-061a, and the following salts Ic-007a-DEA2, IIc-007a-DEA2, IIIc-061a-DEA3 were stable as solids for up to 56d at temperatures of 4°C, 20°C and 40°C; the salt Ic-007a-DEA3 was stable at the same temperatures for up to 36d. b) Solutions General protocole: salts were obtained as solutions by adding the appropriate number of equivalent of base to solutions or suspensions of the desired compounds in water, sonicating until full dissolution, adjusting if needed the pH to values between 7.0 and 7.4 by addition of aqueous HC1 or excess base. The following bases were investigated: ethylamine, triethylamine, ethylenediamine, diethanolamine, triethanolamine, choline, meglumine, lysine and arginine. For examples: Salts of Ic-007a: Soluble salts were obtained with meglumine, lysine and diethanolamine after stirring the mixture for 2d at 40°C. A solid form of the Ic-007a-Lys2 salt was obtained from DMSO by precipitation with ethanol. The salt was stable as a solution in water for at least 7 d at room temperature. Salts of IIc-007a: DEAl-salt: on small scale, the mono-diethylammonium salt was obtained by the general procedure without adjusting the pH. Solubility: 17.4 mg / mL vs 1.8 mg / mL for the parent diacid Large scale process and characterization: To IIc-007a (20g, 42.7mmol) was charged EtOH (200ml). The reaction was stirred at RT to afford a slurry. DEA (4.4ml, 42.7mmol) was charged and the reaction heated at 50°C for 2h. The batch was cooled to RT and the solids filtered off. The filter cake was washed with EtOH (50mL) and oven dried at 40°C to afford 21.5g mono-DEA salt as a yellow solid in a 98% yield. NMR: 1.6% EtOH, 1.04eq DEA. HPLC: 99.6%. The solid-state data for the mono-DEA salt of IIc-007a showed a clear crystalline pattern in the XRPD analysis. The TGA trace showed a loss of minor amount of EtOH <120°C indicating that the EtOH may be dried off at 60-80°C. One then observed the loss ofthe DEA (theory 13.5%wtfor 1:1 salt) associated with the melt endotherm in the DSC (peak at 273.8°C), followed by a melt of the free acid form. DEA2-salt, pH adjusted: obtained by the general procedure with pH adjustment (0.51 additional equiv of Et2NH required to reach pH=7.25). The salt in solution exhibits clear degradation after 21 d at 40°C, and extensive degradation after 24 h at 80°C. DEA2-salt, pH not adjusted: obtained by the general procedure without pH adjustment. pH of solution = 5.87. The salt in solution exhibited no degradation after 21 d at 4°C, 20°C, and 40°C. Lys2-salt, pH not adjusted: obtained by the general procedure using 2 equiv of L-lysine. pH of solution = 5.74. NOTE: by analogy with the bis (N-methyl)amide of 2-hydroxyisophthalic acid (pKa of phenol = 6.81), the 2-OH group of the isophthalic bis-amide core of IIc-007a is remarkably acidic and its ionization leads to degradation of the molecule. This effect is not observed for Ic-007a (expected pKa of the phenolic functions in the range of 9.8-10.0). Thus it is important not to adjust the pH of solutions of dicationic salts of IIc-007a. Salts oflllc-061a: DEA3-salt, pH adjusted: obtained by the general procedure using 3 equiv of Et2NH with pH adjustment (0.8 additional equiv of HC1 (0.5 M) required to reach final pH=7.22). The salt in solution exhibited no degradation after 21 d at 4°C, 20°C, and slight degradation at 40°C after 33 d. Meg3-salt, pH adjusted: obtained by the general procedure using 3 equiv of meglumine with pH adjustment to reach final pH=7.22 (HC1 0.5M). The salt in solution exhibited no degradation after 21 d at 4°C, 20°C, and 40°C after 14 d. Salts of IVc-059a, DEA2-salt, pH adjusted: obtained by the general procedure with pH adjustment (0.32 additional equiv of Et2NH required to reach pH=7.3). The salt in solution exhibits stability after 26 d at 4°C, 20°C and 40°C. Example 1.14: Prodrugs Prodrugs of Ic-007a 1) 2-Morpholinoethyl 5-[[2,5-dihydroxy-4-[[4-hydroxy-3-(2-morpholinoethoxycarbonyl) phenyl] carbamoyl]benzoyl]amino]-2-hydroxy-benzoate (Ic-007a-mpe2) Et3N, DMF, EDC, DMAP, 60 “C 2) Hz. Pd / C, THF, water, AcOH Esterification. A suspension of 5-[[2,5-dibenzyloxy-4-[(3-carboxy-4-hydroxyphenyl) carbamoyl]-benzoyl]amino]-2-hydroxy-benzoic acid (130 mg, 0.2 mmol) in N,N-dimethylformamide (4 ml) was stirred at room temperature. N,N-dimethylpyridin-4-amine (49 mg, 0.4 mmol) and a solution of 2-morpholinoethanol (53 mg, 0.4 mmol) in N,N-dimethylformamide (0.5 ml) was added. l-Ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride (115 mg, 0.6 mmol) was added and the reaction mixture was heated in a microwave reactor at 60°C for 1.5 hours. The reaction mixture was fdtered, the fdtrate was diluted with tetrahydrofuran and the solvent was evaporated. The residue purified by silica gel chromatography eluting with 0-40% methanol in dichloromethane to give the title product as a white solid (80 mg, 45%). LCMS (m / z) [M+H] 875.1. Hydrogenolysis'. A solution of the diester obtained above (80 mg, 0.092 mmol) in tetrahydrofuran (12 ml) and water (4 ml) was prepared and 10% palladium on carbon (50 mg, 10% paste) was added. The reaction mixture was stirred under a hydrogen atmosphere for 17 hours. The catalyst was removed by filtration and the solvent evaporated. The residue was purified by reverse phase preparative HPLC on a C18 column using a gradient of 10-97% (acetonitrile + 0.1% formic acid):(water + 0.1% formic acid). The residue was triturated with diethyl ether and dried under vacuum to yield the title product Ic-007a-mpe2 as a yellow solid (22 mg, 35%). 1HNMR(d6-DMSOppm) 5 11.16-11.00 (brs, 1H), 10.46 (s, 1H), 10.45-10.15 (br s, 1H), 8.25 (d, J=2.7 Hz, 1H), 7.77 (dd, J=9.0, 2.7Hz, 1H), 7.53 (s, 1H), 7.01 (d, J=9.0 Hz, 1H), 4.46 (t, J=5.4 Hz, 2H), 3.623.56 (m, 4H), 2.77-2.69 (m, 2H), 2.56-2.50 (m, 4H, partly obscured by DMSO peak). LCMS (m / z) [M+H] 695.0. 2) 5-[[2,5-Dihydroxy-4-[[4-hydroxy-3-(2-morpholinoethoxycarbonyl)phenyl]carbamoyl] benzoyl] amino]-2-hydroxy-benzoic acid (Ic-007a-mpel) OBn O Et3N, DMF, EDC, DMAP, 60 °C 2) Hz. Pd / C, THF, water, AcOH Esterification. A solution of 5-[[2,5-dibenzyloxy-4-[(3-carboxy-4-hydroxy-phenyl)- carbamoyl]benzoyl]amino]-2-hydroxy-benzoic acid (324 mg, 0.5 mmol) and triethylamine (101 mg, 0.15 ml, 1 mmol) in N,N-dimethylformamide (7ml) was stirred at room temperature. A solution of 2- morpholinoethanol (66 mg, 0.5 mmol) in N,N-dimethylformamide (1 ml) and N,N-dimethylpyridin-4-amine (122 mg, 1 mmol) was added. l-Ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride (115 mg, 0.6 mmol) was added and the reaction mixture was stirred at room temperature for 2 hours was then heated in a microwave at 60°C for 4 hours. The reaction was repeated on a similar scale and the reaction mixtures combined. The solvent was evaporated and the residue was triturated with diethyl ether to give a mixture of the mono and diester (230 mg). LCMS (m / z) [M+H] 762.0 (mono ester). Hydrogenolysis. The mixture of mono and diester (230 mg) obtained above was dissolved in acetic acid (10 ml), tetrahydrofuran (15 ml) and water (5 ml) and 10% palladium on carbon (150 mg, 10% paste) was added. The reaction mixture was stirred under a hydrogen atmosphere for 16 hours. The catalyst was removed by filtration and the solvent evaporated to give a yellow gum (140 mg). The residue was purified by reverse phase preparative HPLC on a C18 column using a gradient of 10-70% (acetonitrile + 0.1% formic acid):(water + 0.1% formic acid). The residue was triturated with diethyl ether and dried under vacuum to yield the title monoester Ic-007a-mpel as a yellow solid (11 mg). XH NMR (d6-DMSO ppm) 8 11.33-11.29 (br s, 1H), 11.13-10.08 (br s, 1H), 10.50-10.44 (br s, 2H), 10.36-10.30 (br s, 1H), 8.25 (d, J=2.4 Hz, 1H), 8.06-8.02 (m, 1H), 7.78 (dd, J=9.0, 2.4Hz, 1H), 7.69-7.60 (m, 2H), 7.52 (s, 1H), 7.01 (d, J=9.0 Hz, 1H), 6.75 (d, J=8.7 Hz, 1H), 4.50-4.45 (m, 2H), 3.65-3.55 (m, 4H), 2.81-2.71 (m, 2H), 2.60-2.50 (m, 4H, partially obscured by DMSO peak). LCMS (m / z) [M+H] 582.0. 3) 1-(2,2-dimethylpropanoyloxy)ethyl 5-[[4-[[3-[1-(2,2-dimethylpropanoyloxy)eth oxycarbonyl]-4-hydroxy-phenyl]carbamoyl]-2,5-dihydroxy-benzoyl]amino]-2-hydroxy-benzoate (Ic-007a-pive2) And 4) 5-[[4-[[3-[l-(2,2-dimethylpropanoyloxy)ethoxycarbonyl]-4-hydroxy-phenyl]carbamoyl]-2,5-dihydroxy-benzoyl]amino]-2-hydroxy-benzoic acid (Ic-007a-pivel) OBn O OBn O Et3N, THE (mixture of mono- and di-esters) Esterification. A solution of 5-[[2,5-dibenzyloxy-4-[(3-carboxy-4-hydroxy-phenyl)carbamoyl] benzoyl]amino]-2-hydroxy-benzoic acid (324mg, 0.5mmol) and triethylamine (152mg, 0.21mmol) in N,N-dimethylformamide (10mL) was stirred at 0°C and 1-iodoethyl 2,2-dimethylpropanoate (572mg, 2mmol) was added. The reaction mixture was allowed to warm to room temperature and stirred at room temperature for 24 hours. The dimethylformamide was evaporated and the residue was partitioned between dichloromethane and aqueous sodium metabisulfite. The organic phase was dried over anhydrous magnesium sulphate and evaporated to give a 1:1 mixture of the mono and diester (187mg). The reaction was repeated and the 1:1 mixtures of esters combined. LCMS (m / z) [M+H] 777.0 (mono ester) and 905.1 (diester). OBn O OH O (mixture of mono- and di-esters) (mixture of mono- and di-esters) Hydrogenolysis The mixture of mono and diesters (320 mg) obtained above was dissolved in tetrahydrofuran (50 ml) and water (5 ml) and 10% palladium on carbon (300 mg, 10% paste) was added. The reaction mixture was stirred under a hydrogen atmosphere for 20 hours. The catalyst was removed by filtration and the solvent was evaporated. LCMS indicated only partial deprotection had been achieved. The residue was dissolved in tetrahydrofuran (36 ml) and water (6 ml) and 10% palladium on carbon (600 mg, 10% paste) was added. The reaction mixture was stirred under a hydrogen atmosphere for 22 hours. The catalyst was removed by filtration and the solvent was evaporated. The residue was purified by reverse phase preparative HPLC on a C18 column using a gradient of 40-97% (acetonitrile + 0.1% formic acid):(water + 0.1% formic acid). The residues were triturated with diethyl ether and dried under vacuum to yield the title products: Diester (Ic-007a-pive2): yellow solid (60 mg). 1HNMR(d6-DMSO ppm) 5 11.05 (s, 1H), 10.46 (s, 1H), 10.18 (s, 1H), 8.18 (br s, 1H), 7.83-7.77 (m, 1H), 7.52 (s, 1H), 7.05-6.96 (m, 2H), 1.58 (d, J=5.5 Hz, 3H), 1.17 (s, 9H). LCMS (m / z) [M+H] 724.9. Biodata: T1 / 2 (mouse plasma): 62.2 min (ester cleaved; 65% remaining after Ih); T1 / 2 (human plasma): > 180 min. Monoester (Ic-007a-pivel): yellow solid (35 mg). *HNMR (d6-DMSO ppm) 5 11.13 (s, IH), 11.06 (s, IH), 10.46 (s, IH), 10.42 (s, IH), 10.18 (s, IH), 8.21-8.18 (m, 2H), 8.78-8.72 (m, 2H), 7.55 (s, IH), 7.52 (s, IH), 7.03-6.92 (m, 3H), 1.58 (d, J=5.5 Hz, 3H), 1.17 (s, 9H). LCMS (m / z) [M+H] 596.9 Biodata: T1 / 2 (mouse plasma): 44.6 min (ester cleaved ; 49% remaining after Ih); T1 / 2 (human plasma): > 180 min. Prodrugs of IIc-007a 1) 2,2-Dimethylpropanoyloxymethyl 5-[[3-[[3-(2,2-dimethylpropanoyloxymethoxycarbonyl)-4-hydroxy-phenyl]carbamoyl]-2,5-dihydroxy-benzoyl]amino]-2-hydroxy-benzoate (IIc-007a-pivm2) o Esterification. A solution of 5-[[2,5-dibenzyloxy-3-[(3-carboxy-4-hydroxy-phenyl)carbamoyl] benzoyl]amino]-2-hydroxy-benzoic acid (280 mg, 0.432 mmol) in N,N-dimethyl formamide was prepared and chloromethyl 2,2-dimethylpropanoate (137 pL, 0.95 mmol) was added, followed by triethylamine (167 pL, 1.2 mmol)) and sodium iodide (143 mg, 0.95 mmol). The stirred solution was heated at 50°C for 18 hours. The solution was then cooled and partitioned between saturated ammonium chloride solution and ethyl acetate. The organic layer was dried over sodium sulfate, filtered and evaporated. The residue was purified by chromatography on a silica column using a gradient of 100% Ao-hexane to 50% ethyl acetate, 50% Ao-hexane to yield the diester as a colourless gum (192 mg, 51%). LCMS (m / z) [M+H] 876.9. Hydrogenolysis: A solution of diester obtained above (192 mg, 0.219 mmol) in tetrahydrofuran (4.5 mL) was prep...

Claims

1. A substituted hydroquinone of formula (I):5                                                              (I)wherein:Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-10   C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;R1 = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, or CONH-R10;one of R2 or R3 is H and the other is R5;R4  = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,      C1-C6acyloxymethyl,      C1-C6acyloxy-1-ethyl,      C1-15    C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R5 = R6, R7, or R8R6 = CONH-R9, CONHCOR9, CONH(CH2)n-R9, CONHCH(COOR4)(CH2)kR9,; wherein k = 0-4;R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4, 20   (CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, 5-membered N-containing heterocycles, or fluorine;R8 = (CH2)mX(CH2)pR9;X = O, S, SO2, NH, NAc, or N(CH2)qR9;R9 = aryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, 5-membered N-containing heterocycles, C=O, or NHCO-R10; or 25 heteroaryl substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4,(CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles], fluorine, C=O, or NHCO-R10;R10 = aryl, heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, 5-membered N-containing heterocycles, or fluorine;30   wherein the aryl of R9 and R10 is an aromatic group containing from 6 to 14 carbon atoms, selectedamong phenyl, naphthyl, biphenyl group; and the heteroaryl of R9 and R10 is an aromatic group containing 1 to 14 carbon atoms and one or more nitrogen; and2021236256   12 Jun 2026n, m, p and q are independently 1-4.

2. The compound of formula (I), according to claim 1:5                                                              (I)wherein:Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-10   C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;R1 = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, or CONH-R10;one of R2 or R3 is H and the other is R5;R4  = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,      C1-C6acyloxymethyl,      C1-C6acyloxy-1-ethyl,      C1-15   C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R5 = R6, or R7,R6 = CONH-R9, CONHCOR9, CONH(CH2)n-R9, or CONHCH(COOR4)(CH2)kR9; wherein k = 04;20   R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4,(CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, 5-membered N-containing heterocycles, or fluorine;R9 = aryl, heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, 5-membered N-containing heterocycles, C=O, or NHCO-R10; or heteroaryl substituted with at least one or more groups selected from COOR4, 25   (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, azoles [5-membered N-containing heterocycles],fluorine, C=O, or NHCO-R10;R10 = aryl substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, 5-membered N-containing heterocycles, or fluorine; wherein the aryl of R9 and R10 is an aromatic group containing from 6 to 14 carbon atoms, selected among phenyl, 30 naphthyl, biphenyl group; and the heteroaryl of R9 and R10 is an aromatic group containing 1 to 14 carbon atoms and one or more nitrogen; and n, is independently 1-4.2021236256   12 Jun 20263.     The compound according to claim 2, wherein:(A)Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-5 C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;R1 = COOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,      C1-C6acyloxymethyl,      C1-C6acyloxy-1-ethyl,      C1-C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);10   R2 = H; R3 = R5; andR5 = R6 = CONH-R9;or(B)Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, 15 phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;R1 = COOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,     C1-C6acyloxymethyl,     C1-C6acyloxy-1-ethyl,     C1-C6alkoxycarbonyloxymethyl,  C1-C6alkoxycarbonyloxy-1-ethyl,  or (oxodioxolyl)methyl;  o-20 methoxyphenyl (guaiacol ester);R3 = H; R2 = R5; andR5 = R6 = CONH-R9;orwherein said compound is selected form the group consisting of:25   4-(2-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-4-(2-sulfophenylaminocarbonyl)benzoic acid; 4-(3-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(3-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;30   2,5-dihydroxy-4-(3-sulfophenylaminocarbonyl)benzoic acid;4-(4-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(4-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-4-(4-sulfophenylaminocarbonyl)benzoic acid;4-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;35   4-(4-carboxy-3-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(4-carboxy-2,5-dihydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(2-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2021236256   12 Jun 20263,5-bis(2,5-dihydroxy-4-carboxybenzoylamino)benzoic acid;3-(4-carboxy-2,5-dihydroxybenzamido)phthalic acid;2-(4-carboxy-2,5-dihydroxybenzamido)terephthalic acid;2-(4-carboxy-2,5-dihydroxybenzamido)isophthalic acid;5    4-(4-carboxy-2,5-dihydroxybenzamido)phthalic acid;5-(4-carboxy-2,5-dihydroxybenzamido)isophthalic acid;2-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid;2-(4-carboxy-2,5-dihydroxybenzamido)isonicotinic acid;6-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid;10    6-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid;2-(4-carboxy-2,5-dihydroxybenzamido)-5-fluoronicotinic acid;6-(4-carboxy-2,5-dihydroxybenzamido)pyridine-2,5-dicarboxylic acid;2-(4-carboxy-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylic acid;3-(4-carboxy-2,5-dihydroxybenzamido)isonicotinic acid;15    5-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid;5-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid;3-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid;5-(4-carboxy-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid;4-(4-carboxy-2,5-dihydroxybenzamido)nicotinic acid;20    4-(4-carboxy-2,5-dihydroxybenzamido)picolinic acid;4-(4-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(3-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-4-(3-(1-hydroxy-1H-pyrazol-4-yl)phenylaminocarbonyl)benzoic acid;4-(2-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;25 ethyl 4-(2-(ethoxycarbonyl)phenylaminocarbonyl)-2,5-diacetoxybenzoate;ethyl 4-(2-(ethoxycarbonyl)phenylaminocarbonyl)-2,5-dihydroxybenzoate;ethyl 4-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-diacetoxybenzoate;ethyl 4-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoate;ethyl 2,5-dihydroxy-4-(4-hydroxy-3-(methoxycarbonyl)phenylaminocarbonyl)benzoate;30 ethyl 3,5-bis(2,5-diacetoxy-4-ethoxycarbonylbenzoylamino)benzoate;ethyl 3,5-bis(2,5-dihydroxy-4-ethoxycarbonylbenzoylamino)benzoate;ethyl 3-(4-(ethoxycarbonyl)-2,5-dihydroxybenzamido)isonicotinate;Ethyl 4-(4-ethoxycarbonyl-2,5-dihydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoate;3-(2-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;35    3-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-3-(2-sulfophenylaminocarbonyl)benzoic acid;3-(3-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2021236256   12 Jun 20263-(3-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-3-(3-sulfophenylaminocarbonyl)benzoic acid;3-(4-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;3-(4-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;5    2,5-dihydroxy-3-(4-sulfophenylaminocarbonyl)benzoic acid;3-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;3-(4-carboxy-3-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;3-(2-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzoic acid;3,5-Bis(2,5-dihydroxy-3-carboxybenzoylamino)benzoic acid;10    3-(3-carboxy-2,5-dihydroxybenzamido)phthalic acid;2-(3-carboxy-2,5-dihydroxybenzamido)terephthalic acid;2-(3-carboxy-2,5-dihydroxybenzamido)isophthalic acid;4-(3-carboxy-2,5-dihydroxybenzamido)phthalic acid;5-(3-carboxy-2,5-dihydroxybenzamido)isophthalic acid;15    2-(3-carboxy-2,5-dihydroxybenzamido)nicotinic acid;2-(3-carboxy-2,5-dihydroxybenzamido)isonicotinic acid;6-(3-carboxy-2,5-dihydroxybenzamido)nicotinic acid;6-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid;2-(3-carboxy-2,5-dihydroxybenzamido)-5-fluoronicotinic acid;20    6-(3-carboxy-2,5-dihydroxybenzamido)pyridine-2,5-dicarboxylic acid;2-(3-carboxy-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylic acid;3-(3-carboxy-2,5-dihydroxybenzamido)isonicotinic acid;5-(3-carboxy-2,5-dihydroxybenzamido)nicotinic acid;5-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid;25   3-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid5-(3-carboxy-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid;4-(3-carboxy-2,5-dihydroxybenzamido)nicotinic acid;4-(3-carboxy-2,5-dihydroxybenzamido)picolinic acid;3-(4-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;30   3-(3-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-3-(3-(1-hydroxy-1H-pyrazol-4-yl)phenylaminocarbonyl)benzoic acid;3-(2-(carboxymethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoic acid;ethyl 3-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzoate; andethyl 3-(2-(ethoxycarbonylmethyl)phenylaminocarbonyl)-2,5-dihydroxybenzoate;354.     The compound according to claim 2, wherein:(A)2021236256   12 Jun 2026Ra, Rb = H;R1 = SO3H;R2 = H; R3 = R5; andR5 = R6 = CONH-R9;5 or(B)Ra, Rb = H;R1 = SO3H;R3 = H; R2 = R5; and10   R5 = R6 = CONH-R9;orwherein said compound is selected form the group consisting of:2-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid;2,5-dihydroxy-4-(2-sulfophenylaminocarbonyl)benzenesulfonic acid;15 3-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid;2,5-dihydroxy-4-(3-sulfophenylaminocarbonyl)benzenesulfonic acid;4-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid;2,5-dihydroxy-4-(4-sulfophenylaminocarbonyl)benzenesulfonic acid;5-(2,5-dihydroxy-4-sulfobenzamido)-2-hydroxybenzoic acid;20 4-(2,5-dihydroxy-4-sulfobenzamido)-2-hydroxybenzoic acid;2-(2,5-dihydroxy-4-sulfobenzamido)-5-hydroxybenzoic acid;3,5-bis(2,5-dihydroxy-4-sulfobenzamido)benzoic acid;3-(2,5-dihydroxy-4-sulfobenzamido)phthalic acid;2-(2,5-dihydroxy-4-sulfobenzamido)terephthalic acid;25 2-(2,5-dihydroxy-4-sulfobenzamido)isophthalic acid;4-(2,5-dihydroxy-4-sulfobenzamido)phthalic acid;5-(2,5-dihydroxy-4-sulfobenzamido)isophthalic acid;2-(2,5-dihydroxy-4-sulfobenzamido)nicotinic acid;2-(2,5-dihydroxy-4-sulfobenzamido)isonicotinic acid;30 6-(2,5-dihydroxy-4-sulfobenzamido)nicotinic acid;6-(2,5-dihydroxy-4-sulfobenzamido)picolinic acid;2-(2,5-dihydroxy-4-sulfobenzamido)-5-fluoronicotinic acid;6-(2,5-dihydroxy-4-sulfobenzamido)pyridine-2,5-dicarboxylic acid;2-(2,5-dihydroxy-4-sulfobenzamido)pyridine-3,5-dicarboxylic acid;35 3-(2,5-dihydroxy-4-sulfobenzamido)isonicotinic acid;5-(2,5-dihydroxy-4-sulfobenzamido)nicotinic acid;5-(2,5-dihydroxy-4-sulfobenzamido)picolinic acid;2021236256   12 Jun 20263-(2,5-dihydroxy-4-sulfobenzamido)picolinic acid;5-(2,5-dihydroxy-4-sulfobenzamido)-2-fluoroisonicotinic acid;4-(2,5-dihydroxy-4-sulfobenzamido)nicotinic acid;4-(2,5-dihydroxy-4-sulfobenzamido)picolinic acid;5    (4-(2,5-dihydroxy-4-sulfobenzamido)phenyl)acetic acid;(3-(2,5-dihydroxy-4-sulfobenzamido)phenyl)acetic acid;(2-(2,5-dihydroxy-4-sulfobenzamido)phenyl)acetic acid;2-(2,5-dihydroxy-3-sulfobenzamido)benzoic acid;2,5-dihydroxy-3-(2-sulfophenylaminocarbonyl)benzenesulfonic acid;10 3-(2,5-dihydroxy-3-sulfobenzamido)benzoic acid;2,5-dihydroxy-3-(3-sulfophenylaminocarbonyl)benzenesulfonic acid;4-(2,5-dihydroxy-3-sulfobenzamido)benzoic acid;2,5-dihydroxy-3-(4-sulfophenylaminocarbonyl)benzenesulfonic acid;5-(2,5-dihydroxy-3-sulfobenzamido)-2-hydroxybenzoic acid;15 4-(2,5-dihydroxy-3-sulfobenzamido)-2-hydroxybenzoic acid;2-(2,5-dihydroxy-3-sulfobenzamido)-5-hydroxybenzoic acid;3-(2,5-dihydroxy-3-sulfobenzamido)-5-(2,5-dihydroxy-4-sulfobenzamido)benzoic acid3-(2,5-dihydroxy-3-sulfobenzamido)phthalic acid;2-(2,5-dihydroxy-3-sulfobenzamido)terephthalic acid;20 2-(2,5-dihydroxy-3-sulfobenzamido)isophthalic acid;4-(2,5-dihydroxy-3-sulfobenzamido)phthalic acid;5-(2,5-dihydroxy-3-sulfobenzamido)isophthalic acid;2-(2,5-dihydroxy-3-sulfobenzamido)nicotinic acid;2-(2,5-dihydroxy-3-sulfobenzamido)isonicotinic acid;25 6-(2,5-dihydroxy-3-sulfobenzamido)nicotinic acid;6-(2,5-dihydroxy-3-sulfobenzamido)picolinic acid;2-(2,5-dihydroxy-3-sulfobenzamido)-5-fluoronicotinic acid;6-(2,5-dihydroxy-3-sulfobenzamido)pyridine-2,5-dicarboxylic acid;2-(2,5-dihydroxy-3-sulfobenzamido)pyridine-3,5-dicarboxylic acid;30 3-(2,5-dihydroxy-3-sulfobenzamido)isonicotinic acid;5-(2,5-dihydroxy-3-sulfobenzamido)nicotinic acid;5-(2,5-dihydroxy-3-sulfobenzamido)picolinic acid;3-(2,5-dihydroxy-3-sulfobenzamido)picolinic acid;5-(2,5-dihydroxy-3-sulfobenzamido)-2-fluoroisonicotinic acid;35 4-(2,5-dihydroxy-3-sulfobenzamido)nicotinic acid;4-(2,5-dihydroxy-3-sulfobenzamido)picolinic acid;(4-(2,5-dihydroxy-3-sulfobenzamido)phenyl)acetic acid;2021236256   12 Jun 2026(3-(2,5-dihydroxy-3-sulfobenzamido)phenyl)acetic acid; and (2-(2,5-dihydroxy-3-sulfobenzamido)phenyl)acetic acid.

5. The compound according to claim 2, wherein:5   (A)Ra, Rb = H,R1 = (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6acyloxymethyl, C1-C6acyloxy-1-ethyl, C1-C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-10 methoxyphenyl (guaiacol ester);R2 = H or R5, R3 = R5; andR5 = R6 = CONH-R9;Or(B)15   Ra, Rb = H;R1 = (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6acyloxymethyl, C1-C6acyloxy-1-ethyl, C1-C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);20   R3 = H; R2 = R5; andR5 = R6 = CONH-R9;or wherein said compound is selected form the group consisting of: 2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid;(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;25    (2,5-dihydroxy-4-(2-sulfophenylaminocarbonyl)phenyl)acetic acid;3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid;(2,5-dihydroxy-4-(3-sulfophenylaminocarbonyl)phenyl)acetic acid;4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid;2-(2,5-dihydroxy-4-(4-sulfophenylaminocarbonyl)phenyl)acetic acid;30   5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid;4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid;2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-5-hydroxybenzoic acid;3,5-Bis(2,5-dihydroxy-4-carboxymethylbenzoylamino)benzoic acid 3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid;35    2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)terephthalic acid;2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid;4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid;2021236256   12 Jun 20265-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid;2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid;2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotinic acid;6-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid;5    6-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-5-fluoronicotinic acid;6-(4-(carboxymethyl)-2,5-dihydroxybenzamido)pyridine-2,5-dicarboxylic acid;2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylic acid;3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotinic acid;10    5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid;5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;5-(4-(carboxymethyl)-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid;4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid;15    4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;(4-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid;(3-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid;(2-(4-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid;methyl 2-(4-(ethoxycarbonylmethyl)-2,5-dihydroxybenzamido)benzoate;20    ethyl (4-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxyphenyl)acetate;diethyl 5-(4-( ethoxycarbonylmethyl)-2,5-dihydroxybenzamido)isophthalate;methyl 3,5-bis(4-(ethoxycarbonylmethyl)-2,5-dihydroxybenzamido)benzoate;2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid;(2,5-dihydroxy-3-(2-sulfophenylaminocarbonyl)phenyl)acetic acid;25   3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid;(2,5-dihydroxy-3-(3-sulfophenylaminocarbonyl)phenyl)acetic acid;4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)benzoic acid;(2,5-dihydroxy-3-(4-sulfophenylaminocarbonyl)phenyl)acetic acid;5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid;30   4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid;2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-5-hydroxybenzoic acid;3,5-Bis(2,5-dihydroxy-3-carboxymethylbenzoylamino)benzoic acid3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid;2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)terephthalic acid;35    2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid;4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)phthalic acid;5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isophthalic acid;2021236256   12 Jun 20262-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid; 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotinic acid;6-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid;6-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;5    2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-5-fluoronicotinic acid;6-(3-(carboxymethyl)-2,5-dihydroxybenzamido)pyridine-2,5-dicarboxylic acid; 2-(3-(carboxymethyl)-2,5-dihydroxybenzamido)pyridine-3,5-dicarboxylic acid;3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)isonicotinic acid;5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid;10    5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;5-(3-(carboxymethyl)-2,5-dihydroxybenzamido)-2-fluoroisonicotinic acid;4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)nicotinic acid;4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)picolinic acid;15    (4-(3-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid;(3-(3-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid; and (2 -(3-(carboxymethyl)-2,5-dihydroxybenzamido)phenyl)acetic acid.

6. The compound according to claim 2, wherein:20   (A)Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;R1 = CONH-R10; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, 25   N-methylpiperazino-C1-C6alkyl,    C1-C6acyloxymethyl,     C1-C6acyloxy-1-ethyl,    C1-C6alkoxycarbonyloxymethyl,  C1-C6alkoxycarbonyloxy-1-ethyl,  or (oxodioxolyl)methyl;  o-methoxyphenyl (guaiacol ester);R2 = H; R3 = R5; andR5 = R6 = CONH-R9;30 Or(B)Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;35 R1 = CONH-R10; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6 acyloxymethyl, C1-C6acyloxy-1-ethyl, C1-2021236256   12 Jun 2026C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R3 = H; R2 = R5; andR5 = R6 = CONH-R9.5 orwherein said compound is selected form the group consisting of:5-(4-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid;N1,N4-bis(2-(1H-tetrazol-5-yl)phenyl)-2,5-dihydroxyterephthalamide;10   5-(4-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoicacid;5-(2,5-dihydroxy-4-(4-hydroxy-3-sulfophenylaminocarbonyl)benzamido)-2-hydroxybenzenesulphonic acid;4-(4-(4-carboxy-3-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic 15 acid;4-(2,5-dihydroxy-4-(3-hydroxy-4-sulfophenylaminocarbonyl)benzamido)-2-hydroxybenzenesulphonic acid;2-(2,5-dihydroxy-4-(4-hydroxy-2-carboxyphenylaminocarbonyl)benzamido)-5-hydroxybenzoic acid;20   2-(2,5-dihydroxy-4-(4-hydroxy-2-sulfophenylaminocarbonyl)benzamido)-5-hydroxybenzenesulphonic acid;methyl          5-(4-(2-(1H-tetrazol-5-yl)phenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoate;methyl 5-(2,5-diacetoxy-4-(4-acetoxy-3-(methoxycarbonyl)phenylaminocarbonyl)benzamido)-25 2-acetoxybenzoate;methyl 5-(2,5-dihydroxy-4-(4-hydroxy-3-(methoxycarbonyl)phenylaminocarbonyl)benzamido)-2-hydroxybenzoate;methyl 2-(2,5-dihydroxy-4-(4-hydroxy-2-(methoxycarbonyl)phenylaminocarbonyl)benzamido)-5-hydroxybenzoate;30 1-(2,2-dimethylpropanoyloxy)ethyl 5-[[4-[[3-[1-(2,2-dimethylpropanoyloxy)ethoxycarbonyl]-4-hydroxy-phenyl]aminocarbonyl]-2,5-dihydroxy-benzoyl]amino]-2-hydroxybenzoate 5-(3-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid;5-(2,5-dihydroxy-3-(4-hydroxy-3-sulfophenylaminocarbonyl)benzamido)-2-35 hydroxybenzenesulphonic acid;4-(3-(3-hydroxy-4-carboxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid;2021236256   12 Jun 20264-(2,5-dihydroxy-3-(3-hydroxy-4-sulfophenylaminocarbonyl)benzamido)-2-hydroxybenzenesulphonic acid;2-(3-(2-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-5-hydroxylbenzoic acid; and5   2-(2,5-dihydroxy-3-(4-hydroxy-2-sulfophenylaminocarbonyl)benzamido)-5-hydroxybenzenesulphonic acid.

7. The compound according to claim 2 having the formula (I):10wherein:Ra, Rb = H;R1 = CONH-R10;R10= phenyl substituted with COOR4 and with OR4;15   R2 = H;R3 = CONH-R9;R9 = phenyl substituted with COOR4 and with OR4; andR4 = H;and wherein said compound is  5-(4-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-20 dihydroxybenzamido)-2-hydroxybenzoic acid.

8. The compound according to claim 2 having the formula (I):25wherein:2021236256   12 Jun 2026Ra, Rb = H;R1 = CONH-R10;R10= phenyl substituted with COOR4 and with OR4;R2 = CONH-R9;5   R3 = H;R9 = phenyl substituted with COOR4 and with OR4; andR4 = H;and wherein said compound is  5-(3-(3-carboxy-4-hydroxyphenylaminocarbonyl)-2,5-dihydroxybenzamido)-2-hydroxybenzoic acid.

109. The compound according to claim 2, wherein:(A)Ra, Rb = H;R1 = COOR4; (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl,15    pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6acyloxymethyl, C1-C6acyloxy-1-ethyl,       C1-C6alkoxycarbonyloxymethyl,       C1-C6alkoxycarbonyloxy-1-ethyl,       or(oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R2 = H; R3 = R5; andR5 = R6 = CONHCOR9;20 or(B)Ra, Rb = H;R1 = COOR4; (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl,pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6acyloxymethyl, C1-C6acyloxy-1-25 ethyl,       C1-C6alkoxycarbonyloxymethyl,       C1-C6alkoxycarbonyloxy-1-ethyl,       or(oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R3 = H; R2 = R5; andR5 = R6 = CONHCOR9;or wherein said compound is selected form the group consisting of:30 N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 4-carboxy-2,5-dihydroxybenzamide;N-(4-carboxy-2,5-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxy-benzamide;N-(3-carboxy-2,5-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxy-benzamide;N-(3,4-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxybenzamide;N-(3,5-dihydroxybenzoyl) 4-carboxy-2,5-dihydroxybenzamide;35 N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 3-carboxy-2,5-dihydroxybenzamide;N-(4-carboxy-2,5-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxy-benzamide;N-(3-carboxy-2,5-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxy-benzamide;2021236256   12 Jun 2026N-(3,4-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxybenzamide;N-(3,5-dihydroxybenzoyl) 3-carboxy-2,5-dihydroxybenzamide;N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 4-carboxymethyl-2,5-dihydroxybenzamide;N-(4-carboxy-2,5-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxy-benzamide;5 N-(3-carboxy-2,5-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxy-benzamide;N-(3,4-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxybenzamide;N-(3,5-dihydroxybenzoyl) 4-carboxymethyl-2,5-dihydroxybenzamide;N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 3-carboxymethyl-2,5-dihydroxybenzamide;N-(4-carboxy-2,5-dihydroxybenzoyl) 3-carboxymethyl-2,5-dihydroxy-benzamide;10 N-(3-carboxy-2,5-dihydroxybenzoyl) 3-carboxymethyl-2,5-dihydroxy-benzamide;N-(3,4-dihydroxybenzoyl) 3-carboxymethyl-2,5-dihydroxybenzamide; andN-(3,5-dihydroxybenzoyl) 3-carboxymethyl-2,5-dihydroxybenzamide.

10. A compound according to claim 2, wherein15   (A)Ra, Rb = H;R1 = COOR4; (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl,pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6acyloxymethyl, C1-C6acyloxy-1-ethyl,       C1-C6alkoxycarbonyloxymethyl,       C1-C6alkoxycarbonyloxy-1-ethyl,       or20 (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R2 = H; R3 = R5; andR5 = R6 = CONH(CH2)n-R9;Or(B)25   Ra, Rb = H;R1 = COOR4; (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl,pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6acyloxymethyl, C1-C6acyloxy-1-ethyl,       C1-C6alkoxycarbonyloxymethyl,       C1-C6alkoxycarbonyloxy-1-ethyl,       or(oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);30   R3 = H; R2 = R5; andR5 = R6 = CONH(CH2)n-R9;or wherein said compound is selected form the group consisting of:4-(3,4-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid;35 4-(3,5-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-4-((3,4,5-trihydroxycyclohexyl)methylaminocarbonyl)benzoic acid;2021236256   12 Jun 20264-(2-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(3-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(4-carboxyphenylmethylaminocarbonyl) 2,5-dihydroxybenzoic acid;3-(3,4-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;5    3-(2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid;3-(3,5-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;3-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-3-((3,4,5-trihydroxycyclohexyl)methylaminocarbonyl)benzoic acid;3-(2-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;10   3-(3-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;3-(4-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;(4-(3,4-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(4-(3,5-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(4-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxyphenyl)acetic15 acid;(2,5-dihydroxy-4-((3,4,5-trihydroxycyclohexyl)methylaminocarbonyl)phenyl)acetic acid;(4-(2-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(4-(3-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(4-(4-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;20   (3-(3,4-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(3-(3,5-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(3-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(2,5-dihydroxy-3-((3,4,5-trihydroxycyclohexyl)methylcarbonylamino)phenyl)acetic acid;25   (3-(2-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid;(3-(3-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid; and(3-(4-carboxyphenylmethylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid.

11. The compound according to claim 2, wherein said compound is selected form the group30 consisting of:N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 4-carboxy-2,5-dihydroxybenzamide;N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 3-carboxy-2,5-dihydroxybenzamide;N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 4-carboxymethyl-2,5-dihydroxybenzamide;N-(1,3,4,5-tetrahydroxycyclohexylcarbonyl) 3-carboxymethyl-2,5-dihydroxybenzamide;35 4-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid;2,5-dihydroxy-4-((3,4,5-trihydroxycyclohexyl) methylaminocarbonyl)benzoic acid;3-(3,5-dihydroxyphenylmethylaminocarbonyl)-2,5-dihydroxybenzoic acid;2021236256   12 Jun 20263-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid; (4-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxyphenyl)  aceticacid;(2,5-dihydroxy-4-((3,4,5-trihydroxycyclohexyl)methylaminocarbonyl)phenyl)acetic acid;5    (3-((4,5-dihydroxy-3-oxocyclohex-1-enyl)methylaminocarbonyl)-2,5-dihydroxyphenyl)  aceticacid; and(2,5-dihydroxy-3-((3,4,5-trihydroxycyclohexyl)methylcarbonylamino)phenyl)acetic acid.

12. The compound according to claim 2, wherein:10   Ra, Rb = H;R1 = SO3H;R2 = H; R3 = R5; andR5 = R6 = CONH(CH2)n-R9;or wherein said compound is selected form the group consisting of:15 2-((2,5-dihydroxy-4-sulfobenzamido)methyl)benzoic acid;3-((2,5-dihydroxy-4-sulfobenzamido)methyl)benzoic acid; and 4-((2,5-dihydroxy-4-sulfobenzamido)methyl)benzoic acid.

13. The compound according to claim 2, wherein:20   (A)Ra, Rb = H;R1 = COOR4; (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl,pyrrolidino-Ci-C6alkyl, N-methylpiperazino-Ci-C6alkyl, , Ci-C6acyloxymethyl, Ci-C6acyloxy-1-ethyl,       C1-C6alkoxycarbonyloxymethyl,       C1-C6alkoxycarbonyloxy-1-ethyl,       or25 (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R2 = H; R3 = R5; andR5 = R6 = CONHCH(COOR4)(CH2)kR9;or(B)30   Ra, Rb = H;R1 = COOR4; (CH2)nCOOR4; R4 = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl,pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl, C1-C6acyloxymethyl, C1-C6acyloxy-1-ethyl,       C1-C6alkoxycarbonyloxymethyl,       C1-C6alkoxycarbonyloxy-1-ethyl,       or(oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);35   R3 = H; R2 = R5; andR5 = R6 = CONHCH(COOR4)(CH2)kR9;or wherein said compound is selected form the group consisting of:2021236256   12 Jun 20264-(1-carboxy-2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid;4-(carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid; 3-(1-carboxy-2-(3,4-dihydroxyphenyl)ethylaminocarbonyl)-2,5-dihydroxybenzoic acid 3-(carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)-2,5-dihydroxybenzoic acid;5   (4-(carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid; and(3-(carboxy(3,4-dihydroxyphenyl)methylaminocarbonyl)-2,5-dihydroxyphenyl)acetic acid.

14. The compound according to claim 2, wherein:(A)10   Ra, Rb = H;R1 = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, CONH-R10;R4  = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,      C1-C6acyloxymethyl,      C1-C6acyloxy-1-ethyl,      C1-C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-15 methoxyphenyl (guaiacol ester);R2 = H; R3 = R5; andR5 = R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, 5-membered N-containing heterocycles, or fluorine; or20   (B)Ra, Rb = H;R1 = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, CONH-R10;R4  = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,      C1-C6acyloxymethyl,      C1-C6acyloxy-1-ethyl,      C1-25 C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);R3 = H; R2 = R5; andR5= R7 = benzoheteroaryl substituted with at least one or more groups selected from: COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, OR4, 5-membered N-containing heterocycles, or fluorine; 30 or wherein said compound is selected form the group consisting of:2-(4-Carboxy-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-4-carboxylic acid;Methyl 2-(4-ethoxycarbonyl-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-4-carboxylate;2-(2,5-Dihydroxy-4-sulfophenyl)-1H-benzo[d]imidazole-4-carboxylic acid;2-(4-Carboxy-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylic acid;35 2-(2,5-Dihydroxy-4-sulfophenyl)-1H-benzo[d]imidazole-5-carboxylic acid;2-(3-Carboxy-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-4-carboxylic acid;2-(2,5-Dihydroxy-3-sulfophenyl)-1H-benzo[d]imidazole-4-carboxylic acid;2021236256   12 Jun 20262-(3-Carboxy-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylic acid;2-(2,5-Dihydroxy-3-sulfophenyl)-1H-benzo[d]imidazole-5-carboxylic acid;2-(4-(Carboxymethyl)-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-4-carboxylic acid;2-(4-(Carboxymethyl)-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylic acid;5   2-(3-(Carboxymethyl)-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-4-carboxylic acid; and2-(3-(Carboxymethyl)-2,5-dihydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylic acid.

15. The compound of formula (I), according to claim 1:10                                                       (I)wherein:Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-15   C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;R1 = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, or CONH-R10;one of R2 or R3 is H and the other is R5;R4  = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,     C1-C6acyloxymethyl,     C1-C6acyloxy-1-ethyl,     C1-C620 alkoxycarbonyloxymethyl,  C1-C6alkoxycarbonyloxy-1-ethyl,  or (oxodioxolyl)methyl;  o-methoxyphenyl (guaiacol ester);R5 = R8R8 = (CH2)mX(CH2)pR9;X = O, S, SO2, NH, NAc, or N(CH2)qR9;25    R9 = aryl, or heteroaryl, substituted with at least one or more groups selected from COOR4,(CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, 5-membered N-containing heterocycles, fluorine, C=O, or NHCO-R10;R10 = aryl, heteroaryl, substituted with at least one or more groups selected from COOR4, (CH2)nCOOR4, (CH2)nSO3H, OR4, SO3H, 5-membered N-containing heterocycles, or fluorine;30 wherein the aryl of R9 an R10 is an aromatic group containing from 6 to 14 carbon atoms, selected among phenyl, naphthyl, or biphenyl group; and2021236256   12 Jun 2026the heteroaryl R9 and R10 is an aromatic group containing 1 to 14 carbon atoms and one or more nitrogen; andn, m, p and q are an integer independently equal to 1-4.5    16. The compound according to claim 14, wherein:(A)Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO, phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;10   R1 = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, CONH-R10;R4  = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-methylpiperazino-C1-C6alkyl,      C1-C6acyloxymethyl,      C1-C6acyloxy-1-ethyl,      C1-C6alkoxycarbonyloxymethyl, C1-C6alkoxycarbonyloxy-1-ethyl, or (oxodioxolyl)methyl; o-methoxyphenyl (guaiacol ester);15   R2 = H; R3 = R5; andR5 = R8 = (CH2)mX(CH2)pR9;wherein X = O, S, SO2, NH, NAc, or N(CH2)qR9; or(B)20   Ra, Rb = H, C1-4acyl, arylC1-4alkyl, C6-C10arylCO, HOOC(CH2)nCO, C1-C7alkylNHCO,phosphono, phosphonooxymethyl,   C1-C6acyloxymethyl,   C1-C6acyloxy-1-ethyl,   C1-C6alkoxycarbonyloxymethyl, or C1-C6alkoxycarbonyloxy-1-ethyl;R1 = COOR4, (CH2)nCOOR4, SO3H, (CH2)nSO3H, CONH-R10;R4  = H, C1-4alkyl, arylC1-4alkyl, morpholino-C1-C6alkyl, pyrrolidino-C1-C6alkyl, N-25    methylpiperazino-C1-C6alkyl,     C1-C6acyloxymethyl,     C1-C6acyloxy-1-ethyl,     C1-C6alkoxycarbonyloxymethyl,  C1-C6alkoxycarbonyloxy-1-ethyl,  or (oxodioxolyl)methyl;  o-methoxyphenyl (guaiacol ester);R3 = H; R2 = R5; andR5 = R8 = (CH2)mX(CH2)pR9;30 wherein X = O, S, SO2, NH, NAc, or N(CH2)qR9;or wherein said compound is selected form the group consisting of:Bis(4-carboxy-2,5-dihydroxyphenylmethyl)amine;4-((2,5-Dihydroxy-4-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid;4-((2,5-Dihydroxy-3-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid;35 Bis(2,5-dihydroxy-4-sulfophenylmethyl)amine;N,N-Bis(4-carboxy-2,5-dihydroxyphenylmethyl)acetamide;N-(2,5-dihydroxy-4-sulfophenylmethyl) N-(4-carboxy-2,5-dihydroxyphenylmethyl)acetamide;2021236256   12 Jun 2026N-(2,5-dihydroxy-3-sulfophenylmethyl) N-(4-carboxy-2,5-dihydroxyphenylmethyl)acetamide;N,N-Bis(2,5-dihydroxy-4-sulfophenylmethyl)acetamide;4-((2,5-Dihydroxy-4-carboxyphenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid;4-((2,5-Dihydroxy-4-sulfophenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid;5 4-((2,5-Dihydroxy-3-sulfophenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid;4-((2,5-Dihydroxy-4-sulfophenyl)methylthiomethyl)-2,5-dihydroxybenzenesulfonic acid;4-((2,5-Dihydroxy-4-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid;4-((2,5-Dihydroxy-4-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid;4-((2,5-Dihydroxy-3-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid;10 4-((2,5-Dihydroxy-4-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzenesulfonic acid;4-((2,5-Dihydroxy-4-carboxyphenyl)methoxymethyl)-2,5-dihydroxybenzoic acid;4-((2,5-dihydroxy-4-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid;4-((2,5-dihydroxy-3-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid;4-((2,5-Dihydroxy-4-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzenesulfonic acid;15 Tris (4-carboxy-2,5-dihydroxyphenylmethyl)amine;Tris (4-ethoxycarbonyl-2,5-dihydroxyphenylmethyl)amine;Bis(3-carboxy-2,5-dihydroxyphenylmethyl)amine;3-((2,5-Dihydroxy-3-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid;3-((2,5-Dihydroxy-4-sulfophenylmethylamino)methyl)-2,5-dihydroxybenzoic acid;20 Bis(2,5-dihydroxy-3-sulfophenylmethyl)amine;N,N-Bis(3-carboxy-2,5-dihydroxyphenylmethyl)acetamide;N-(2,5-dihydroxy-3-sulfophenylmethyl) N-(3-carboxy-2,5-dihydroxyphenylmethyl)acetamide;N-(2,5-dihydroxy-4-sulfophenylmethyl) N-(3-carboxy-2,5-dihydroxyphenylmethyl)acetamide; N,N-Bis(2,5-dihydroxy-3-sulfophenylmethyl)acetamide;25 3-((2,5-Dihydroxy-3-carboxyphenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid;3-((2,5-Dihydroxy-3-sulfophenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid;3-((2,5-Dihydroxy-4-sulfophenyl)methylthiomethyl)-2,5-dihydroxybenzoic acid;3-((2,5-Dihydroxy-3-sulfophenyl)methylthiomethyl)-2,5-dihydroxybenzenesulfonic acid;3-((2,5-Dihydroxy-3-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid;30 3-((2,5-Dihydroxy-3-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid;3-((2,5-Dihydroxy-4-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid;3-((2,5-Dihydroxy-3-sulfophenyl)methylsulfonylmethyl)-2,5-dihydroxybenzenesulfonic acid; 3-((2,5-Dihydroxy-3-carboxyphenyl)methoxymethyl)-2,5-dihydroxybenzoic acid;3-((2,5-dihydroxy-3-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid;35 3-((2,5-dihydroxy-4-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzoic acid;3-((2,5-Dihydroxy-3-sulfophenyl)methoxymethyl)-2,5-dihydroxybenzenesulfonic acid;2021236256   12 Jun 2026Methyl              3-((2,5-diacetoxy-3-methoxycarbonylphenyl)methylsulfonylmethyl)-2,5-diacetoxybenzoate;Methyl              3-((2,5-dihydroxy-3-methoxycarbonylphenyl)methylsulfonylmethyl)-2,5-hydroxybenzoate;5 2-Morpholinoethyl                                                    3-((2,5-dihydroxy-3-(2-morpholinoethoxycarbonyl)phenyl)methylsulfonylmethyl)-2,5-hydroxybenzoate;Tris (3-carboxy-2,5-dihydroxyphenylmethyl)amine; andTris (3-ethoxycarbonyl-2,5-dihydroxyphenylmethyl)amine.10    17. The compound according to claim 2, having the formula (I):(I)wherein:Ra, Rb = H;15 R1 = COOR4;R2 = H;R3 = R8;R4 = H;R8 = (CH2)mX(CH2)pR9;20   R9 = phenyl substituted with COOR4 and with OR4;X = N(CH2)qR9; andm, p and q = 1; andwherein said compound is Tris (4-carboxy-2,5-dihydroxyphenylmethyl)amine.25    18. The compound according to claim 2, having the formula (I):(I)2021236256   12 Jun 2026wherein:Ra, Rb = H;R1 = COOR4;R2 = (CH2)mX(CH2)pR95   R3 = H;R9 = phenyl substituted with COOR4 and with OR4;R4 = H;X = SO2; andm and p = 1;10 and said compound is 3-((2,5-Dihydroxy-3-carboxyphenyl)methylsulfonylmethyl)-2,5-dihydroxybenzoic acid.

19. A pharmaceutical composition comprising a therapeutically effective amount of the compound according to any one of claims 1-18 or a pharmaceutically acceptable salt, or 15 stereoisomer thereof, and a pharmaceutically acceptable excipient.

20. A method of treating and / or preventing autoimmune, immunological, rheumatology, vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic and gastro-intestinal disorders, neuroinflammatory and neurodegenerative diseases, neoplasms and cancer associated 20 disorders, hormone related diseases, or immunological disorders resulting from viral and / or bacterial infectious diseases and / or complications thereof, said method including the step of administering an effective amount of a compound according to anyone of claims 1-19.

21. Intermediates in the synthesis of compounds according to claim 2, said intermediates 25 being chosen among 2,5-bis(benzyloxy)-4-(ethoxycarbonyl)benzoic acid; 2,5-bis(benzyloxy)isophthalaldehyde; 2,5-bis(benzyloxy)isophthalic acid; ethyl 2,5-bis(benzyloxy)-4-(hydroxymethyl)benzoate; or ethyl 2,5-bis(benzyloxy)-3-(hydroxymethyl)benzoate.

22. Use of a compound according to anyone of claims 1-19 in the manufacture of a 30 medicament for treating and / or preventing autoimmune, immunological, rheumatology, vascular disorders, ophthalmologic disorders, fibrotic disorders, metabolic and gastro-intestinal disorders, neuroinflammatory and neurodegenerative diseases, neoplasms and cancer associated disorders, hormone related diseases, or immunological disorders resulting from viral and / or bacterial infectious diseases and / or complications thereof.35

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