Alpha-hydroxylated fatty acid metabolites, their medical uses, and their use as biomarkers

Abstract

Fatty acids with one or more unsaturations and an odd-numbered hydrocarbon chain are described, wherein these fatty acids have the chemical structure of the therapeutically active metabolites of alpha-hydroxylated mono- or polyunsaturated fatty acids with an even-numbered chain. The compositions comprising these fatty acids, their medical uses, and their use as indicators of a patient's efficacy and / or response to treatment with the alpha-hydroxylated mono- or polyunsaturated fatty acids with an even-numbered chain from which they are derived are also described.

Description

Alpha-hydroxylated fatty acid metabolites, their medical uses, and their use as biomarkers TECHNICAL FIELD OF THE INVENTION The present invention relates to fatty acids with one or more unsaturations, of odd-numbered hydrocarbon chains, wherein the chemical structure of said fatty acids corresponds to that of the metabolites of mono- or polyunsaturated alpha-hydroxylated fatty acids. The present invention also relates to compositions comprising said odd-numbered fatty acids, their medical uses, and their use as indicators of the efficacy of treatment of a patient with the mono- or polyunsaturated alpha-hydroxylated fatty acids of which they are metabolites. BACKGROUND OF THE INVENTION It is known that changes in the lipid composition of membranes influence cell signaling, potentially leading to the development of diseases, reversing them, or even preventing them. Similarly, therapeutic interventions focused on regulating membrane lipid levels can prevent and reverse (cure) pathological processes. In general, fatty acids whose chemical structure has an odd number of carbon atoms have not been considered of therapeutic relevance, since, in humans and, in general, in mammals, the vast majority of fatty acids present are even chain, normally between 14 and 24 carbon atoms, the presence of odd chain fatty acids being very uncommon, limited to traces. Currently, the data available in the scientific literature indicate that small structural differences in fatty acids have significant effects on biological activity and, therefore, on therapeutic activity. It is well known that many drugs produce known adverse effects or are toxic to various cells or tissues. Prodrugs are compounds that, when ingested, undergo metabolic reactions and give rise to a drug or medication—their metabolite—which produces an effect on the health of a patient or subject. Thus, on the one hand, administering a therapeutically active compound as a prodrug allows for modulating its distribution and absorption over time, since its metabolism generates the drug—that is, the metabolite—only in those cells or tissues where the metabolic reactions that transform the prodrug into its active metabolite occur. In this sense, these prodrugs offer other advantages, such as allowing for delayed or controlled administration of the active metabolite, preventing its accumulation, which could produce harmful effects on the body. On the other hand, the identification and synthesis of these therapeutically active metabolites allow for a more potent effect, enabling the administration of higher therapeutically active doses over controlled periods than would be achieved through the spontaneous metabolism of the corresponding prodrug.Therefore, it is an objective of the present invention to provide therapeutically active compounds (metabolites) derived from other compounds or prodrugs, such that the administration of said metabolites, alone, through their prodrugs, or in combination with their respective prodrugs, allows modulation of the therapeutic effect and possible adverse side effects, depending on the patient's condition and the pathological condition to be treated. BRIEF DESCRIPTION OF THE INVENTION A compound selected from the group consisting of: a compound of formula (II), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)t,-(CH2)c-CH3 (II) and a compound of formula (III), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)íW(CH2)c-CH3(III) where a is an integer between 1 and 14; b is an integer between 1 and 7; cesO, 3o6ym=0; and where a+3b+c+3 is an even integer. More particularly, the present invention relates to a compound selected from the group consisting of: a compound of formula (II), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(II) where: a=6, b=1 and c=6; oa=6, b=2 and c=3; oa=6, b=3 and c=0; oa=3, b=3 and c=3; oa=2, b=4 and c=3; oa=2, b=5 and c=0; and a compound of formula (III), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)w(CH2)c-CH3 (III) where a=1, b=6, c=0 and m= 0. The present invention also relates to a compound selected from the group consisting of a compound of formula (II) and a compound of formula (III), as described herein, for use as a medicament and, in particular, for use in the induction of neuroregeneration and in the prevention and / or treatment (including maintenance treatment) of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. The present invention also relates to a pharmaceutical or nutraceutical composition comprising at least a first compound selected from the group consisting of a compound of formula (II) and a compound of formula (III) and, optionally, a compound of formula (I), as described in the present invention. Finally, the present invention relates to an in vitro method for determining the efficacy of a therapeutic or preventive treatment for a disease or pathology with a compound of formula (I), or with a pharmaceutically acceptable salt or ester thereof, in a subject, wherein said method comprises determining in vitro in a biological sample from said subject, the amount of a compound of formula (II) or formula (III), as described in the present invention, or of its carboxylate anion, or of a derivative formed therefrom in vivo or in vitro, wherein said amount is related to the efficacy of the treatment for said disease or pathology DESCRIPTION OF THE INVENTION The present invention relates to a compound selected from the group consisting of: a compound of formula (II), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) and a compound of formula (III), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH -(CH2)3-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fW.mr(CH2)c-CH3(III) where a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and wherein a+3b+c+3 is an even integer. All values ​​of a, b, c, and m in the present invention are integers greater than or equal to zero. Once the value of b is defined in a formula, the value of m is defined as an integer between 0 and b, where said value of b is the one already defined between 0 and b-1. For the purposes of the present invention, when a specific formula or composition is not indicated, the values ​​of a, b, c, and m are applicable to all formulas and compositions described herein. In one embodiment of the invention, a is an integer between 1 and 7; b is an integer between 2 and 7; c is 0, 3, or 6; m is 0; and a + 3b + c + 3 is an even integer. In another embodiment of the invention, a is an integer between 1 and 14; b is 1; c is 0, 3, or 6; m is 0; and a + 3b + c + 3 is an even integer. Preferably, for all embodiments of the present invention m=0 and, therefore, the present invention relates to a compound selected from the group consisting of: a compound of formula (II), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(II) and a compound of formula (III), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-(CH2)a+r(CH=CH-CH2W(CH2)c^ (III); where a is an integer between 1 and 14; b is an integer between 1 and 7; c is 0, 3 or 6; and where a+3b+c+3 is an even integer. cenAnn / zznz / E / YiAi A preferred embodiment of the invention relates to a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (II) or formula (III). More preferably, said salt is a sodium salt, and said ester is a methyl or ethyl ester. The compounds of formula (II) or formula (III) of the present invention correspond to the formulas of the metabolites of a compound of formula (I), or of a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(I) where a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b - 1); and where a+3b+c+3 is an even integer. Compounds of formula (I) are therefore mono- or polyunsaturated alpha-hydroxylated fatty acids with an even number of carbon atoms (a+3fi+c+3 is an even integer). On the one hand, 2-hydroxymonounsaturated fatty acids of formula (I), with an even chain, are prodrugs of other monounsaturated fatty acids of formula (II), with an odd chain, when these prodrugs undergo a decarboxylation process. On the other hand, 2-hydroxypolyunsaturated fatty acids of formula (I), with an even chain, are prodrugs of other mono- or polyunsaturated fatty acids, with an odd chain. If decarboxylation occurs but hydrogenation of one of the double bonds of the compound of formula (I) does not take place, the compound derived from the prodrug of formula (I) will be a compound of formula (II). However, if hydrogenation of one of the double bonds and decarboxylation of the compound of formula (I) occur, the compound derived from the prodrug of formula (I) will be a compound of formula (III), in which the hydrogenated double bond can be in a different position depending on the value of m. For illustrative purposes, Figure 1A and Figure 8F show a schematic of the α-oxidation metabolism of 2-hydroxydocosahexaenoic acid (DHA-H), a compound of formula (I), at the cellular level, yielding (6Z,9Z,12Z,15Z,18Z)-heneicosa-6,9,12,15,18-pentaenoic acid (HPA), its metabolite of formula (III). According to this pathway, the prodrug DHA-H is a 2-hydroxylated polyunsaturated fatty acid, which is converted to HPA through a sequence of metabolic steps: (1) activation of DHA-H by conjugation with coenzyme A; (2) cleavage mediated by 2-hydroxyacyl-CoA lyase, yielding an aldehyde with an odd number of carbon atoms; (3) action of aldehyde dehydrogenase on the aldehyde, hydrogenating one of the double bonds, to transform it into an acid (HPA). Thus, HPA, according to the invention, is a compound of formula (III), wherein m=0, if HPA is the metabolite of a prodrug of formula (I) wherein a=1, b=6, c=0, which is a polyunsaturated omega-3 alpha-hydroxylated fatty acid with 22 carbon atoms and 6 conjugated double bonds (DHA-H). However, HPA can be a compound of formula (II) when HPA is the metabolite of a prodrug of formula (I), wherein a=4, b=5, and c=0, which is a polyunsaturated omega-3 alpha-hydroxylated fatty acid with 22 carbon atoms and 5 double bonds (2-hydroxydocosapentaenoic acid). One embodiment of the present invention relates to a compound of formula (III), wherein a=1, b=6, c=0, and m=0. cenAnn / zznz / E / YiAi Additionally, Figure 8A-8F shows the metabolism schemes for other fatty acids of formula (I). Specifically, Figure 8A shows the metabolism scheme of 2-hydroxylinoleic acid (LA-H), a compound of formula (I) in which a=6, b=2 and c=3, to produce, after decarboxylation, (8Z,11Z)-heptadeca-8,11-dienoic acid (HDA, C17:2 ω-6), which is a compound of formula (II) in which a=6, b=2 and c=3. Figure 8B shows the scheme of the metabolism of 2-hydroxy-alpha (a)-linolenic acid (ALA-H), which is a compound of formula (I) in which a=6, b=3 and c=0, to produce, after undergoing decarboxylation, (8Z,11Z,14Z)-heptadeca-8,11,14-trienoic acid (HTA ω-3, C17:3 ω-3), which is a compound of formula (II) in which a=6, b=3 and c=0.On the other hand, Figure 8C shows the scheme of the metabolism of 2-hydroxy-gamma (y)-linolenic acid (GLA-H), which is a compound of formula (I) in which a=3, b=3 and c=3, to produce, after undergoing decarboxylation, the (5Z,8Z,11Z)-heptadeca-5,8,11-trienoic acid (HTAω-6, C17:3 ω6), which is a compound of formula (II) in which a-3, b-3 and c=3. Figure 8D shows the scheme of the metabolism of 2-hydroxyarachidonic acid (ARA-H), which is a compound of formula (I) in which a-2, ύ=4 and c=3, to produce, after undergoing decarboxylation, (4Z,7Z,10Z, 13Z)-nonadeca-4,7,10,13-tetraenoic acid (NTA, C:19:4 ω-6), which is a compound of formula (II) in which a=2, b=4 and c=3.Finally, Figure 8E shows the scheme of the metabolism of 2-hydroxy-eicosapentaenoic acid (EPA-H), which is a compound of formula (I) in which a=2, b=5 and c=0, to produce, after undergoing decarboxylation, (4Z,7Z,10Z,13Z,16Z)-nonadeca-4,7,10,13,16-pentaenoic acid (NPA, C19:5 ω-3), which is a compound of formula (II) in which a-2, b=5 and c=0. On the other hand, according to the metabolic scheme in Figure 11, compounds of formula (I) can also be monounsaturated alpha-hydroxylated fatty acids with an even number of carbon atoms. According to this pathway, the prodrug sodium salt of 2-hydroxyoleic acid (2OHOA) is a 2-hydroxylated monounsaturated fatty acid, which is converted to 8Z-heptadecenoic acid (8Z-heptadecenoic or C17:1n-9) through a sequence of metabolic steps: (1) activation by an acyl-CoA ligase, in a process dependent on ATP (adenosine triphosphate) and magnesium (Mg2+); (2) 2OHOA-CoA would be subject to the activity of 2-hydroxyphytanoyl-CoA lyase (2-hydroxyacyl-CoA lyase 1, HACL1), forming an intermediate monounsaturated aldehyde; (3) The aldehyde dehydrogenase enzyme would be responsible for the conversion of said intermediate aldehyde into 8Z-heptadecenoic acid in an NAD+ (Nicotinamide Adenine Dinucleotide) dependent process.Therefore, 8Z-heptadecenoic acid, according to the invention, is a compound of formula (II), wherein a=6, b=1 and c=6, which is a monounsaturated omega-9 alpha-hydroxylated fatty acid of 17 carbon atoms, resulting from the metabolism of 2-hydroxyoleic acid, or a pharmaceutically acceptable salt or ester thereof, which is a prodrug of formula (I). While the medical uses of compounds of formula (I) are known, the present invention describes the formula of their metabolites, compounds of formula (II) or formula (III), which provide a specific and differentiated therapeutic action in the body after the metabolism of said compounds of formula (I), thus acting as prodrugs of these compounds. In this way, the present invention provides a means of tailoring a therapeutic treatment depending on the nature of the disease and the prognosis of the patient being treated. Specifically, the present invention reveals specific formulations of mono- or polyunsaturated alpha-hydroxylated fatty acid metabolites that are therapeutically effective. Thus, the present invention further describes the uses as a medicament of said metabolites of formula (II) or formula (III), either alone, allowing control of the administered amount; or their use as a medicament in combination with their prodrug of formula (I); or their use as a medicament by administering said prodrug of formula (I), allowing regulation of the intensity and dose administered over time during treatment.Furthermore, administering compounds of formula (II) or formula (III) via their prodrug of formula (I) allows for modulation of drug distribution and absorption. This is because the prodrug's metabolism enables the generation of the corresponding drug only in those cells or tissues where the metabolic reactions that transform the prodrug occur, resulting in the active compound in those cells. In any case, this document refers to both compounds of formula (II) and compounds of formula (III), whether obtained through chemical synthesis (see example 1) or during the metabolism of compounds of formula (I). In this respect, for the purposes of the present invention, the term “metabolites” is used to designate said compounds of formula (II) or formula (III), whether their origin is the metabolism of a compound of formula (I) in the organism of a subject, or whether said compounds of formula (II) or formula (III) are synthetically obtained products.Therefore, for the purposes of the present invention, the term compound of formula (I) is used interchangeably with the term "prodrug of formula (I)" and, likewise, the terms "compound of formula (II)" and "compound of formula (III)" are used interchangeably, respectively, with the terms "metabolite of formula (II)" and "metabolite of formula (III)", because, these compounds of formula (II) and formula (III), whether obtained by chemical synthesis or resulting from the natural metabolism of a compound of formula (I), have the chemical structure or chemical formula of a metabolite of the compound of formula (I) that consequently acts as a prodrug of these. To illustrate the invention, the examples of the present invention show how the therapeutic effect exerted by the prodrugs of formula (I) is directly related to the therapeutic effect exerted by the metabolite of formula (II) or formula (III) in the body, and also show the therapeutic effect exerted per se by the compounds of formula (II) and formula (III). Thus, as shown in example 7.3, the administration of the sodium salt of 2-hydroxyoleic acid (OHOA), compound of formula (I), produced a greater reduction in the size of xenoblastic tumors in mice as the cellular accumulation of the C17:1 n-9 metabolite of formula (II) increased. Therefore, the therapeutic action of the sodium salt of 2-OHOA is related, in part, to its conversion into the C17:1 n-9 metabolite. On the other hand, example 6.Paragraph 2 of the present invention shows that the formation of the C17:1 n-9 metabolite (8Z-heptadecenoic acid), from the incorporation of 2OHOA, differs between tumor and non-tumor cells. Glioma cells showed a significant increase in their C17:1 n-9 levels compared to 2OHOA (Figures 13B and 13D), while in non-tumor cells, the detected levels of 2OHOA were significantly higher than those of its C17:1 n-9 metabolite. Furthermore, the examples and figures show that the anti-proliferative effect mediated by the compounds of formula (I), exemplified by DHA-H, is mediated, at least in part, by its metabolite HPA (compound of formula (III)), since the inhibition of the formation of this compound from DHA-H results in a reduced anti-proliferative effect of DHA-H (Figure 4B).These results show that the therapeutic value of compounds of formula (I) is partly linked to the biological activity of their metabolite of formula (II) or formula (III), with said compound of formula (I) acting as a true prodrug of the compound of formula (II). On the other hand, the administration of a compound of formula (II) or formula (III), such as HPA, under the same experimental conditions as the administration of a compound of formula (I), such as DHA-H, results in HPA levels an order of magnitude higher than those produced by DHA-H, implying that the therapeutic activity of HPA could be superior to that of DHA-H. This effect is due to the structural differences between the prodrug of formula (I) (DHA-H) and its metabolite of formula (III) (HPA). In fact, in the present invention, it is demonstrated that the uptake of the alpha-hydroxylated form of DHA (DHA-H) is inhibited compared to that of the non-hydroxylated analogue (Figure 5C).If DHA-H uptake is impaired compared to non-hydroxylated fatty acids, then the different intracellular HPA levels observed after DHA-H and HPA administration must be due to the different uptake of these compounds by cells from the extracellular environment. Furthermore, as shown in Example 6.3, the IC50 values ​​of the C17:1 n-9 metabolite were lower than those of its prodrug 2OHOA, confirming its greater antiproliferative potency. Additionally, as shown in Figure 3B, HPA levels in a tumor are inversely correlated with tumor size in xenographic models. Therefore, the therapeutic action of the prodrug (I) is enhanced by the greater presence of the metabolite. On the other hand, as shown in Figure 5A-5C, treatment with HPA sodium (a metabolite obtained by chemical synthesis, as described in Example 1) induces a much greater degree of mortality in the culture than treatment with DHA-H sodium (a prodrug) or DHA sodium (a natural analogue) under the same conditions. Therefore, administering the metabolite provides a more pronounced therapeutic effect than that obtained by administering the prodrug. However, as shown in Example 6.3, C17:1 n-9 had an antiproliferative effect when administered directly instead of its prodrug, in both tumor and non-tumor cells. Therefore, administering this metabolite of formula (II), C17:1 n-9, via its prodrug of formula (I), 2OHOA, provides a selective way to produce a therapeutic effect, allowing for longer administration of this therapy without undesirable adverse effects and proving equally useful in maintenance therapy. Specifically, odd-chain fatty acids are metabolized by β-oxidation, yielding propionyl-CoA. Unlike even-chain fatty acids, whose metabolism ends in the production of acetyl-CoA, which, in turn, is metabolized via the Krebs cycle. Propionyl-CoA can be transformed into propionic acid, which, as an adverse effect, causes metabolic acidosis if it accumulates.Propionyl-CoA can be metabolically transformed into succinyl-CoA (which is metabolized via the Krebs cycle) in a process dependent on biotin and vitamin B12. This process is not a typical metabolic pathway for fatty acids because, in mammals, the vast majority of fatty acids are even-chain. Consequently, this metabolic pathway selectively affects odd-chain polyunsaturated fatty acids, such as the metabolites of formula (II) and formula (III), and can become saturated if there are excessively high intracellular concentrations of these odd-chain metabolites or in specific pathological conditions involving biotin or vitamin B12 deficiency, leading to the adverse effect of propionic acidosis. Thus, the metabolite administered directly to cells possesses a toxicity that is undesirable in some cases. This toxicity is modulated when the prodrug or compound of formula (I) is administered, regulating the effect and toxicity of the metabolite of formula (II) or (III). In this regard, the slower uptake of the prodrug compared to non-hydroxylated fatty acids could be useful in preventing excessively high intracellular concentrations of the metabolite and, consequently, a possible accumulation of propionic acid.Thus, depending on the metabolic condition, the administration regimen and the pathology to be treated, and in particular in those cases where a more intense therapeutic action is desired, or in treatments of reduced duration, it may be convenient to use a metabolite of formula (II) or formula (III), or a pharmaceutically acceptable salt or ester thereof; whereas in other cases, such as in treatments prolonged over time, or maintenance treatments, it may be convenient to administer controlled over time, by using the prodrug of formula (I), or a pharmaceutically acceptable salt or ester thereof, such as the sodium salt of DHA-H.Thus, the administration of the metabolites of formula (II) or formula (III) by using the compounds of formula (I), with an even chain, as prodrugs, allows a time-regulated administration of their metabolites of formula (II) or formula (III), which have an odd chain. Therefore, the present invention demonstrates how the administration of compounds of formula (II) or formula (III) by means of the administration of their prodrugs of formula (I), allows a time-regulated administration of their odd-chain metabolites. Therefore, the present invention allows the therapy to be adapted, depending on the nature of the disease and the prognosis of the patient being treated, to use the metabolite, or the compound of formula (I), i.e., the prodrug, as a medicinal product. On the one hand, in cases where short-term acute therapeutic activity is required, the use of the metabolite would be more appropriate or prioritized to obtain a rapid and significant effect. On the other hand, when long-term treatment is required, in chronic diseases, for example, or if maintenance treatment is required, the use of the prodrug, or of compositions that combine different ratios of prodrug and metabolite, may be recommended or prioritized, depending on the timing and severity of the disease. Therefore, in general, the use of the compounds of formula (II) and (III), and their pharmaceutically or nutraceutically acceptable salts, is beneficial to the body, as shown in the examples in this application. The action of these compounds of formula (II) and (III), through the administration of their corresponding prodrug of formula (I), allows for the avoidance of adverse effects resulting from their metabolism and accumulation when prolonged administration or high doses are required, by administering said compounds of formula (II) and (III) in a controlled manner, as a result of their metabolism.In this way, prodrugs with formula (I) provide a means of administering metabolites of formula (II) or formula (III) with a lower risk of adverse side effects and while delivering a therapeutically effective amount of these metabolites over time, as the prodrug with formula (I), once administered, is metabolized. Thus, depending on the metabolic condition, the administration regimen, and the pathology being treated, it may be appropriate to use a compound of formula (II) or formula (III) directly, or a pharmaceutically acceptable salt or ester thereof (metabolites), or it may be appropriate to administer it over time using the prodrug of formula (I), or a pharmaceutically acceptable salt or ester thereof (prodrug), or a combination thereof (prodrug + metabolites). Thus, one aspect of the invention relates to a compound selected from the group consisting of a compound of formula (II), or a pharmaceutically acceptable salt or ester thereof: COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) and a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof: COOH -(CH2)3-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)(M.mr(CH2)c-CH3(III); wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b - 1); and wherein a + 3b + c + 3 is an even integer, for use as a medicament, and in particular for use in the induction of neuroregeneration and in the prevention and / or treatment (including maintenance treatment) of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. For the purposes of the present invention, the term “maintenance treatment” or “maintenance therapy” is defined as a therapeutic treatment administered as a complement to a primary or main treatment or therapy, with the purpose of either preventing or delaying the recurrence of the disease, which has completely or partially remitted after treatment with a primary treatment or therapy, or to slow the development of a disease after the end of treatment with a primary therapy. Preferably, the present invention relates to a compound of formula (II) or a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof, for use in a treatment or maintenance therapy for a disease or pathology, and more preferably in a treatment or maintenance therapy for cancer. One embodiment of the invention relates, therefore, to the use of a compound selected from the group consisting of a compound of formula (II), or a pharmaceutically acceptable salt or ester thereof, and a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof, as described in the present invention, in the preparation of a medicament for the induction of neuroregeneration or for the prevention and / or treatment (including maintenance treatment) of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. Another embodiment of the present invention relates to a method of preventing and / or treating a disease or pathology, or to a method of inducing neuroregeneration; in a patient, wherein said method comprises administering to said patient an effective amount of a compound selected from the group consisting of a compound of formula (II), or a pharmaceutically acceptable salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(II) and a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof: COOH -(CH2)a-(CH=CH-CH2)„r(CH2)3-(^ (III); where a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b - 1); and where a+3b+c+3 is an even integer. For the purposes of the present invention, the effective quantity, or the therapeutically effective quantity, is understood to be that which provides a therapeutic effect without producing unacceptable toxic effects in the patient. The effective quantity or dose of the drug depends on the compound and the pathology or disease being treated, and on, for example, the age, weight, and clinical condition of the patient, the route of administration, the patient's medical history, the severity of the disease, and the potency of the administered compound. Additionally, one embodiment of the invention relates to a compound selected from the group consisting of a compound of formula (II): COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) and a compound of formula (III): COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fM.mr(CH2)c-CH3 (III); for use in the prevention and / or treatment of a disease or pathology or in the induction of neuroregeneration, wherein the prevention and / or treatment or the induction of neuroregeneration is characterized by the administration of a compound or prodrug of formula (I), or a pharmaceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) and wherein said compound of formula (I) is metabolized to produce a therapeutically effective amount of: a compound of formula (II): COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) or of a compound of formula (III): COOH -(CH2)a-(CH=CH-CH2)nr(CH2)3-(CH=CH-CH2)(W(CH2)c-CH3(III); and where a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; cenAnn / zznz / E / YiAi m is an integer between 0 and (b -1); and in which a+3b+c+3 is an even integer. Preferably, the disease is selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a skin and subcutaneous tissue pathology; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. Therefore, another aspect of the present invention relates to a method for administering an effective amount of a compound of formula (II), or of a compound of formula (III), as described in the present invention, for the prevention and / or treatment of a disease or pathology, or for the induction of neuroregeneration and / or the prevention of neurodegeneration, wherein said compound of formula (II) or said compound of formula (III), is administered as a prodrug of formula (I), or as a pharmaceutically acceptable salt or ester thereof, as described in the present invention. The invention further relates to a method for the prevention and / or treatment of a disease or pathology; wherein said method comprises administering an effective amount of a prodrug of a compound of formula (II), or of a pharmaceutically acceptable salt or ester thereof; or of a prodrug of a compound of formula (III), or of a pharmaceutically acceptable salt or ester thereof, as described in the present invention; wherein said prodrug of the compounds of formula (II) or of formula (III) has formula (I), or a pharmaceutically acceptable salt or ester thereof, as described in the present invention. Additionally, the present invention relates to a method for the prevention and / or treatment of a disease or pathology, or for the induction of neuroregeneration and / or the prevention of neurodegeneration, wherein said method comprises administering to a patient in need an effective amount of a compound of formula (I), or a pharmaceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(I) wherein the compound of formula (I) is metabolized in the body of said patient to produce a therapeutically effective amount of a metabolite: which has a formula (II): COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) or which has formula (III): COOH -(CH2)3-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fM.mr(CH2)c-CH3 (III); where a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b - 1); and a + 3b + c + 3 is an even integer, wherein said metabolite is responsible for the prevention and / or treatment of said disease or pathology and for the induction of neuroregeneration and / or the prevention of neurodegeneration in the patient. Preferably, when an effective amount of a compound of formula (I) is administered, the metabolite having formula (II), or having formula (III), is present in the body of said patient. In a preferred embodiment, said compound of formula (I) is metabolized to more than 1%, 10%, more than 40%, more than 50%, and up to 99% into a metabolite of formula (II) or formula (III) upon administration. Another embodiment relates to a method for the prevention and / or treatment of a selected disease or pathology from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a skin and subcutaneous tissue pathology; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease, and for the induction of neuroregeneration and / or the prevention of neurodegeneration; wherein said method comprises administering to a patient an effective amount of a prodrug having the structure of formula (I), or a pharmaceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH^^ (I) wherein said prodrug is converted in vivo to release an active compound in cells of said patient; wherein said active compound has a structure: of formula (II): COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(II) or formula (III): COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fb.M-(CH2)c-CH3(III) where a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and a+3b+c+3 is an even integer. Preferably, this conversion is a chemical or physiological process. For the purposes of the present invention, the term “chemical process” refers to the in vivo conversion of the prodrug to release the active compound through a chemical reaction, wherein the prodrug is a reactant or substrate of the chemical reaction, and the active compound is a reaction product. Furthermore, for the purposes of the present invention, the term “physiological process” refers to a conversion due to an event or process that occurs naturally in an organism, for example, due to enzyme activity. Moreover, although the compounds of formula (I) act therapeutically through their metabolites of formula (II) or formula (III), these compounds of formula (I) also exhibit biological activity independent of this metabolic pathway, as shown in Example 6.4 of the present invention. Thus, another embodiment of the invention relates to a compound selected from the group consisting of a compound of formula (II) and a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof, as described in the present invention, for use as a medicament and, in particular, for use in the induction of neuroregeneration and / or the prevention of neurodegeneration and / or for use in the prevention and / or treatment of a disease or pathology, according to the present invention, characterized in that said compound is administered before, after, or in conjunction with a compound of formula (I), or with a pharmaceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14 and a+3b+c+3 is an even integer; and wherein said values ​​of a, b and c are equal to or different from the values ​​of a, b and c of the compound of formula (II) or of the compound of formula (III). Additionally, the present invention relates to a method for inducing neuroregeneration and / or preventing neurodegeneration, or to a method for preventing and / or treating a disease or pathology, comprising administering an effective amount of a compound of formula (II), or a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof, to a patient, and wherein said method is characterized in that it comprises the additional administration of a compound of formula (I), or a pharmaceutically acceptable salt or ester thereof, as described in the present invention; and wherein said compound of formula (I) is administered before, after, or in conjunction with said compound of formula (II) or formula (III). For the purposes of the present invention, the term “prodrug” refers to a compound that, when administered to a subject, is transformed, through a metabolic process, into a second therapeutically active compound. On the other hand, the term “subject” refers, for the purposes of the present invention, to a human or an animal. The term “pharmaceutically acceptable” refers, for the purposes of the present invention, to a compound or substance authorized or authorizable by a regulatory agency of the federal or state government or listed in the European, American, or other generally recognized pharmacopoeia for use in animals or humans. Throughout this specification, this term applies primarily to the salts and esters of the compounds of formulas (I), (II), and (III), which are defined in accordance with this description. Thus, the term “pharmaceutically acceptable salt” refers to a salt of a compound that also possesses the desired pharmacological activity of the parent compound from which it is derived. Preferably, the pharmaceutically acceptable salt is the sodium salt. For the purposes of the present invention, the term “ester” refers to any compound in which the hydroxyl group belonging to a carboxylic acid moiety has been replaced by an alkoxide group. In a preferred embodiment of the invention, the ester is a methyl or ethyl ester. More preferably, the ester is an ethyl ester. The term “nutraceutically acceptable” refers, for the purposes of the present invention, to anything used in nutraceutical products. Thus, for the purposes of the present invention, the term “nutraceutical” or “nutraceutical composition” refers to a dietary supplement, to be taken alone or in combination with other foods, that produces a beneficial effect on the health of the person ingesting it, especially in the prevention of disease. Throughout this specification, this term applies primarily to the salts and esters of the compounds of formulas (I), (II), and (III), which are defined in accordance with this description. For the purposes of the present invention, the term “stereoisomer” refers to compounds that have the same chemical formula and the same sequence of atoms, but have a different three-dimensional orientation in space, and includes the R and S stereoisomers (also using the (+) and (-) nomenclature) resulting from the presence of a chiral carbon, as well as the E and Z stereoisomers (also using the cis / trans nomenclature) resulting from the arrangement of the substituents on the carbons that form a double bond. Thus, since prodrugs of formula (I) comprise a chiral carbon (the alpha carbon to the carboxylic group), the invention also includes the two R and S stereoisomers, as well as any mixture of both, with respect to the configuration of said chiral carbon.On the other hand, since both the prodrugs of formula (I) and their metabolites of formula (II) or (III) comprise C=C double bonds, the invention also includes all the E and Z stereoisomers for each of their double bonds. In a preferred embodiment, all the double bonds of the prodrug of formula (I), the compound of formula (II), and the compound of formula (III) have an all-cis configuration. Thus, if the prodrug of formula (I) has a specific cis / trans (or E / Z) stereochemical configuration of its double bonds, the metabolite of formula (II) or formula (III) will also have that configuration for the double bonds it contains. For the purposes of the present invention, the term “comprises” indicates that it includes a group of certain features (for example, a group of features A, B, and C). It is interpreted to mean that it includes those features (A, B, and C) but does not exclude the presence of other features (for example, features D or E), provided they do not render the claim impracticable. Additionally, the terms “contains,” “includes,” “has,” or “encompasses,” and their plural forms, are to be taken as synonymous with the term “comprises” for the purposes of the present invention. On the other hand, if the expression “consists of” is used, then no additional features are present in the apparatus / method / product other than those following that expression. In this sense, for the purposes of the present invention, the term “comprises” may be replaced by either the terms “consists of” or “consists essentially of.”Accordingly, “comprises” may refer to a group of features A, B and C, which may additionally include other features, such as E and D, on the condition that such features do not render the claim impracticable, but the term “comprises” also includes the situation in which the group of features “consists of” or “consists essentially” of A, B and C. Furthermore, the present invention supports the administration of a compound of formula (I), in particular 2OHOA, or a pharmaceutically acceptable salt or ester thereof, more preferably the sodium salt of 2OHOA, in a maintenance treatment (maintenance therapy), wherein said compound of formula (I), or a pharmaceutically acceptable salt or ester thereof, is administered at different intervals over a period of time, the cumulative concentration of its metabolite of formula (II), or of formula (III), being a measure of the efficacy of the treatment. Therefore, said in vitro method for determining the efficacy of a treatment with a compound of formula cenAnn / zznz / E / YiAi (I), or with a pharmaceutically acceptable salt or ester thereof, comprises determining the amount of a compound of formula (II), or of formula (III), or of its carboxylate anion, or of a derivative formed therefrom. In this sense, for the purposes of the present invention, the term “biomarker” refers to a first compound or substance, or a derivative of that first compound or substance, that can be used to determine the response and / or efficacy of a treatment with a second compound or substance. Thus, for the purposes of the present invention, metabolites of formula (II) or formula (III) can be used as biomarkers for determining the response and / or efficacy of a treatment with a compound of formula (I). Therefore, another aspect of the invention relates to an in vitro method for determining the efficacy of a therapeutic or preventive treatment for a disease or pathology, or of a neuroregeneration induction treatment, with a compound of formula (I), or with a pharmaceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(C^ (I) in a subject, wherein said method comprises determining in vitro in a biological sample of said subject, the amount of a compound: of formula (II): COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) or formula (III): COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fM.mr(CH2)c-CH3 (III) or of its carboxylate anion, or of a derivative formed from the same in vivo or in vitro, wherein said amount is related to the efficacy of the treatment; and wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and wherein a+3b+c+3 is an even integer. Therefore, this method comprises determining the amount of a compound of formula (II), or of formula (III), of its respective carboxylate anions, or of a derivative formed from it. Said derivative of the compound of formula (II) or (III) can be formed in vitro by reacting said compound of formula (II) or (III), present in the in vitro sample, with a substance to obtain a derivative thereof. In this case, the method of the invention comprises determining the amount of said derivative of formula (II) or formula (III) formed in vitro. For example, some techniques for the detection of fatty acids require their prior chemical modification, and thus, it is common for detection by gas chromatography to require that the fatty acid sample (in this case a compound of formula (II) or formula (III)) be transformed into its respective methyl ester for detection and quantification. crnRnn / zznz / B / YiAi On the other hand, said derivative of the compound of formula (II), or of formula (III), may be a metabolic derivative or a derivative formed in vivo (result of a reaction occurring in vivo), formed as a result of the reaction of said compound of formula (II), or of formula (III), with another lipid, protein, enzyme, nucleotide, carbohydrate, etc. Thus, said derivative may be an ester of said compound of formula (II), or of formula (III), such as, for example, a glycerophospholipid (such as phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol, phosphatidylglycerol, phosphatidic acid or any of its lyso forms, such as lysophosphatidylcholine, lysophosphatidylethanolamine, etc.), a plasmalogen (alkyl or alkenyl), a cholesterol ester, a glycerolipid such as triacylglycerol (triglyceride) or diacylglycerol, a cardiolipin, a sphingolipid, a thioester with coenzyme A (acyl-CoA), or an acylcarnitine, among others.In this case, the method of the invention comprises determining in vitro the amount of said metabolic derivative (or derivative formed in vivo) in the biological sample. Thus, the amount of said compound of formula (II), or of formula (III), or of their respective carboxylate anions, or of a derivative formed from them in vivo or in vitro, is related to the efficacy in the treatment and / or prevention of a disease or pathology, or to a neuroregeneration induction treatment, in a subject with the compound of formula (I), wherein the levels of said compound of formula (II), or of formula (III), or of its carboxylate anion, or of its derivative, compared to a control group, are related to the efficacy in the therapeutic or preventive treatment of a disease or pathology, with said compound of formula (I), or with a pharmaceutically acceptable salt, or ester thereof, Another aspect of the invention relates to the use of a compound: of formula (II): COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) or formula (III): COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fft.M-(CH2)c-CH3 (III) or of its respective carboxylate anion, or of a derivative formed from the same in vivo or in vitro, to determine in vitro the efficacy of a therapeutic or preventive treatment of a disease or pathology, or of a neuroregeneration induction treatment, with a compound of formula (I), or with a pharmaceutically acceptable salt, or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) in a subject, wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and wherein a+3b+c+3 is an even integer. More preferably, the disease or pathology is selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; cenRnn / zznz / E / YiAi a skin and subcutaneous tissue pathology; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. Even more preferably, the disease or pathology is selected from among a neurological or neurodegenerative disease; a cancer; an inflammatory disease; and a metabolic disease. In a more preferred embodiment, the method determines the efficacy of a treatment with a pharmaceutically acceptable salt of the compound of formula (I) and even more preferably with the sodium salt of the compound of formula (I). In one embodiment of the invention, the biological sample is a blood sample (including plasma or serum), a urine sample, a saliva sample, a tissue biopsy, cerebrospinal fluid, or a sweat sample. The present invention also relates to a pharmaceutical composition comprising at least a first compound selected from the group consisting of: a compound of formula (II), or a pharmaceutically acceptable salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) and a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof: COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)(W(CH2)c-CH3(III) wherein said composition optionally comprises a second compound of formula (I), or a pharmaceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) and wherein a is an integer between 1 and 14; or is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and a+3b+c+3 is an even integer; and at least one pharmaceutically acceptable excipient. The present invention also relates to a pharmaceutical composition comprising at least a first compound selected from the group consisting of: a pharmaceutically acceptable salt or ester of a compound of formula (II): COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(II) and a pharmaceutically acceptable salt or ester of a compound of formula (III): COOH -(CH2)3-(CH=CH-CH2)m-(CH2)3-(CH <H-CH2)^mH^ (III) en donde dicha composición comprende, opcionalmente, una sal o un éster farmacéuticamente aceptables de un compuesto de fórmula (I): COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(I) and wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and a+3b+c+3 is an even integer; and at least one pharmaceutically acceptable excipient. Another embodiment of the invention relates to a pharmaceutical composition comprising at least a first compound selected from the group consisting of a compound of formula (II) and a compound of formula (III), wherein said composition optionally comprises a pharmaceutically acceptable salt or ester of a compound of formula (I), as described above; and at least one pharmaceutically acceptable excipient; for use as a medicament; and in particular, for use in the induction of neuroregeneration and / or the prevention of neurodegeneration, and for use in the prevention and / or treatment of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology;a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. In a preferred embodiment of the invention, said at least first compound is a pharmaceutically acceptable salt or ester of a compound of formula (II), or of a compound of formula (III), and / or said second compound is a pharmaceutically acceptable salt or ester of a compound of formula (I). One embodiment of the invention relates to the use of a pharmaceutical composition comprising at least a first compound selected from the group consisting of a compound of formula (II) and a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof, wherein said composition optionally comprises a compound of formula (I), or a pharmaceutically acceptable salt or ester thereof, as described above; and at least one pharmaceutically acceptable excipient; in the preparation of a medicament for the induction of neuroregeneration and / or the prevention of neurodegeneration, and / or for the prevention and / or treatment of a disease or pathology. Another embodiment of the invention relates to a method for the prevention and / or treatment of a disease or pathology, or for the induction of neuroregeneration and / or the prevention of neurodegeneration; wherein said method comprises administering, to a patient in need, an effective amount of a pharmaceutical composition comprising at least a first compound selected from the group consisting of a compound of formula (II) and a compound of formula (III), or a pharmaceutically acceptable salt or ester thereof, wherein said composition optionally comprises a compound of formula (I), or a pharmaceutically acceptable salt or ester thereof, as described above; and at least one pharmaceutically acceptable excipient. Preferably, the disease or pathology is selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. The expert in the field may select one or more pharmaceutically acceptable vehicles or excipients known in the state of the art, so that the pharmaceutical compositions are suitable for administration to both a human subject and an animal. In a preferred embodiment of the invention, said excipient is albumin, for example: ovalbumin, lactalbumin, native or recombinant albumin of human, bovine, murine, or rabbit origin, more preferably, human serum albumin or bovine serum albumin. The pharmaceutical compositions disclosed in the present invention can also be administered concurrently with, or after, additional therapy. Preferably, such additional therapy is radiotherapy, tumor treatment fields, immunotherapy, or chemotherapy. More preferably, the pharmaceutical compositions disclosed in the present invention can also be administered concurrently with, or after, therapy comprising the administration of temozolomide. This administration may be within the treatment of an adult or a pediatric patient. In a preferred embodiment, this pharmaceutical composition is administered concurrently with, before, or after radiotherapy, chemotherapy, tumor treatment fields, or immunotherapy. In one embodiment of the invention, the pharmaceutical compositions disclosed herein comprise at least one additional therapeutic component or active ingredient. This additional therapeutic component or active ingredient provides additive or synergistic biological activities. For the purposes of this description, the terms “active ingredient” and “therapeutic ingredient” are to be taken as synonymous and mean a chemical or biological entity that exerts therapeutic effects when administered to humans or animals. This additional active ingredient or therapeutic ingredient may be a cell therapy, a small molecule therapy, an immunotherapy, a radiotherapy, or other similar product. The therapeutic components or additional active compounds include compounds for the treatment of neurodegenerative diseases, anticancer agents, metabolism-regulating compounds, cardiovascular agents, and agents that regulate obesity and overweight. The therapeutic components or additional active compounds also include compounds for the treatment of neurodegenerative diseases, chemotherapeutic agents, metabolism regulators, cardiovascular agents, and agents for regulating obesity and overweight. Preferably, such an active compound or therapy is a chemotherapeutic agent, a cell therapy agent, or an immunotherapeutic agent. In a preferred embodiment, said pharmaceutical composition further comprises a chemotherapeutic agent selected from the group consisting of: platinum-based antineoplastic agents; antimitotic chemotherapeutic agents; a polyadenosine diphosphate ribose polymerase (PARP) inhibitor; type I topoisomerase inhibitors; crnRnn / zznz / B / YiAi type II topoisomerase inhibitors; epothilones; skeletal cyclodisruptors; alkylating agents; histone deacetylase inhibitors; kinase inhibitors; antifolates; peptide antibiotics; retinoids; vinca alkaloids and thymidylate synthase inhibitors.More preferably, the chemotherapeutic agent is selected from the group consisting of: bevacizumab, carmustine, cyclophosphamide, melphalan, ifosfamide, busulfan, temozolomide, mechlorethamine, chlorambucil, melphalan, dacarbazine, daunorubicin, doxorubicin, epirubicin, idarubicin, mitoxantrone, valrubicin, paclitaxel, docetaxel, abraxane, taxotere, epothilone, vorinostat, romidepsin, irinotecan, topotecan, camptothecin, exatecan, lurtotecan, etoposide, teniposide, tafluposide, bortezomib, erlotinib, gefitinib, imatinib, vemurafenib, vismodegib, azacitabine, azathioprine, capecitabine, cytarabine, cladribine, fludarabine, doxyfluridine, fluorouracil, gemcitabine, hydroxyurea, mercaptopurine, methotrexate, pemetrexed, azathioprene, thioguanine, retinoic acid, bleomycin, actinomycin, carboplatin, cisplatin, oxaliplatin, tretinoin, alitretinoin, bexarotene, topotecan, vinblastine, vincristine, vindesine, and vinorelbine.More preferably, the additional chemotherapeutic agent is temozolomide. In this regard, the fact that lipids, when integrated into the cell membrane, can control cell signaling implies that they can also regulate the physiological state of cells and, consequently, the overall state of health. Therefore, the compounds described herein are useful in inducing neuroregeneration and in the prevention and / or treatment of various diseases and pathologies, particularly those selected from the group consisting of a neurological or neurodegenerative disease; cancer; neoplasia; inflammatory disease; cardiovascular disease; skin and subcutaneous tissue pathology; metabolic pathology; neuropathic pain; paralysis; sleep disorders; digestive pathology; musculoskeletal and connective tissue disease; genitourinary pathology; and metabolic disease. For the purposes of the present invention, diseases of the nervous system are all those diseases that affect the nervous system (both central and peripheral). Within this group are neurodegenerative diseases, which, for the purposes of the present invention, are a heterogeneous group of disorders characterized by the progressive degeneration of the structure and function of the central or peripheral nervous system. Preferably, the neurodegenerative disease is selected from the group consisting of spinal cord injury and pain of neurological origin. For the purposes of the present invention, the term “induction of neuroregeneration” refers to the regeneration of neurological functions.On the other hand, for the purposes of the present invention, the term “prevention of neurodegeneration” indicates that the treatment produces the arrest of a neurodegenerative process already underway, or that the treatment prevents the onset or progression of neurodegeneration. Some of these neurodegenerative processes result in a significant decline in patients' cognitive abilities or motor impairments. Neurodegenerative processes, neurological disorders, and neuropsychiatric disorders share a common basis of neuronal degeneration or alterations in their components, such as lipids (e.g., myelin) or membrane proteins (e.g., adrenergic receptors, serotonergic receptors, etc.). In particular, neurodegenerative diseases are selected from the group consisting of: (i) inflammatory diseases of the central nervous system such as bacterial meningitis, non-bacterial meningitis, acute necrotizing hemorrhagic encephalopathy, other encephalitis, myelitis and encephalomyelitis, cerebral ventriculitis not otherwise specified (NEOM), intracranial and intraspinal abscess and granuloma, extradural and subdural abscess, phlebitis, intracranial and intraspinal thrombophlebitis and sequelae of inflammatory diseases of the central nervous system; (ii) systemic atrophies mainly affecting the central nervous system such as Guillain-Barré, diabetic neuropathy, Wallerian degeneration, Levy body dementia, frontotemporal dementia, Huntington's chorea, Huntington's dementia, hereditary ataxia; spinal muscular atrophy and related syndromes such as Werdnig-Hoffman;systemic atrophies mainly affecting the central nervous system, post-polio syndrome; motor neuron diseases such as amyotrophic lateral sclerosis and progressive bulbar palsy; (iii) extrapyramidal and movement disorders such as Parkinson's disease, secondary parkinsonism, neuroleptic malignant syndrome, drug-induced secondary parkinsonism, post-encephalitic parkinsonism, vascular parkinsonism, degenerative diseases of the basal ganglia, Hallervorden-Spatz, progressive supranuclear ophthalmoplegia, progressive supranuclear palsy, striatonigral degeneration, dystonia, essential tremor, drug-induced tremor, myclonia, drug-induced chorea, drug-induced tics, tics of organic origin, drug-induced movement disorders, akathisia, restless legs syndrome, stiff-person syndrome, and benign attacks of chills;(iv) other degenerative diseases of the nervous system such as Alzheimer's disease, early-onset or late-onset Alzheimer's disease, frontotemporal dementia such as Pick's disease, degeneration of the nervous system due to alcohol, Alpers disease, Leigh disease, Lewy body dementia, mild cognitive impairment, corticobasal degeneration, primary degenerative dementia including Alzheimer's dementia, senile and presenile forms, stroke; (v) demyelinating diseases of the central nervous system such as multiple sclerosis of the spinal cord, brainstem, disseminated, generalized or otherwise unspecified (NEOM); acute disseminated demyelinations, diffuse sclerosis of the central nervous system;(vi) episodic and paroxysmal disorders such as epilepsy and recurrent seizures, idiopathic epilepsy and seizures, grand mal seizures, unspecified atonic or clonic epilepsy, Lennox-Gastaut syndrome, epileptic spasms, unspecified type of epilepsy, migraine, headache, transient ischemic attacks and related syndromes, sleep disorders and vertigo; (vii) disorders of the nerves, nerve roots and nerve plexuses such as trigeminal nerve disorders, facial nerve disorders, cranial nerve disorders, nerve root and plexus disorders, mononeuropathies of the upper or lower extremity and Wallerian degeneration; (viii) polyneuropathies and other disorders of the peripheral nervous system including hereditary and idiopathic neuropathy such as Roussy-Levy syndrome, Refsum disease; inflammatory polyneuropathy;sequelae of polyneuropathy such as sequelae of Guillain-Barré syndrome, serum neuropathy; other polyneuropathies such as drug-induced, alcoholic, toxic, or radiation-induced neuropathy; sequelae of inflammatory and toxic polyneuropathies; (x) muscular and neuromuscular junction diseases such as myasthenia gravis and other myoneural disorders, disorders of muscle and neuromuscular junction; (x) cerebral palsy and other paralytic syndromes including hemiplegia, paraplegia, and tetraplegia; (x) other disorders of the nervous system such as complex regional pain syndrome, neuropathic pain, disorders of the autonomic nervous system, peripheral autonomic neuropathy, hydrocephalus, brain cysts, Riley-Day syndrome, multisystem degeneration of the autonomic nervous system, hippocampal sclerosis, mesial sclerosis, diabetic neuropathy or Wolfram syndrome, adrenoleukodystrophy, leukodystrophy and spinal cord injury;and (xii) mental and behavioral disorders due to physiological conditions such as vascular dementia, unspecified dementia, depression; behavioral disorders related to the use of psychoactive substances; schizophrenia, schizotypal disorder, delusional disorder and other psychotic disorders not related to mood; mood (affective) disorders such as manic episode, bipolar disorder, major depressive disorder, cyclothymic disorder, dysthymic disorder; anxiety disorder, dissociative disorder, stress-related disorder and other non-psychotic somatoform mental disorders; behavioral syndromes associated with physiological disorders and physical factors such as eating disorders, sleep disorders; personality disorder, impulse control disorder, gambling disorder; intellectual disability;speech disorders, writing disorders, learning disorders, disorders due to the use of psychoactive substances, and adjective behaviors.; For the purposes of the present invention, "neuropathic pain" is defined as pain caused by an injury or disease of the somatosensory nervous system, according to the definition of the International Association for the Study of Pain (IASP). The somatosensory nervous system comprises sensory neurons and neural pathways that respond to changes on the surface or within the body. The term paralysis, for the purposes of the present invention, refers to the partial or total loss of mobility in any part of the body, caused by an injury or disease of the central or peripheral nervous system. Furthermore, the term sleep disorders refers to disorders that include problems initiating and maintaining sleep caused by a problem or pathology of the central or peripheral nervous system.Non-limiting examples of such sleep disorders include insomnia, hypersomnias such as narcolepsy, sleep apnea, restless legs syndrome, circadian rhythm disorders, and parasomnia, among others. Certain neurodegenerative diseases can lead to processes that result in blindness, hearing loss, disorientation, mood disorders, and other symptoms. Alzheimer's disease is a well-characterized example of a neurodegenerative disorder, in which plaques have been observed to form, primarily composed of the β-amyloid peptide resulting from altered protein processing, followed by accumulation on the cell exterior. Conversely, tangles of neurofilaments composed of hyperphosphorylated tau protein appear inside the cells. This process has been associated with alterations in cholesterol metabolism and the consequent alteration of levels of certain membrane lipids, such as docosahexaenoic acid (DHA).On the other hand, several neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, and senile dementia (or Lewy body dementia), have been linked to the pathological accumulation of fibrillar aggregates of the α-synuclein protein, which lead to a significant alteration in cellular triglyceride metabolism. In fact, the development of these and other neurodegenerative diseases is related to alterations in serum or cellular lipid levels, such as cholesterol, triglycerides, sphingomyelin, phosphatidylethanolamine, etc. This, again, suggests that lipids play a crucial role in the proper functioning of neurons, glial cells, nerves, the brain, cerebellum, and spinal cord, which is logical considering the high abundance of lipids in the central nervous system. Alzheimer's disease (AD) is a neurodegenerative disease for which there is currently no effective therapy or treatment, and whose pathophysiology remains largely unknown. Multiple drugs and therapies have been designed and developed in the last decade with the aim of halting or slowing the neurodegenerative process characteristic of this disease. However, no treatment has yet successfully completed a phase III clinical trial in humans. Most therapies have been based on the amyloid cascade hypothesis, which is currently being questioned due to the near-complete failure of clinical trials of anti-amyloid / tau therapies.On the other hand, different types of multiple sclerosis and other neurodegenerative processes are related to demyelination, the net result of which is the loss of lipids in the myelin sheath of neuronal axons, with the consequent alterations in the propagation of electrical signals. Myelin is a lipid layer that surrounds the axons of many neurons and is formed by a series of spiral folds of the plasma membrane of glial cells (Schwann cells and oligodendrocytes, peripherally and centrally, respectively). Therefore, it is well established that lipids play an important role in the development of neurodegenerative diseases. Furthermore, it has been shown that natural polyunsaturated fatty acids have a moderate preventive effect on the development of neurodegenerative processes.In fact, the most abundant lipid in the central nervous system is docosahexaenoic acid (DHA), whose abundance is altered in many neurodegenerative processes, such as Alzheimer's disease. On the other hand, metabolic disease is primarily selected from the group that includes obesity, overweight, hypercholesterolemia, hypertriglyceridemia, diabetes, and insulin resistance. Metabolic diseases comprise a set of pathologies characterized by the accumulation or deficiency of certain molecules. A typical example is the accumulation of glucose, cholesterol, and / or triglycerides above normal levels. Increased levels of glucose, cholesterol, and / or triglycerides, both systemically (e.g., increased plasma levels) and cellularly (e.g., in cell membranes), are associated with alterations in cell signaling that lead to dysfunctions at various levels, typically due to errors in the activity of certain enzymes or the regulation of these proteins.Among the most important metabolic disorders are hypercholesterolemia (high cholesterol levels) and hypertriglyceridemia (high triglyceride levels). These diseases have high incidence, morbidity, and mortality rates, making their treatment a top priority. Other important metabolic disorders include diabetes and insulin resistance, characterized by problems controlling glucose levels. These metabolic disorders are implicated in the development of other pathological processes, such as cancer, hypertension, obesity, and arteriosclerosis. Another pathological process related to the previously described metabolic disorders has been identified and could constitute a new metabolic disorder in itself: metabolic syndrome. For the purposes of the present invention, a neoplasm is defined as an abnormal mass of tissue that occurs when cells multiply excessively or are not destroyed at the appropriate time. Neoplasms are either benign (non-cancerous) or malignant (cancerous). The term “neoplasm” is equivalent to “tumor.”There are multiple types of cancer, including, for example, cancer of the oral cavity and pharynx, cancer of other digestive organs, cancer of other respiratory organs, cancer of bone and articular cartilage, melanoma and other malignant neoplasms of the skin, cancer of mesothelial tissues and soft tissues, cancer of genital organs, cancer of the urinary tract, cancer of the eye, brain and other regions of the nervous system, cancer of the thyroid and other endocrine glands, malignant neuroendocrine tumors, cardiovascular inflammation; inflammation caused by tumors; inflammation of rheumatoid origin; respiratory inflammation; acute and chronic inflammation; inflammatory hyperalgesia; and edema and inflammation caused by trauma or burns. For the purposes of the present invention, the term digestive pathology refers to diseases of the oral cavity and salivary glands; diseases of the esophagus, stomach and duodenum; diseases of the appendix; non-infectious enteritis and colitis; diseases of the peritoneum and retroperitoneum; diseases of the liver; and diseases of the gallbladder, bile ducts and pancreas. For the purposes of the present invention, a musculoskeletal and connective tissue disease refers to pathologies of muscles, joints, and bones that may or may not have an autoimmune origin. Such musculoskeletal and connective tissue diseases are selected from the group consisting of: arthropathies, connective tissue disorders, disorders of muscles and soft tissues; disorders of synovial membrane and tendon; osteopathies; and chondropathies. For the purposes of the present invention, the term genitourinary pathology refers to glomerular diseases; tubulointerstitial kidney diseases; acute renal failure; chronic kidney disease; lithiasis; and inflammatory and non-inflammatory disorders of the renal tract. The present invention also relates to a nutraceutical composition comprising at least a first compound selected from the group consisting of: a nutraceutically acceptable compound of formula (II), or a salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) and a nutraceutically acceptable compound of formula (III), or a salt or ester thereof: COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fM.mr(CH2)c-CH3 (III) wherein said composition optionally comprises a second compound of formula (I), or a nutraceutically acceptable salt or ester thereof: COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) and wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and a+3b+c+3 is an even integer; and at least one nutraceutically acceptable excipient. The present invention also relates to a nutraceutical composition comprising at least a first compound selected from the group consisting of: a nutraceutically acceptable salt or ester of a compound of formula (II): COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) and cenRnn / zznz / E / YiAi a nutraceutically acceptable salt or ester of a compound of formula (III): COOH -(CH2)3-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)ib.^ (III) wherein said composition optionally comprises a nutraceutically acceptable salt or ester of a compound of formula (I): COOH -CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3(I) and wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b-1); and a+3b+c+3 is an even integer; and at least one nutraceutically acceptable excipient. The present invention also relates to a nutraceutical composition comprising at least a first compound selected from the group consisting of a compound of formula (II) and a compound of formula (III), or a nutraceutically acceptable salt or ester thereof, wherein said composition optionally comprises a compound of formula (I), or a nutraceutically acceptable salt or ester thereof, as described above, for use in the prevention of a disease or pathology. Additionally, the present invention also relates to a method of preventing a disease or pathology, wherein said method comprises administering to a subject an effective amount of a nutraceutical composition comprising at least a first compound selected from the group consisting of a compound of formula (II) and a compound of formula (III), or a nutraceutically acceptable salt or ester thereof, wherein said composition optionally comprises a compound of formula (I), or a nutraceutically acceptable salt or ester thereof, as described above. Preferably, the disease or pathology is selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease. Preferably m=0 and, each of the embodiments of the present invention described, including those embodiments relating to compounds of formula (II), or of formula (III), pharmaceutical and nutraceutical compositions comprising them, their first and second medical uses, methods of inducing neuroregeneration and / or preventing neurodegeneration, or methods of preventing and / or treating a disease or pathology, as well as the use and in vitro method of determining the efficacy of a treatment, relate to a compound selected from the group consisting of a compound of formula (II), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3cenAnn / zznz / E / YiAi (II) and a compound of formula (III), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-(CH2)a+3-(CH=CH-CH2W(CH2)c-CH3(III) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is 0.3 or 6; and wherein a+3b+c+3 is an even integer. Also preferably m=0 and, each of the embodiments of the present invention described, including those embodiments relating to compounds of formula (II), or of formula (III), pharmaceutical and nutraceutical compositions comprising them, their first and second medical uses, methods of inducing neuroregeneration and / or preventing neurodegeneration, or methods of preventing and / or treating a disease or pathology, as well as the use and in vitro method of determining the efficacy of a treatment, relate to a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (II): COOH -(CH2)a-(CH=CH-CH2)HCH2)c-CH3 (II) or a pharmaceutically acceptable salt or ester of a compound of formula (III): COOH -(CH2)a+3-(CH=CH-CH2W(CH2)c-CH3 (III) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is 0, 3 or 6; and wherein a+3b+c+3 is an even integer. More preferably m=0 and each of the embodiments of the present invention described, including those embodiments relating to compounds of formula (II), or of formula (III), pharmaceutical and nutraceutical compositions comprising them, their first and second medical uses, methods of inducing neuroregeneration and / or preventing neurodegeneration, or methods of preventing and / or treating a disease or pathology, as well as the use and in vitro method of determining the efficacy of a treatment, relate to a compound selected from the group consisting of: a compound of formula (II), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) wherein: a=6, b=1 and c=6; oa=6, b=2 and c=3; oa=6, b=3 and c=0; oa=3, b=3 and c=3; oa=2, b=4 and c=3; oa=2, b=5 and c=0; and a compound of formula (III), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH -(CH2)a+3-(CH=CH-CH2)Mr(CH2)c-CH3 (III) wherein a=1,b=6 andc=0. Also, more preferably, each of the embodiments of the present invention described herein, including those embodiments relating to compounds of formula (II) or formula (III), pharmaceutical and nutraceutical compositions comprising them, their first and second medical uses, methods of inducing neuroregeneration and / or preventing neurodegeneration, or methods of preventing and / or treating a disease or pathology, as well as the use and in vitro method of determining the efficacy of a treatment, relate to a compound selected from the group consisting of: a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (II): COOH -(CH2)a-(CH <H-CH2)b-(CH2)c-CH3 (II) en donde: a=6, b=1 y c=6; o a=6, b=2 y c=3; o a=6, b=3 y c=0; o a=3, b=3 y c=3; o a=2, b=4 y c=3; o a=2, b=5 y c=0; and a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (III): COOH -(CH2)a+r(CH=CH-CH2)Mr(CH2)c-CH3 (III) wherein a=1,b=6 andc=0. Even more preferably, said salt is a sodium salt, and said ester is an ethyl ester. In one embodiment of the invention, the pharmaceutical and nutraceutical compositions described herein comprise a compound of formula (I), together with a compound of formula (II) or a compound of formula (III), in a concentration of 0.01% to 99.99% w / w, preferably the composition comprising 10% to 80% w / w, or even more preferably in a concentration of 20% to 80% w / w. In another embodiment of the invention, the compositions described herein comprise a prodrug of formula (I) together with a compound of formula (II) or a compound of formula (III), wherein said combination is in a ratio in the range of 0.01:100 to 100:0.01, preferably 1:5 to 5:1, and even more preferably 1:2 to 2:1. In an additional aspect, the pharmaceutical or nutraceutical compositions of the invention can be presented in vials, ampoules, powders, capsules, tablets, sachets, solutions, syrups, ointments, creams, emulsions, gels, patches, controlled-release formulations, suppositories, ovules, etc. The formulations are suitable for administration by various routes, including oral, sublingual, gastroenteric, rectal, parenteral (intravenous, intra-arterial, intramuscular, and subcutaneous), respiratory, and topical (ophthalmic, otic, and transdermal). The route of administration can be easily determined by a person skilled in the art. The compositions of the present invention may be in the form of a gastro-resistant composition to prevent degradation of their components by the low pH of the gastric environment. In certain embodiments, the composition of the invention further includes one or more additional components or excipients, such as diluents, antioxidants, sweeteners, gelling agents, flavorings, fillers, or other carriers, such as colloidal anhydrous silica and glyceryl monostearate. Such compositions may be in the form of a capsule, sachet, paper, or other container. Conventional techniques for the preparation of pharmaceutical compositions may be used in producing the compositions. For example, the compounds disclosed herein may be mixed with a carrier, diluted by means of a carrier, or enclosed within a carrier, which may be in the form of a blister, capsule, sachet, paper, or other container.When the carrier is a diluent, it can be a solid, semi-solid, or liquid material that acts as a vehicle, excipient, or medium for the active compound. Some examples of suitable diluents are water, saline solutions, alcohols, polyethylene glycols, polyhydroxyethoxylated castor oil, peanut oil, olive oil, lactose, terra alba, sucrose, cyclodextrin, amylose, magnesium stearate, talc, gelatin, agar, pectin, gum arabic, stearic acid or lower alkyl ethers of cellulose, silicic acid, fatty acids, fatty acid amines, mono- and diglycerides of fatty acids, pentaerythritol fatty acid esters, polyoxyethylene, hydroxymethylcellulose, and polyvinylpyrrolidone. Similarly, the carrier or diluent may include any sustained-release material known in the art, such as glyceryl monostearate or glyceryl distearate, alone or mixed with a wax.These compositions may also include wetting agents, antioxidants, emulsifying and suspending agents, preservatives, sweeteners, and flavoring agents. The compositions of the invention may be formulated to provide rapid, sustained, or delayed release of the compounds disclosed herein after administration to the patient using well-known procedures in the art. The described compositions may be solid compositions or liquid solutions. In one embodiment, not limiting the invention, said composition is a solid composition that may comprise 20-80% of the compound of formula (I) and / or the compound of formula (II) or formula (III), 20-80% of a diluent, 0.1-20% of an antioxidant, 0.01-10% of a sweetener, 0.1-20% of a gelling agent, and 0.01-10% of a flavoring agent. In another embodiment, not limiting the invention, said composition is a solution for oral administration comprising 20 to 80% of the compound of formula (I) and / or the compound of formula (II) or formula (III), 20 to 80% of diluent, 0.1 to 20% of antioxidant, 0.01 to 10% of a sweetener, 0.1 to 20% of a gelling agent and 0.01 to 10% of a flavoring agent. Pharmaceutical compositions may be sterilized and mixed, if desired, with auxiliary agents, emulsifiers, salt to influence osmotic pressure, buffers and / or coloring substances and the like, which do not react detrimentally with the compounds disclosed earlier in this document. BRIEF DESCRIPTION OF THE FIGURES Figure 1A Illustrative scheme of the cellular metabolism of 2-hydroxydocosahexaenoic acid (DHA-H) yielding (6Z,9Z,12Z,15Z,18Z)-heneicosa-6,9,12,15,18-pentaenoic acid (HPA) via α-oxidation. DHA-H requires activation by an acyl-CoA synthetase, in a process dependent on ATP (adenosine triphosphate) and magnesium (Mg2+). DHAH-CoA would be subject to the activity of 2-hydroxyphytanoyl-CoA lyase (2-hydroxyacyl-CoA lyase 1, HACL1), leading to the formation of an intermediate polyunsaturated aldehyde containing 5 or 6 double bonds. HACL1 activity depends on thiamine pyrophosphate (TPP) and Mg2+, and can be inhibited by a competitive antagonist (e.g., oxythiamine). The enzyme aldehyde dehydrogenase is responsible for the conversion of the intermediate aldehyde to HPA in an NAD+ (Nicotinamide Adenine Dinucleotide)-dependent process. Fig. 1B. DHA-H is metabolically transformed into HPA by α-oxidation in HEK293T cells.The intracellular levels of DHA-H (B1 and B3) and HRA (B2 and B3) are represented. B4) on the y-axis (nmoles / mg of protein), versus treatment concentration with the sodium salt of DHA-H (μM) for 24 hours (B1 and B2) or incubation time (h) with a constant concentration of the sodium salt of DHA-H of 30 μM (B3 and B4), including untreated controls (C), on the x-axis. Black bars represent the result in cells without additional stimulation, white bars represent the result after simultaneous treatment with 1 mM oxythiamine, and striped bars represent the result after treatment with 10 mM oxythiamine. Both DHA-H and HPA increased with concentration and incubation time, with HPA levels significantly higher than those of DHA-H at exposure to 30 μM of the sodium salt of DHA-H after 24 hours. This increase in HPA is inhibited in the presence of 10 mM of oxythiamine (which inhibits the HCLA1 enzyme), demonstrating the involvement of α-oxidation in this metabolic conversion.The bars represent the mean ± standard error, and statistical analysis was performed using one-way ANOVA and Tukey's multiple range test: * p < 0.05 when comparing HPA levels with DHA-H levels under the same condition; #, p < 0.05 when comparing values ​​in the presence and absence of 10 mM oxythiamine. Fig. 1C. Endogenous DHA (native non-hydroxylated form of docosahexaenoic acid) levels in HEK293T are not altered after treatment with the sodium salt of DHA-H. Intracellular DHA levels are plotted on the y-axis (nmoles / mg of protein), versus treatment concentration with the sodium salt of DHA-H (μM) for 24 hours (C1) or incubation time (h) with a constant concentration of the sodium salt of DHA-H of 30 μM (C2), including untreated controls (C), on the x-axis.Treatment with the sodium salt of DHA-H had no significant effect on DHA levels, regardless of concentration or incubation time. The bars represent the mean ± standard error, and statistical analysis was performed using one-way ANOVA and Tukey's multiple range test. Based on these results, it can be concluded that the administration of DHA-H, or its sodium salt in this case, does not alter endogenous levels of DHA (docosahexaenoic acid) or other cellular fatty acids studied. Instead, treatment with DHA-H results exclusively in an increase in HPA levels, implying that the therapeutic effect obtained through treatment with DHA-H, and particularly with its sodium salt, is mediated by HPA and not by modulation of the levels of other endogenous fatty acids. Figure 2A. Mice treated with the sodium salt of DHA-H exhibit dose-dependent brain accumulation of HPA, with DHA-H being undetectable in the brain. Brain levels of HPA (A1) or DHA (A2) are plotted on the y-axis (nmoles / mg of protein) against treatment doses of the sodium salt of DHA-H (A1) and the sodium salt of DHA (A1 and A2) (mg / kg). A1: WT animals; or 5xFAD. A2: Black bars represent WT animals and white bars represent 5xFAD. HPA and DHA levels were determined in the brains of WT and 5xFAD mice after chronic administration of the sodium salt of DHA-H (4 months; 5 doses / week LV; between 3 and 7 months of age; sacrifice at 7 months). HPA accumulation in the brain of both mouse strains is similar, depending on the dose of the sodium salt of DHA-H administered (A1: r2= 0.9292, p= 0.0002; or r2= 0.9704, p<0.0001). DHA levels did not vary significantly between the experimental conditions (A2).Data are shown as mean ± standard error, and statistical analysis was performed using one-way ANOVA and Tukey's multiple range test: * p < 0.05 compared to the control (vehicle-treated mice). Therefore, when the prodrug DHA-H, particularly its sodium salt, is administered to healthy mice and transgenic models of Alzheimer's disease, a significant accumulation of HPA occurs in the brain, without the prodrug (DHA-H) being detected, nor any changes in endogenous DHA levels. Fig. 2B. 5xFAD mice treated with the sodium salt of DHA-H exhibit cognitive improvement that directly correlates with brain HPA levels.The number of total errors (B1), reference memory errors (RME) (B2), or working memory errors (WME) (B3) committed are plotted on the y-axis against brain HPA levels (nmol / mg of protein) on the x-axis. Cognitive assessment was performed using the 8-arm radial maze test during the last month of treatment for the same animals shown in Figure 2A. Individual experimental points for the entire animal population under study were plotted, and data from the 5xFAD animals were fitted to an inverse polynomial regression f(x)=yo+(a / x). The r² and p values ​​corresponding to the regression of each parameter—total errors, RME, and WME—against brain HPA concentration are shown below: C1: r²=0.9146 and p=0.0311; C2: r2=0.9252 and p=0.0243; C3: r2=0.7785 and p=0.0346.The data obtained suggest that minimal increases in brain HPA levels are associated with improved spatial cognition. Each point in the graphs represents the mean ± standard error for each pathology / treatment condition: · WT + vehicle; ▼ WT + DHA-H 20 mg / kg; ♦ WT + DHA-H 200 mg / kg; or 5xFAD + vehicle; Δ 5xFAD + DHA-H 5 mg / kg; V 5xFAD + DHA-H 20 mg / kg; □ 5xFAD + DHA-H 50 mg / kg; O 5xFAD + DHA-H 200 mg / kg. These results show that moderate increases in brain HPA levels are significantly associated with improved spatial cognition, which is one of the cognitive abilities most affected in Alzheimer's disease. Figure 3A. Mice treated with the sodium salt of DHA-H show tumor accumulation of HPA, with DHA-H being undetectable, in xenographic U118 cell tumors. DHA (black bars) and HPA (white bars) levels (pmol / mg of tissue) in the tumor are plotted on the y-axis against the treatment condition (vehicle and DHA-H 200 mg / kg) on ​​the x-axis. Three-month-old NUDE (immunocompromised) mice were injected subcutaneously with 7.5 x 10⁶ U118 cells (grade IV human multiforme glioblastoma). Tumor growth was allowed subcutaneously for 10 days before the start of oral treatments (vehicle or DHA-H sodium salt 200 mg / kg), which were maintained for 42 days until sacrifice. Lipid analysis of xenographic tumors revealed the absence (undetectable levels) of DHA-H. The bars represent the mean ± standard error for each treatment condition. Fig. 3B.HPA levels in tumors are inversely correlated with tumor size in xenographic models. Tumor size (cm³) is plotted on the y-axis against HPA levels (pmol / mg of tissue) in the tumor on the x-axis for two treatment conditions: vehicle and DHA-H sodium salt 200 mg / kg. The presence of HPA in the tumors of animals treated with DHA-H sodium salt shows a statistically significant linear relationship with tumor volume (A²), where r² = 0.4296 and p = 0.0029. The results demonstrated that HPA levels in xenographic tumors have a statistically significant inverse linear relationship with tumor size. In the absence of the DHA-H parent molecule in the target organ, this evidence shows that the presence of HPA in the target organ has a therapeutic effect in vivo. Figure 4A. DHA-H is a prodrug that is metabolically transformed into HPA by α-oxidation in U118 cells. Intracellular levels of DHA (black bars), DHA-H (white bars), and HPA (dashed bars) are plotted on the y-axis (nmoles / mg of protein) against the treatment conditions: Control (C) and DHA-H sodium salt 150 μM (48 h), in the presence or absence of concurrent treatment with 1 and 10 mM oxythiamine, on the x-axis. Both DHA-H and HPA increased in cells treated with the DHA-H sodium salt. This increase in HPA is inhibited in the presence of 1 and 10 mM oxythiamine, demonstrating the involvement of α-oxidation in this metabolic conversion. The bars represent the mean ± standard error, and the statistical analysis was performed using one-way ANOVA and Tukey's multiple evaluation test: * p < 0.05 when comparing only HPA levels. Fig. 4B.The metabolic conversion of DHA-H to HPA is necessary for an anti-tumor effect. Cell viability (% of the control -C- without oxythiamine) is plotted on the y-axis against the treatment conditions: Control (C- black bars) and DHA-H sodium salt 150 μM, 48 h (white bars) in the presence and absence of simultaneous treatment with 1 mM oxythiamine, on the x-axis. Treatment with DHA-H on U118 cells significantly reduces culture viability, while treatment with oxythiamine (alone) has no effect on cell viability. However, when treatment with DHA-H sodium salt is administered simultaneously with oxythiamine, the anti-proliferative effect of this compound is significantly reduced compared to the effect without oxythiamine.The bars represent the mean ± standard error, and the statistical analysis was performed using one-way ANOVA and Tukey's multiple evaluation test: * p < 0.05 when compared with the control (C); # p <0.05 when comparing the effect of DHA-H in the presence and absence of oxythiamine. Figure 5A. Viability of U118 cells in culture after treatment with the sodium salt of DHA-H, the sodium salt of DHA, and HPA. Cell viability (% of untreated control) is plotted on the y-axis against the different treatment conditions on the x-axis: Control (black bar), sodium salt of DHA-H (150 μM, 48 h - white bar), DHA (150 μM, 48 h - dashed bar), and HPA (150 μM, 48 h - gridded bar). Treatment with HPA under the same conditions induces a much more pronounced degree of cell mortality than that induced by DHA-H (prodrug) or DHA (natural analogue). This effect could be due to a mixture of anti-proliferative effect and toxic effects of HPA itself, which would not be attributable to DHA-H or DHA under the same experimental conditions.The bars represent the mean ± standard error, and statistical analysis was performed using one-way ANOVA and Tukey's multiple range test: * p < 0.05 when compared to the control. Fig. 5B. Intracellular HPA levels in cultured U118 cells treated with the sodium salt of DHA-H and HPA. HPA levels (nmoles / mg of protein) are plotted on the y-axis against treatment conditions on the x-axis: sodium salt of DHA-H (150 μM, 48 h - black bar) and HPA (5-150 μM, 48 h - white bars). Administration of 150 μM of the sodium salt of DHA-H results in HPA levels equivalent to those generated by treatment with HPA at 5 μM. Treatment with HPA 150 μM results in significantly higher intracellular HPA levels than those generated by the same concentration of the prodrug. Bars represent mean ± standard error. Fig. 5C. DHA-H and DHA levels in HEK293T cells in the presence (C1) or absence (C2) of culture medium. DHA-H (·) and DHA (o) levels in the culture medium (% of initial levels at time 0) are plotted on the y-axis against incubation time (h) on the x-axis. The lipid concentration in the culture medium was 30 μM, and the culture plates were incubated for up to 72 h. In the presence of cell culture (C1), DHA levels in the medium decreased significantly at 48 and 72 h as a result of DHA uptake by the cells, while DHA-H levels remained unchanged up to 72 h. In the absence of cell culture (C2), the levels of both DHA and DHA-H remained constant over time.The bars represent the mean ± standard error, and the statistical analysis was performed using one-way ANOVA and Tukey's multiple evaluation test: * p < 0.05 when compared with the control. Figures 6A, 6B, and 6C: Chronic treatment with HPA acid or its prodrug, DHA-H, prevents the cognitive decline characteristic of Alzheimer's disease in the transgenic murine model (5xFAD). Cognitive assessment was performed using the 8-arm radial maze test. Animals were treated between 3 and 7 months of age, and the test was administered during the last month of treatment. Total errors made during the test (Fig. 6A), working memory errors (RME) (Fig. 6B), and reference memory errors (WME) (Fig. 6C) were recorded. Each column represents the mean ± SEM of errors during the last week of the radial maze test. Black columns represent errors made by wild-type (WT) mice. White columns represent errors made by 5xFAD transgenic mice treated with the vehicle (5% ethanol).The striped columns represent errors made by 5xFAD mice treated with DHA-H (20 mg / kg / day). The checkered columns represent errors made by 5xFAD mice treated with HPA (20 mg / kg / day). The results show a similar cognitive improvement in 5xFAD mice treated with DHA-H and HPA. The bars represent the mean ± standard error for each treatment condition, and statistical analysis was performed using one-way ANOVA and Tukey's multiple range test: * p < 0.05 when compared to the healthy control (WT) and # p < 0.05 when compared to the vehicle-treated 5xFAD control condition. Figure 7A: Tumor growth is inhibited in vivo in the presence of HPA sodium salt or its prodrug, DHA-H, in xenographic models. Tumor size (cm³) is plotted on the y-axis against the number of days of treatment on the x-axis. To induce xenographic tumors in 3-month-old NUDE (immunocompromised) mice, 7.5 x 10⁶ grade IV human glioblastoma cells (U-118 MG) were inoculated subcutaneously on both sides of the dorsal flank of the animal (8–12 weeks old, 30–35 g). After 10 days, tumors became visible with an approximate volume of 0.1 cm³. The animals were randomly divided into groups with a similar mean tumor volume and received daily oral treatments for 42 days: vehicle (no treatment control), ▲ DHA-H (200 mg / kg / day) and HPA (200 mg / kg / day).Tumor volumes (v) were calculated as v = A² × L / 2, where A is the tumor width and L is its length. Data obtained for each treatment condition were fitted to an exponential growth curve. Fig. 7B: HPA and the prodrug, DHA-H, significantly reduced xenographic tumor volume compared to the untreated control. The volume of induced tumors 42 days after the start of treatment is plotted on the y-axis versus the treatment conditions on the x-axis. Individual data for the animals participating in the study are shown: vehicle (untreated control), DHA-H (200 mg / kg / day), and HPA (200 mg / kg / day). The bars represent the mean ± standard error for each treatment condition, and statistical analysis was performed using one-way ANOVA and Tukey's multiple range test: p < 0.05 when compared to the control condition. Figure 8A-8F. Illustrative diagrams of the cellular metabolism of 2-hydroxylated polyunsaturated fatty acids (prodrugs, PUFA-H), giving rise via o-oxidation to their corresponding non-hydroxylated metabolites, the latter having one less carbon atom than the initial molecule. The hydroxylated fatty acid requires activation by an acyl-CoA synthetase, in a process dependent on ATP (adenosine triphosphate) and magnesium (Mg2+). This PUFA-H-CoA would be subject to the activity of 2-hydroxyacyl-CoA lyase (HACL, isoforms 1 or 2 depending on the cell type), which would lead to the formation of an intermediate polyunsaturated aldehyde. The activity of HACL depends on thiamine pyrophosphate (TPP) and Mg2+, and can be inhibited by a competitive antagonist, such as oxythiamine. The enzyme aldehyde dehydrogenase would be responsible for the conversion of the intermediate aldehyde into the final fatty acid in a process dependent on NAD+ (Nicotinamide Adenine Dinucleotide). Fig. 8A.Schematic of the cellular conversion of 2-hydroxylinoleic acid (LA-H) to (8Z,11Z)-heptadeca-8,11-dienoic acid (HDA). Fig. 8B. Schematic of the cellular conversion of 2-hydroxy-alpha (α)-linolenic acid (ALA-H) to (8Z,11Z,14Z)-heptadeca-8,11,14-trienoic acid (HTAω-3). Fig. 8C. Schematic of the cellular conversion of 2-hydroxy-gamma (γ)-linolenic acid (GLA-H) to (5Z,8Z,11Z)-heptadeca-5,8,11-trienoic acid (HTAω-6). Fig. 8D. Schematic of the cellular conversion of 2-hydroxyarachidonic acid (ARA-H) to (4Z,7Z,10Z,13Z)-nonadeca-4,7,10,13-tetraenoic acid (NTA). Fig. 8E. Schematic of the cellular conversion of 2-hydroxyeicosapentaenoic acid (EPA-H) to (4Z,7Z,10Z,13Z,16Z)-nonadeca-4,7,10,13,16-pentaenoic acid (NPA). Fig. 8F. Schematic of the cellular conversion of 2-hydroxydocosahexaenoic acid (DHA-H) to (6Z,9Z,12Z,15Z,18Z)-heneicosa-6,9,12,15,18-pentaenoic acid (HPA). Figure 9 (A1-F2). Amplified regions of the different chromatograms obtained by gas chromatography with flame ionization detection (GC-FID) when HEK293T cells were treated with the corresponding prodrug: A1) control (vehicle) and A2) LA-H (100 μM, 24 h). The white arrow indicates the chromatographic peak of the parent molecule LA-H, the black arrow indicates the chromatographic peak corresponding to the metabolite HDA. HDA formation is inhibited in the presence of 10 mM oxythiamine. B1) control (vehicle) and B2) ALA-H (100 μM, 24 h). The white arrow indicates the chromatographic peak of the parent molecule ALA-H, the black arrow indicates the chromatographic peak corresponding to the metabolite ΗTA ω-3. The formation of HTA ω-3 is inhibited in the presence of 10 mM oxythiamine. C1) control (vehicle) and C2) GLA-H (100 μM, 24 h). The white arrow indicates the chromatographic peak of the GLA-H parent molecule, the black arrow indicates the chromatographic peak corresponding to the HTA ω-6 metabolite.The formation of ω-6 HTA is inhibited in the presence of 10 mM oxythiamine. D1) control (vehicle) and D2) ARA-H (100 μM, 24 h). The white arrow indicates the chromatographic peak of the parent molecule ARA-H, the black arrow indicates the chromatographic peak corresponding to the NTA metabolite. The formation of NTA is inhibited in the presence of 10 mM oxythiamine. E1) control (vehicle) and E2) EPA-H (100 μM, 24 h). The white arrow indicates the chromatographic peak of the parent molecule EPA-H, the black arrow indicates the chromatographic peak corresponding to the NPA metabolite. The formation of NPA is inhibited in the presence of 10 mM oxythiamine. F1) control (vehicle) and F2) DHA-H (100 μM, 24 h). The white arrow indicates the chromatographic peak of the parent molecule HPA, and the black arrow indicates the chromatographic peak corresponding to the HPA metabolite. HPA formation is inhibited in the presence of 10 mM oxythiamine. Figure 10. Treatment with HPA and other odd-chain polyunsaturated fatty acids prevents excitotoxicity-induced neuronal death. Neuronal cultures were obtained by differentiation from human SH-SY5Y neuroblastomas using retinoic acid and BDNF (Brain-Derived Neurotrophic Factor). Excitotoxic neuronal death was induced by the addition of NMDA (10 mM) and calcium / glycine (530 μM / 10 mM) to the culture medium for 1 hour. To test the neuroprotective effect of the different compounds under study (HDA or C17:2 ω-6, HTA ω-3 or C17:3 ω-3, HTA ω6 or C17:3 ω-6, NTA or C19:4 ω-6, and HRA or C21:5 ω-3), a 24-hour pre-treatment was administered: vehicle (black bars), 1 μM (white bars), 3 μM (dotted bars), and 10 μM (striped bars). The treatments tested under these experimental conditions demonstrated that these compounds can prevent excitotoxicity-induced cell death starting at a concentration of 3 μM.The bars represent the mean ± standard error for each treatment condition and the statistical analysis was performed using one-way ANOVA and Tukey's multiple evaluation test: * p < 0.05 when compared to the control condition (pre-treatment with vehicle). Figure 11. Illustrative scheme of the cellular metabolism of 2-OHOA (LAM561) yielding 8Z-heptadecenoic acid (C17:1n9) via α-oxidation. 2-OHOA requires activation by an acyl-CoA ligase in a process dependent on ATP (adenosine triphosphate) and magnesium (Mg2+). 2OHOA-CoA is then subject to the activity of 2-hydroxyphytanoyl-CoA lyase (2-hydroxyacyl-CoA lyase 1, HACL1), leading to the formation of an intermediate monounsaturated aldehyde. HACL1 activity is dependent on thiamine pyrophosphate (TPP) and Mg2+, and can be inhibited by a competitive antagonist (e.g., oxythiamine). The enzyme aldehyde dehydrogenase would be responsible for the conversion of the intermediate aldehyde into 8Z-heptadecenoic acid in a process dependent on NAD+ (Nicotinamide Adenine Dinucleotide). Figure 12A-12B Analysis of fatty acid composition in U-118 MG glioma cells. (Fig. 12A) Representative chromatograms showing the fatty acid composition in U-118 MG cells incubated in the presence of 400 μM of 2OHOA sodium salt or no treatment (Control) for 24 h, determined by gas chromatography. Retention times (min): C17:1 n-9 (10.12), OA (13.01), 2OHOA (16.87), and C17:0 margaric acid as an internal control (10.81). (Fig. 12B) Quantification of different fatty acids identified in the chromatograms (OA, 2OHOA, and C17:1 n-9). The black bar represents the concentration of each fatty acid in the control, and the white bar represents the fatty acid concentration after treatment with the sodium salt of 2OHOA. The columns show the mean ± SEM of three independent experiments, expressed in nmoles and normalized per mg of protein.Statistical significance is determined with a Student's t test (***p<0.001 compared to the control). Figure 13A-13H. Analysis of fatty acid composition in different glioma and non-tumor cell lines after treatment with the sodium salt of 2OHOA. Representative chromatograms showing the fatty acid composition (left) and quantification of different fatty acids identified in the chromatograms (C17:0, OA, 2OHOA and C17:1 n9) (right) in glioma cells: (Fig.13A) and (Fig.13B) U-251 MG; (Fig.13C) and (Fig.13D) SF-295; and non-tumor cells: (Fig.13E) and (Fig.13F) MRC-5 (human fibroblasts); (Fig. 13G) and (Fig. 13H) mouse astrocytes, after treatment in the absence (control) or presence of 2OHOA sodium salt (400 μM, 24 hours) determined by gas chromatography analysis. The black bar corresponds to the concentration of each fatty acid in the control, and the white bar corresponds to the concentration of the fatty acid after treatment with the 2OHOA sodium salt. C17:0 margaric acid is included as an internal control.The columns show the mean ± SEM of three independent experiments expressed in nmoles and normalized per mg of protein. Statistical significance was determined using a Student's t-test (**p<0.01, ***p<0.001 compared to the control). Figure 14 (A1-C3). Effect of 2OHOA sodium salt, OA, and C17:1 n-9 sodium salt on the viability and proliferation of glioma cells. Viability curves of different glioma cell lines (A1-A3) U-118 MG; (B1-B3) U-251 MG; and (C1-C3) SF-295 treated with increasing doses of 2OHOA sodium salt (0-1000 μM) (A1, B1, and C1); OA (0-300 μM) (A2, B2, and C2); and C17:1 n-9 sodium salt (0-300 μM) (A3, B3, and C3) for 72 hours. Viability was determined by crystal violet staining. Each value represents the mean ± SEM of three independent experiments with at least three biological replicates, expressed as a percentage of the cells treated with vehicle (100%). Figure 15 (A1-B3). Effect of 2OHOA sodium salt, C17:1 n-9 sodium salt, and OA on the viability and proliferation of non-tumor cells. Viability curves of non-tumor cells (A1-A3) MRC-5 (human fibroblasts); and (B1-B3) mouse astrocytes treated with increasing doses of 2OHOA sodium salt (0-1000 μM) (A1 and B1); OA (0-300 μM) (A2 and B2); and C17:1 n-9 sodium salt (0-300 μM) (A3 and B3) for 72 hours. Viability was determined by crystal violet staining. Each value represents the mean ± SEM of three independent experiments with at least three biological replicates, expressed as a percentage of the cells treated with vehicle (100%). Figure 16A-16E. Analysis of the effect of different fatty acids on markers of proliferation and death in different cell lines. Representative immunoblots of the effect of fatty acids (200 μM of OA, 200 μM of C17:1 n-9 sodium salt and 400 μM sodium salt of 2OHOA) on several proteins involved in the signaling and cell death pathways regulated by 2OHOA in glioma cells: (Fig.16A) U-118 MG; (Fig.16B) U-251 MG; and (Fig.16C) SF-295; and non-tumor cells: (Fig.16D) MRC-5 (human fibroblasts); and (Fig.16E) mouse astrocytes, after 72h of treatment. Figure 17A-17B. Analysis of fatty acid composition in U-118 MG glioma cells after α-oxidation inhibition and effect of oxythiamine on cell survival. (Fig. 17A) Quantification of the fatty acids 2OHOA and C17:1n-9 in U-118 MG cells treated with 400 μM of 2OHOA for 24 hours, pre-incubated with increasing doses (1-10 mM) of oxythiamine (α-oxidation inhibitor) for 90 minutes, determined by gas chromatography. Results are shown as the mean ± SEM of three independent experiments, expressed in nmoles and normalized per mg of protein. Statistical significance was determined using a Student's t-test (*p<0.05, ***p<0.001 comparing the amount of 2OHOA with that detected after 400 μM of 2OHOA in the absence of oxythiamine; $$p<0.01, $$$p<0.001 comparing the amount of C17:1 n-9 with that formed after 400 μM of 2OHOA in the absence of oxythiamine). (Fig.17B) Viability of U-118 MG cells pre-incubated with oxythiamine (for 90 minutes) and treated in the absence (Control) or in the presence of 2OHOA sodium salt (400 μM, 72 hours), determined by trypan blue vital exclusion staining. Results are presented as the mean cell count ± SEM of three independent experiments. Statistical significance was determined using a Student's t-test (p<0.001 for the absence of 2OHOA and oxythiamine, Control-0; and p<0.01 for treatment with 2OHOA without pre-incubation with oxythiamine). Figures 18A-18D. Effect of the C17:1n-9 metabolite on the action of 2OHOA. Viability of different human glioma cell lines: (Fig. 18A) U-251 MG and (Fig. 18B) SF-295; and non-tumor cells: (Fig. 18C) human MRC fibroblasts and (Fig. 18D) mouse astrocytes; all treated in the absence or presence of 2OHOA sodium salt (400 μM, 72 hours) and pre-incubated or not with oxythiamine (for 90 minutes). Cell viability was determined by trypan blue vital exclusion staining. Results are presented as the mean cell count ± SEM of three independent experiments. Statistical significance was determined using a Student's t-test (**p<0.01 and ***p<0.001 regarding the absence of 2OHOA and oxythiamine; and $p<0.05 regarding treatment with 2OHOA alone). Figure 19A-19E. Analysis of the effect of the C17:1 n-9 metabolite on the action of 2OHOA on proliferation and death markers in different cell lines by inhibition of its formation by oxythiamine. Representative immunoblots of the effect of 2OHOA (400 μM) combined or not with oxythiamine (2 mM) on several proteins involved in the signaling and cell death pathways regulated by 2OHOA in glioma cells: (Fig.19A) U-118 MG; (Fig.19B) U-251 MG; and (Fig.19C) SF-295; and non-tumor cells: (Fig.19D) MRC-5 (human fibroblasts); and (Fig.19E) mouse astrocytes, after 72 h of treatment. Figures 20A-20B. Analysis of fatty acid composition in rat plasma after 24 hours of treatment with the sodium salt of 2OHOA. (Fig. 20A) Representative chromatograms showing the fatty acid composition in rat plasma samples obtained at different time points (0, 1, 2, 3, 4, 6, 8, and 24 hours) after acute treatment with 2OHOA (2 mg / kg, 24 hours) determined by gas chromatography. C17:0 margaric acid was quantified as an internal control in the chromatogram. (Fig. 20B) Quantification of the 2OHOA and C17:1n-9 fatty acids identified in the chromatograms. Results are shown as the mean ± SEM of 4 animals and expressed in nmoles, normalized per mL of plasma. Statistical significance was determined using a Wilcoxon test (*p<0.05 and **p<0.01 with respect to baseline levels at 0 hours; $p<0.05 and $$p<0.01 with respect to 2OHOA fatty acid levels). Figures 21A-21B. Analysis of fatty acid composition in rat plasma after 15 days of treatment with the sodium salt of 2OHOA. (Fig. 21A) Representative chromatograms showing the fatty acid composition in rat plasma samples obtained at different time points (0, 1, 2, 3, 4, 6, 8, and 24 hours) after chronic treatment with 2OHOA (2 mg / kg, 15 days) determined by gas chromatography. C17:0 margaric acid was quantified as an internal control. (Fig. 21B) Quantification of the 2OHOA and C17:1 n-9 fatty acids identified in the chromatograms. Results are shown as the mean ± SEM of 4 animals, expressed in nmoles and normalized per mL of plasma. Statistical significance was determined using a Wilcoxon test (*p<0.05 and **p<0.01 with respect to baseline levels at 0 hours; $p<0.05 and $$p<0.01 with respect to 2OHOA fatty acid levels). Figure 22A-22B. Fatty acid composition analysis of xenographic tumors from immunocompromised mice. (Fig. 22A) Representative chromatograms showing the fatty acid composition of xenographic tumors derived from U-118 MG glioblastoma cells in mice treated orally and daily with 2OHOA sodium salt (200 mg / kg, 42 days) as determined by gas chromatography. (Fig. 22B) Quantification of the OA and C17:1 n-9 fatty acids identified in the chromatograms. C17:0 margaric acid was quantified as an internal control. The white bar represents the concentration of each fatty acid in the control, and the black bar represents the fatty acid concentration after treatment with the 2OHOA sodium salt. Results are shown as the mean ± SEM of at least 7 xenographic tumors and expressed in nmoles, normalized per g of tissue. Statistical significance was determined using a Mann-Whitney test (***p<0.01 compared to the control). Figure 23. Inverse correlation between tumor volume and the amount of the C17:1 n-9 metabolite. Representation of the amount of metabolite quantified by gas chromatography in xenographic mouse tumors, with respect to the tumor volume measured on day 42 of treatment with 200 mg / kg of 2OHOA sodium salt (black squares) or its vehicle (Control, white circles). Significance determined by the Pearson correlation coefficient (p = 0.0001; r = 0.825). Figure 24A-24C. Fatty acid composition analysis in human patients with advanced glioma. (Fig. 24A) Representative chromatogram of the fatty acid composition of a glioma patient responding to treatment with 2OHOA sodium salt (12 g / day, 21 days) and determined in plasma samples obtained at different times during treatment (0, 4 and 360 hours, 15 days) by gas chromatography. (Fig. 24B) Quantification of the fatty acids 2OHOA and C17:1n-9 identified in the chromatograms of patients responding and non-responding to 2OHOA treatment in plasma samples obtained at different times on the first day of treatment (0, 1, 2, 4, 6, 8 hours) and on days 8 (192 hours), 15 (360 hours), 21 (504 hours) and the first day of the second treatment cycle (574 hours). (Fig.24C) Quantification of the 2OHOA and C17:1 n-9 fatty acids identified in the chromatograms of the same responder and non-responder patients together.C17:0 margaric acid in the chromatograms was quantified as an internal control. Results are shown as the mean ± SEM of 8 patients (4 responders and 4 non-responders) and expressed in nmoles, normalized per mL of plasma. Statistical significance was determined using a Mann-Whitney test (*p<0.05 and **p<0.01 with respect to the amounts of 2-OHOA fatty acid). EXAMPLES The examples described below are illustrative and are not intended to limit the scope of the present invention. Example 1: Fatty acids, reagents, and organic solvents 1.1. DHA, DHA-H and HPA DHA (sodium salt of docosahexaenoic acid; C22:6 n-3), DHA-H (sodium salt of 2-hydroxy-docosahexaenoic acid; 2OHC22:6 n-3), EPA-H (sodium salt of 2-hydroxy-eicosapentaenoic acid), ARA-H (sodium salt of 2-hydroxyarachidonic acid), GLA-H (sodium salt of 2-hydroxy-gamma (y)-linolenic acid), ALA-H (sodium salt of 2-hydroxy-alpha (a)-linolenic acid), LA-H (2-hydroxy-linoleic acid), HPA (sodium salt of (6Z,9Z,12Z,15Z,18Z)-heneicosa-6,9,12,15,18pentaenoic acid), NTA (sodium salt of acid (4Z,7Z,10Z, 13Z)-nonadeca-4,7,10,13-tetraenoic acid), HTA ω-6 (sodium salt of (5Z,8Z, 11Z)-heptadeca-5,8,11-trienoic acid), HTA ω-3 (sodium salt of (8Z,11Z,14Z)-heptadeca-8,11,14-trienoic acid) and HDA ((8Z,11Z)-heptadeca-8,11-dienoic acid) were obtained from Lipopharma Therapeutics (Spain).Margaric acid (C17:0) was purchased from Sigma-Aldrich, and heneicosapentaenoic acid (HPA free acid; C21:5 n-3) and (4Z,7Z,10Z,13Z,16Z)-nonadeca-4,7,10,13,16-pentaenoic acid (NPA free acid; C19:5 ω-3) were purchased from Cayman Chemicals (Michigan, USA). D(+)-Glucose (cell culture tested), sodium pyruvate, L-Gin (cell culture tested), acetyl chloride, N,O-bis(trimethylsilyl)acetamide, sodium chloride, sodium phosphate, EDTA (ethylenediaminetetraacetic acid), and Tris-base were purchased from Sigma-Aldrich. Conversely, chloroform, ethanol, methanol, cenRnn / zznz / E / YiAi carried out in the absence of light and under a nitrogen atmosphere. go L·)d) ---► RCH2CO2Me ► Scheme 1. crnRnn / zznz / B / YiAi Hydrochloric acid and hexane were obtained from Scharlab (Spain). Heparin (5000 units / ml) was purchased from Hospira Invicta SA (Spain), ketamine (Anesketin 100 mg / ml) from Eurovet Animal Health BV (Netherlands), xylazine (Xilagesic 20 mg / ml) from Laboratorios Calier SA (Spain), and oxythiamine hydrochloride from Santa Cruz Biotechnology (Germany). For the production of HPA, the chemical synthesis is carried out starting from (5Z,8Z,11Z,14Z,17Z)-eicosa-5,8,11,14,17pentaenoic acid (EPA (C20:5, ω-3)), according to reaction scheme 1. The chemical synthesis of HPA is disclosed in the prior art (Larsen et al., 1997, Lipids 32(7), 707-714. doi: 10.1007 / s11745-997-0090-4). The reactions were h) RCOC1 ------* rcohn2 3 rch2co2h Reagents and conditions: a) (COCl)2 / PhH 1.5h rt., b) CH2N2 / ether 20 min. 0°C, c) AgOBz(cat.), Et3N / THF / H2O The synthesis of the HPA sodium salt of the present invention was carried out starting from the compound designated with the number 5 when R is CH3-CH2-(CH=CH-CH2)5-CH2CH2-, which corresponds to HPA (C21). The salt is obtained under an acid-base reaction, a liquid-liquid extraction is performed with MTBE / HCl, and the pH is adjusted with NaOMe to obtain the HPA sodium salt in good yields. A similar procedure can be carried out for the synthesis of HDA, HTA ω-3, HTA ω-6, NTA, and NRA, by adjusting the starting substrate. 1.2. OHOA, OAy C17:1 n-9 The lipid compounds sodium salt of 2OHOA, sodium salt of OA and sodium salt of C17:1n-9 were acquired from Medalchemy, SL (Spain). The chemical synthesis of C17:1 n-9 is disclosed in WO1997049667. A solution of 8Z-heptadecene (66 mg, 0.26 mmol, 1 equivalent) and 2-methyl-2-butane (1.6 mL, 15.1 mmol, 58 equivalents) in tBuOH (6.5 mL) at 25°C, in an atmosphere of N2, is treated by adding dropwise (2.5 mL) of a solution of NaClO2 (80%, 208 mg, 2.3 mmol, 9 equivalents) and NaH2PO4.H2O (250 mg, 1.8 mmol, 7 equivalents) in deionized water. The reaction mixture was left to stir for a further 15 minutes, before concentrating it under vacuum. The residue is treated with water (30 mL) and the aqueous layer is extracted with EtOAc (3 x 30 mL). The organic layers are dried with Na₂SO₄, filtered, and concentrated under vacuum. Chromatography (SiO₂, 2 x 13 cm, 10–20% EtOAc—hexane gradient elution) yielded 27 mL (66 mg, 95%) as clear oil. The synthesis of the sodium salt of C₁₇:1n–9 of the present invention was carried out starting from the compound C₁₇:1n–9.The salt is obtained under an acid-base reaction, a liquid-liquid extraction is carried out with MTBE / HCI and the pH is adjusted with NaOMe to obtain the C17:1 n-9 sodium salt with good yields. Example 2: Compositions with DHA-H and HPA The following are some general examples of composition that do not limit the scope of the invention. cenAnn / zznz / E / YiAi Component Composition %w / w Composition %w / w Composition %w / w DHA-H 3.6 0 1.3 HPA 0 3.6 1.3 DMSO 80.0 80.0 80.0 Water 16.4 16.4 16.4 Total 100 100 100 Table 1. Example of topical use formulation Component Composition %w / P Composition %w / P Composition %w / P DHA-H 5 0 2.5 HPA 0 5 2.5 Ethanol (96%v / v) 5 5 5 water 90 90 90 Total 100 100 100 Table 2. Example of oral formulation Component Composition %w / w HPA 63.3 Triglycerides 25.5 Glyceryl monostearate 6.66 Aroma 2.22 Superoxide dismutase 1.11 Colloidal silica 1.11 Total 100 Table 3. Example soft capsule oral formulation: Example 3: Cell assays with DHA-H and HPA To describe the metabolic conversion of DHA-H into HPA(C21:5 ω-3), as well as the conversion of LA-H into HDA ​​(C17:2 ω-6), ALA-H into ΗΤΑ ω-3 (C17:3 ω-3), GLA-H into ΗΤΑ ω-6 (C17:3). ω-6), ARA-H in NTA (C19:4 ω-6), EPA-H in NPA (C19:5 ω-3), were employed cultures of HEK293T cells (Human Embryonic Kidney Cells 293T}, which is an embryonic, non-tumor cell line widely used in human metabolism studies under conditions physiological. HEK293T cells were cultured in Dulbecco's Modified Eagle's Medium (DMEM; Biowest, France), supplemented with 10% FBS (Fetal Bovine Serum; Gibco, Thermo-Fisher), 2 mM L-Gin, 25 mM D(+)-glucose, 1 mM sodium pyruvate, and penicillin / streptomycin. Mouse neuroblastoma N2a cells were maintained in a 1:1 (v:v) mixture of DMEM and Opti-Mem (Gibco, Thermo-Fisher), supplemented with 5% FBS and penicillin / streptomycin. Both cell lines were incubated in a 5% CO2 atmosphere at 37°C. HEK293T cells were incubated with DHA-H and DHA at 10, 30, and 100 μM for 24 hours, and with 30 μM for 6, 48, and 72 hours. These cells were also incubated with LA-H, ALA-H, GLA-H, ARA-H, and EPA-H at 100 μM for 24 hours. HEK293T cells were also incubated with oxythiamine in the presence of DHA-H under the same conditions, at final oxythiamine concentrations of 1 and 10 mM. HEK293T cells were separated from the plates using pipettes with cold phosphate-buffered saline (PBS). The cells were recovered by centrifugation (1000 x g, 10 min at 4°C) and washed twice with cold PBS before being frozen at -80°C. To analyze the levels of DHA-H and DHA in the cell culture medium, 90 mm diameter plates were filled with 11 ml of complete cell culture medium containing 30 pM DHA-H or DHA in the presence or absence of attached HEK293T cells (5.105 cells / plate).The plates were incubated as described above, and 1 ml aliquots were collected from the plates at 0, 6, 24, 48, and 72 hours. Aliquots of the cell culture medium were immediately centrifuged at 1000 x g for 10 min at 4°C to remove any cell suspension, and the cell-free aliquots were stored at -20°C. The U-118 MG, MIA-PaCa 2, and A549 cell lines were obtained from the European Cell Culture Collection (ECACC) through Sigma-Aldrich Co. (St. Louis, MO) and maintained in RPMI (Roswell Park Memorial Institute) (U-118 MG and A549) or DMEM (MIA-PaCa 2) culture medium supplemented with 10% FBS (Gibco, Thermo Fisher) in a 5% CO2 atmosphere at 37°C. The U-118 MG, MIA-PaCa 2, and A549 cells were treated under the conditions described in the assay description to obtain the results in Table 4, optionally in the presence or absence of oxythymine (1 or 10 mM). Cell survival was analyzed in a Bürker chamber using trypan blue vital exclusion staining (Scharlab) or the Cell Proliferation Kit II (Roche).Briefly, cells were seeded in 96-well plates at a density of 3 × 10³ cells per well 24 h before treatment, and then cultured in the presence or absence of compounds of interest at the concentrations and for the times indicated in the figures. After different times, viable cells on the plate were determined by adding XTT according to the manufacturer's instructions. Cells were incubated at 37 °C in 5% CO₂ until a consistent color developed, and absorbance was recorded at 495 nm using a microplate reader with a reference wavelength of 650 nm (FLUOstar Omega, BMG LABTECH, Germany). Human SH-SY5Y neuroblastoma cells were maintained in DMEM-F12 (Invitrogen) supplemented with 10% FBS (Sigma), penicillin / streptomycin (PAA), non-essential amino acids (Sigma), and 2 mM L-Gin (Sigma). Differentiation of these cells to a neuronal phenotype was performed following a standard procedure. Briefly, cells were seeded onto plates pretreated with poly-L-lysine, and 24 h later, the medium was replaced with fresh medium supplemented with 10 μM retinoic acid (Sigma). The cells were then incubated in the dark for 5 days, and the medium was replaced with serum-free medium supplemented with 50 ng / ml human brain-derived neurotrophic factor (hBDNF; Alomone Labs; Tel Aviv, Israel). Finally, the cells were incubated for 6 days to complete differentiation.Neurons were treated for 24 h with the compounds HDA, HTA ω-3, HTA ω-6, NTA, NRA and HRA, at 1, 3 and 10 pm, for 24 hours, before induction of excitotoxicity with NMDA (n-Methyl-DAspartate, 10 mM, Sigma) in a medium containing glycine (530 μM, Sigma) and calcium (10 mM, Sigma). cenAnn / zznz / E / YiAi Treatment with DHA-H results in high cellular levels of HPA compared to prodrug levels in cell cultures (Figure 1B). Figure 1B shows intracellular levels of DHA-H and HPA in HEK293T cells under DHA-H treatment. The accumulation of both compounds is evident depending on the treatment concentration or incubation time, but HPA levels are significantly higher than those of the prodrug after 24 hours of incubation and 30 μM of treatment. The increase in HPA levels is inhibited in the presence of concomitant oxythiamine treatment (partial inhibition at 1 mM and almost total inhibition at 10 mM), a competitive antagonist of 2-hydroxyacyl-CoA lyase (see Figure 1A). In this regard, it has also been shown that endogenous levels of DHA (the native non-hydroxylated form) are not altered by this treatment with DHA-H (Figure 1C). Similarly, Figures 8A-8F show that this same metabolic pathway is valid for other 2-hydroxylated polyunsaturated fatty acids used as prodrugs, such as LA-H, ALA-H, GLA-H, ARA-H, and EPA-H, yielding HDA, HTA ω-3, HTA ω-6, NTA, and NRAP, respectively (chromatograms shown in Figure 9 (A1-F2)). All of these metabolites have demonstrated therapeutic activity, as shown in Figure 10 and Table 4 below. IC50 (μΜ) LI118MG MIA-PaCa2 A549 HDA(C17:2 n-6) 144 ±32 234 ± 18 159 ± 10 HTAn-3 (C17:3 n-3) 129 ±03 216 ±24 166 ±30 HTAn-6 (C17:3 n-6) 235 ± 26 95 ±31 212 ±48 NTA (C19:4 n-6) 113 ± 13 62 ±02 216 ±03 NPA(C19:5 n-3) 90 ±09 91 ± 18 143 ±39 HPA (C21:5 n-3) 124 ±16 58 ±17 228 ± 03 Table 4. IC50 values ​​in cell lines of human glioblastoma (U118 MG), pancreatic cancer (MIA-PaCa 2) and human lung adenocarcinoma (A549) The antitumor activity of the different metabolites described in Figures 8A-8F and 9 (A1-F2) was determined by direct treatment with these molecules (HDA or C17:2 ω-6, HTA ω-3 or C17:3 ω-3, HTA ω-6 or C17:3 ω-6, NTA or C19:4 ω6, NRA or C19:5 ω-3 and HPA or C21:5 ω-3) in tumor cell cultures, on which the IC50 value was determined for each of these compounds (Inhibitory Concentration 50: concentration of compound under study that induces the death of 50% of the tumor cell population). The cell cultures used correspond to different cancer types: U118-MG (grade IV human glioblastoma), MIA-PaCa 2 (pancreatic carcinoma), and A549 (small cell lung adenocarcinoma). The different compounds showed varying IC50 values ​​across the different tumor cell lines, demonstrating the selectivity of some of them in inducing the selective death of certain types of tumor cells. Example 4: In vivo assays with DHA-H and HPA. The 5xFAD model of Alzheimer's disease is a double transgenic PS1 / APP mouse that harbors five human mutations associated with familial AD (Tg6799 line): Swedish (K670N / M671L), Florida 151(I716V), and London (V717I) in APP; and the clinical mutations M146L and L286V in human PS1. Both transgenes are expressed under the control of the Thy-1 promoter, and the mice exhibit cognitive decline starting at 4 months of age (Oackley et al., 2006, Neurosci 26(40), 10129-10140. doi: 10.1523 / jneurosci.1202-06.2006). The 5xFAD transgenic and wild-type (WT) animals were obtained from Jackson Laboratories (USA) and maintained in a B6 / SJL genetic background by crossing heterozygous transgenic mice with B6 / SJL WT (F1) breeders. The animals were housed at a controlled temperature of 22 °C (±2 °C) and 70% humidity, on a 12h-12h light-dark cycle, with free access to a standard laboratory diet (Panlab A03, Barcelona, ​​Spain). Male WT and 5xFAD transgenic mice received orally DHA-H (or DHA) dissolved in 5% ethanol at daily doses of 5, 20, 50, and 200 mg / kg, or the vehicle alone. In a separate trial, these animals were also treated with HPA (20 mg / kg) and DHA-H (20 g / kg) to compare the effect of both compounds in this model. These treatments were initiated when the mice reached 3 months of age (dosed 5 days / week) and continued until 7 months of age. During the final month of treatment, all animals were maintained on a hypocaloric diet to perform selected behavioral spatial learning and memory tests (radial arm maze).A total of 46 animals were used for the study shown in Figure 2A-2B: WT treated with vehicle (n=3), WT treated with DHA-H (20 mg / kg, n=3; and 200 mg / kg, n=3), WT treated with DHA (20 mg / kg, n=3); 5xFAD (n=5) treated with DHA-H (5 mg / kg, n=6; 20 mg / kg, n=5; 50 mg / kg, n=6; and 200 mg / kg, n=7), and 5xFAD (20 mg / kg, n=5) treated with DHA. A total of 20 animals were used in the study shown in Figure 6A–6C: vehicle-treated WT mice (n=5), vehicle-treated 5xFAD mice (n=5), and 5xFAD mice treated with DHA-H (20 mg / kg, n=5) and HPA (20 mg / kg, n=5). After the behavioral test, the mice were maintained on a normal diet (and treatment) for one more week, after which they were anesthetized with an intraperitoneal injection of ketamine / xylazine (100 / 10 mg / kg) and perfused intracardially with 50 mL of heparinized saline. The animals' brains were immediately removed and dissected along the midline on a cold surface.Once the cerebellum was removed, each cerebellar-free half was frozen in liquid nitrogen and stored at -80 °C. NUDE (Swiss) Crl:NU (Ico)Foxn1nu mice (8–12 weeks old, 30–35 g, Charles River Laboratories, Paris, France) were kept in a thermostatically controlled cabinet (28 °C, EHRET, Labor-U-Pharmatechnik) with sterile airflow at 40–60% relative humidity and 12-hour light / dark cycles. Their diet consisted of a standard feed diet (Labdiet 22% rat-mouse breeding, Sodispan) ad libitum. To induce xenographic tumors, 7.5 x 10⁶ U-118 MG cells were inoculated subcutaneously on both sides of the animal's dorsal flank, and after one week the tumors became visible with an approximate volume of 100 mm³. The animals were randomly divided into groups with a similar mean tumor volume and received daily oral treatments for 42 days: vehicle, DHA-H (200 mg / kg) and HPA (200 mg / kg).In the study shown in Figure 3A-3B, animals treated with vehicle (untreated controls; n=6) and animals treated with DHA-H (200 mg / kg; n=9) were included. In Figure 7A-7B, animals treated with vehicle (untreated controls; n=6), animals treated with DHA-H (200 mg / kg; n=8), and animals treated with HPA (200 mg / kg; n=8) were included. Tumor volumes (v) were calculated as v = A² x L / 2, where A is the tumor width and L is its length. After treatment, the mice were euthanized by cervical dislocation, and the xenographic tumors were dissected and frozen in liquid nitrogen at -80°C. All protocols used were approved by the Bioethics Committee of the University of the Balearic Islands and comply with national and international guidelines on animal welfare.In the use of healthy and transgenic mice models of Alzheimer's disease (5xFAD), it was observed that a significant accumulation of HPA occurred at the brain level, while the parent molecule (DHA-H) could not be detected, nor changes in endogenous levels of DHA (native non-hydroxylated form) (Figure 2A). Radial arm maze test. The spatial behavior test was performed as previously described, with some modifications (FiolDeroque et al., 2013, Biogerontology 14(6), 763-775. doi: 10.1007 / s10522-013-9461-4). All animals were isolated and subjected to caloric restriction until reaching 80-85% of their normal body weight, and were maintained under these conditions for one week before the start of the trial and until its conclusion. After dietary restriction and 3 days before the start of the trials, the animals were trained twice daily in the eight-arm radial maze test (LE766 / 8, Panlab SL, Spain) for 3 days. Each mouse was placed in the center of the maze and allowed to search for the reward, a 45 mg food pellet (Dustless Precision Pellets, Bio-Serv, USA), located at the end of each arm. Each session ended when the animal managed to find all eight baited arms or failed to complete all the arms within 10 minutes.The movement of each animal was recorded using a digital video tracking system (LE 8300 with Sedacomv1.3 software, Panlab, SL, Spain). After training, the experimental paradigm began. In all experimental sessions (one session per day), only four arms were baited, compared to the training protocol. Each session ended when the animals successfully located all four baited arms or failed to do so after 10 minutes. Performance was assessed by considering: (1) the time taken to complete the test; (2) the number of working memory errors (WME, re-entry into a previously visited baited arm); (3) the number of reference memory errors (RME, entry into an unbaited arm); and (4) the total number of errors (WME + RME). The test was repeated five days per week for three weeks.Once the test was completed, the animals were fed ad libitum for an extra week before slaughter. In this regard, it can be observed that brain HPA levels in Alzheimer's mouse models show a statistically significant inverse relationship with behavioral parameters in a test assessing spatial and associative memory (radial maze test) (Figure 2B). These results suggest that moderate increases in brain HPA levels are significantly associated with improved spatial cognition. Similarly, direct administration of HPA has effects similar to DHA-H administration on the same behavioral parameters analyzed (Figure 6A-6C). Example 5: Lipid extraction and fatty acid transmethylation relative to Examples 3 and 4 The HEK293T or U-118 MG cells used in the previous examples were lysed with cold hypotonic buffer (1 mM EDTA, 20 mM Tris-HCl [pH 7.4]) by up-and-down pipetting. The cell lysates were pulsed with ultrasound (4 cycles, 10 s / cycle, 10 W) prior to lipid extraction. For brain analysis, tissue from each animal was homogenized in cold PBS at a 1:10 (w:v) ratio in the presence of protease inhibitors (Roche), using a blade homogenizer (Polytron PT3100). The homogenates were sonicated, aliquoted, and stored at -80 °C. Only one aliquot of each sample, containing approximately 8 mg of protein / aliquot, was subjected to lipid extraction. The protein content before lipid extraction was determined by a modified Lowry method (Bio-rad DC Protein Assay). Margaric acid (C17:0) was added to the samples undergoing lipid extraction as an internal standard, and the lipids were extracted with chloroform:methanol (Eggers and Schwudke, 2016). Briefly, 0.75 volumes of the aqueous phase (already containing the biological sample) were mixed with 2 volumes of chloroform and 1 volume of methanol. This mixture was vortexed for 1 minute and centrifuged at 1000 x g for 10 minutes. The lower organic phase was collected and washed with 1 mL of PBS:methanol (1:1, v:v), and the resulting organic phase was dried under argon flow. The film containing the extracted lipids was transmethylated by incubating the lipid mixture for 90 minutes at 100°C in 3 ml of methanol:acetyl chloride (10:1, v:v), under an argon atmosphere (Christie, 1993).The resulting fatty acid methyl esters (FAMEs) were extracted with hexane by adding 3 mL of water and 1 mL of hexane to the transmethylation reaction and thoroughly vortexing the mixture. After centrifugation at room temperature (1000 x g for 10 min), the upper phase containing the FAMEs was collected, and the remaining volume was washed twice with 1 mL of hexane. The hexane phases were combined, evaporated under argon flow, and resuspended in 60 mL of hexane (for the analysis of cell samples, cell culture medium, and blood plasma) or in 200 mL (for the analysis of brain samples). To check if a fatty acid compound is hydroxylated, the isolated FAMEs were subjected to a second derivatization with trimethylsilyl (Alderson et al., 2004, J Biol Chem 279(47), 48562-48568. dol: 10.1074 / jbc.M406649200).Briefly, the FAMEs were dried under argon flow, and the lipid film was dissolved in N,O-bis(trimethylsilylyl) acetamide (0.1–5.0 mg of lipids per 200–400 µL of trimethylsilylation reagent), which was then heated in a capped vial at 70°C for 30 min. The solvent was evaporated, and the lipid film was resuspended in hexane for analysis. When the fatty acid under study is hydroxylated, the retention time of the FAME changes as a result of this second derivatization. However, if the fatty acid under study is not hydroxylated, the resulting FAME exhibits the same retention time regardless of the second derivatization. HPA levels generated by treatment with the prodrug DHA-H in these cells were evaluated in the presence or absence of oxythiamine (a competitive inhibitor of α-oxidation) (Figure 4A). The results showed that the addition of DHA-H to a culture of U-118 MG cells led to a significant increase in HPA levels. This increase was inhibited in the presence of simultaneous treatment with 1 or 10 mM oxythiamine, demonstrating that the transformation of DHA-H to HPA is mediated by α-oxidation. Treatment of cultured U-118 MG cells with DHA-H had no effect on endogenous DHA levels (native, non-hydroxylated form). On the same cultured cells, viability tests were carried out with DHA-H in the presence or absence of 1 mM oxythiamine (Figure 4B), confirming that 1 mM oxythiamine has no effect on cell viability. On the other hand, the addition of DHA-H (150 μM, 48 h) exhibits a significant anti-proliferative effect on U118MG cells. However, this effect is partially reversed (statistically significant) in the presence of 1 mM oxythiamine. It should be noted that this concentration of oxythiamine is sufficient to completely inhibit the increase in HPA levels induced by DHA-H. Therefore, these results show that the anti-proliferative effect mediated by DHA-H on U-118 MG cells is mediated, at least in part, by HPA, since the inhibition of the formation of this compound from DHA-H results in a lower anti-proliferative effect of DHA-H (Figure 4B). The anti-proliferative effect of HPA on a culture of U-118 MG cells was also studied, in comparison with the administration of the prodrug DHA-H and the native form of DHA.The anti-proliferative effect of U-118 MG is significantly greater for HPA compared to DHA-H and DHA (see Figure 5A). When compared to DHA-H, this effect can be explained by differences in intracellular HPA levels induced by DHA-H and HPA (see Figure 5B). In fact, Figure 5C shows that the uptake of the hydroxylated form of DHA is inhibited compared to that of the non-hydroxylated analog. Example 6: In vitro assays with 2OHOA and C17:1n-9. The concentrations of 2OHOA sodium salt used in the experiments described below and the duration of the treatments varied according to the type of assay, being 200 μM or 400 μM and 24 or 72 hours. In some experimental series, C17:1 n-9 sodium salt solutions were used at a concentration of 200 μM for 24 or 72 hours. To prepare these solutions, a 100mM stock aliquot was used. To prepare this starting aliquot, the corresponding milligrams of the lipid compound (in powder form) were dissolved in absolute ethanol and autoclaved distilled water (1:1 volume, normally a 1 ml aliquot is prepared, so 500 ml of ethanol and 500 ml of water are added) inside a culture chamber. The solution was then placed in the culture oven at 37°C for 10 minutes to dissolve the lipid compound and subsequently subjected to agitation. 6.1. Incorporation and metabolism of 2OHOA in U-118 MG and non-tumor glioma cells. To confirm the incorporation of 2OHOA into glioma cell membranes and to determine whether changes in the fatty acid profile occurred after 2OHOA treatment, total lipids were analyzed by gas chromatography in human U-118 MG glioma cells incubated in the absence (control) or presence of 400 μM of 2OHOA sodium salt for 24 h. Analysis of fatty acid levels in glioma cells revealed no change in OA levels after treatment with 2OHOA sodium salt compared to the control (Figure 12A-12B). Furthermore, cellular incorporation of 2OHOA was observed after 24 h of treatment due to the identification of a peak in the chromatogram, exclusively in treated cells, that corresponded to the standard. Notably, a new peak appeared almost exclusively in the chromatogram of the treated cells.High levels of this new peak were detected in the treated cells, accumulating almost twice as much (19.71 ± 0.39 nmol / mg protein) as 2OHOA (10.81 ± 0.34 nmol / mg protein). After various studies to determine its identity, it was confirmed that this new peak corresponded to the fatty acid cis-8-heptadecenoic acid (C17:1n-9). The formation of C17:1n-9 is a consequence of the oxidation of 2OHOA (Figure 11). 6.2. Analysis of fatty acid composition in different glioma and tumor cells after treatment with 2OHOA sodium salt. The fatty acid composition of lipid membranes in other glioma cell lines (U-251 MG and SF-295) was analyzed and compared to non-tumor cells, human fibroblasts (MRC-5), and primary mouse astrocyte cultures after incubation in the absence or presence of 2OHOA sodium salt (400 μM, 24 hours) using gas chromatography. No significant change in the amount of OA was observed after treatment with 2OHOA sodium salt in any of the cell lines analyzed (Figure 13A-13H). However, incorporation of 2OHOA, as well as the formation of the C17:1n-9 metabolite, was observed in both other glioma and non-tumor cell lines after 24 hours of treatment with 2OHOA (Figure 13A-13H). The formation of the C17:1n-9 metabolite, from the incorporation of 2OHOA, differs between tumor and non-tumor cells.Glioma cells (U-251 MG and SF-295) showed a significant increase in their C17:1n-9 levels, accumulating 97.42% and 108.03% more than 2OHOA (19.16 ± 0.53 vs. 9.21 ± 0.41 and 18.38 ± 1.97 vs. 9.31 ± 1.44 nmol / mg, respectively) (Figure 13B and 13D, Table 5). In contrast, in non-tumor cells, the detected levels of 2OHOA were significantly higher than those of its metabolite C17:1 n-9. 46% more 2OHOA was accumulated compared to its C17:1 n-9 metabolite in human MRC-5 fibroblasts (26.31 ± 4.32 vs. 14.00 ± 1.92 nmol / mg) and 38.27% more in mouse astrocytes (12.28 ± 0.90 vs. 7.58 ± 0.70 nmol / mg) (Figure 13F and 13H, Table 5). U-118MG_____________U-251MG______________ Control 2OHOA Control 2OHOA Control 2OHOA 2OHOA 0.00 = 0.00 10.81 = 0.34 0.00 = 0.00 9.31 = 1.44 0.00 = 0.00 9.21 = 0.41 C17:ln-9 0.00 = 0.57 19.71 = 0.39 1.65 = 0.66 18.38 = 1.97 1.08 = 0.59 19.16 = 0.53 MRC-5 ASTROCYTES 2OHOA Control 2OHOA Control 2OHOA 0.00 = 0.00 26.31 = 4.32 0.00 = 0.00 12.28 = 0.90 C17:ln-9 1.08 = 0.46 14.00=1.92 2.30 = 0.34 7.58 = 0.70 Table 5: Levels of the fatty acids 2OHOA and C17:1 n-9 in different glioma and non-tumor cell lines after treatment with 2OHOA. Values ​​of the fatty acids 2OHOA and C17:1 n-9 in different glioma cell lines, U-118 MG, U-251 MG, and SF-295 (top) and non-tumor cell lines, MRC-5 and astrocytes (bottom), after treatment with 2OHOA (400 μM for 24 hours) determined by gas chromatography. The results correspond to the mean ± SEM of three independent experiments, expressed in nmoles and normalized per mg of protein. 6.3. Effect of 2OHOA, C17:1 n-9 on the viability and cell proliferation of glioma cells To evaluate the antiproliferative effect of C17:1 n-9, its IC50 was determined. This IC50 represents the amount of a compound required to reduce cell viability in vitro by 50%. The IC50 was also assessed to determine its effect on the regulation of proteins involved in the 2OHOA mechanism of action. Glioma cell lines (U-118 MG, U-251 MG, and SF-295) and non-tumor cell lines (MRC-5 and astrocytes) were treated with increasing concentrations of C17:1n-9 sodium salt, OA, and sodium 2OHOA for 72 hours. After treatment, the IC50 was determined using crystal violet staining. The results of the cell viability assays showed how the three compounds, 2OHOA, OA and C17:1 n-9, had an antiproliferative effect on all glioma cells analyzed, in a concentration-dependent manner, after 72 hours of treatment.On the other hand, in the non-tumor cells studied, MRC-5 and astrocytes, no effect of 2OHOA on cell viability was observed, but the fatty acids OA and C17:1 n-9 did produce an antiproliferative effect in the same non-tumor cells (Figures 14 (A1-C3) and 15 (A1-B3)). The IC50 values ​​of the sodium salt of 2OHOA were 432.75 ± 10.77, 429.96 ± 9.67, and 399.14 ± 11.47 μM in U-118 MG, U-251 MG, and SF-295 glioma cells, respectively (Table 6). In the non-tumor cells, MRC-5 and astrocytes, the IC50 values ​​of 2OHOA were 1000 μM in both cases. Regarding the C17:1 n-9 compound, the IC5o values ​​were 222.04 ± 9.09, 220.35 ± 7.93 and 248.85 ± 6.02 μM in U-118 MG, U-251 MG and SF-295 glioma cells, respectively. Therefore, C17:1 n-9 induced a very similar antiproliferative effect in both glioma and non-tumor cells. In contrast, treatment with 2OHOA only affected the viability of the different glioma cell lines, without affecting the viability of non-tumor cells. The IC50 values ​​of 2OHOA were 1.90, 1.95, and 1.60 times higher than those of its metabolite C17:1n-9 in U-118 MG, U-251 MG, and SF-295 glioma cells, respectively (Table 6). Furthermore, the IC50 values ​​of 2OHOA were 1.92, 1.80, and 1.56 times higher than those of its non-hydroxylated analogue, OA. The fact that C17:1 n-9 has shown greater antiproliferative potency may be due to its greater capacity to accumulate in cells than 2OHOA. crnRnn / zznz / B / YiAi U-118MG U-251 MG SF-295 MRC-5 Astrocytes 2OHOA 432.75=10.77 429.96=9.67 399.14=11.47 1000 1000.00 OA 225.68=7.30 236.96=6.52 256.06=5.79 236.31=6.73 256.35 5.14 C17:ln-9 222.04 = 9.09 220.35=7.93 248.85=6.02 248.03=7.28 231.816.41 Table 6. IC50 values ​​of different cell lines after treatment with 2OHOA, OA and C17:1n-9. Summary of IC50 values ​​for glioma cell lines (U-118 MG, U-251 MG and SF-295) and non-tumor cells (MRC-5 and astrocytes), calculated from the results obtained in Figures 16A-16E and 17A-17B. The IC50 values ​​obtained correspond to the mean of three independent experiments and were calculated using a dose-response equation with the statistical program GraphPad Prism 6.0 (sigmoid model). 6.4. Analysis of the effect of different fatty acids on markers of proliferation and death in different cell lines The effect of the C17:1n-9 metabolite on different signaling pathways altered by the effect of 2OHOA was analyzed. To this end, different glioma cell lines (U-118 MG, U-251 MG and SF-295) and non-tumor cell lines (MRC-5 and mouse astrocytes) were treated with doses close to the IC50 of each of the compounds (200 μM of C17:1 n.9, 200 μM of OA or 400 μM of 2OHOA) for 72 hours and their effect on different signaling proteins was analyzed by Western Blot. The results showed that treatment with 2OHOA increased BIP and CHOP levels and cJun phosphorylation, while decreasing Akt phosphorylation and cyclin D3 levels. In contrast, treatment with C17:1 n-9 produced no changes in any of these proteins (Figure 16A-16E). This suggests that cell death induced by the C17:1 n-9 metabolite is triggered through pathways different from those of 2OHOA. 6.5. Analysis of the fatty acid composition in U-118 MG glioma cells after inhibition of oxidation and determination of the effect of oxythiamine on cell survival of cytotoxic U-118 glioma cells of oxythiamine at these concentrations. 6.6. Effect of the C17:1 n-9 metabolite on the action of 2OHOA To investigate whether the C17:1 n-9 metabolite can participate in the action of 2OHOA, the effect of oxythiamine pre-incubation on cell survival and 2OHOA-regulated proteins was studied. Cell survival in different glioma and non-tumor cell lines treated with 2OHOA (400 μM, 72 hours) and pre-incubated or not with 2 mM oxythiamine (90 minutes) was analyzed by counting cells using trypan blue vital exclusion staining. In addition, 2OHOA-modulated proteins were studied by Western blot. In glioma cells, a significant decrease in cell survival was observed after incubation with 2 mM oxythiamine for 72 hours. Oxythiamine induced 18.51 ± 0.58% and 17.35 ± 0.63% cell death in U-251 MG and SF-295 cells, respectively (Figure 18A and 18B). These results support the in vitro antitumor effect of oxythiamine in glioma cells.Treatment of cells with 2OHOA induced 23.22 ± 1.32% and 23.97 ± 1.25% cell death in U251 MG and SF-295 cells, respectively. Following combination with 2 mM oxythiamine, a significant recovery in cell viability was observed, with 12% (14.07 ± 1.62% cell death in U-251 MG cells) and 17.25% (10.85 ± 0.58% cell death) in SF-295 cells. In contrast, in non-tumor cells, none of the tested treatments had any effect on cell survival (Figure 18C and 18D). Regarding the study of proteins involved in different signaling and cell death pathways in glioma cells, oxythiamine showed an effect on the levels of BIP, CHOP, c-Jun phosphorylation, Akt phosphorylation, and cyclin D3 in glioma cells in the same direction as 2OHOA, although to a lesser extent (Figure 19A-19C). When combined, oxythiamine inhibited the modulation induced by 2OHOA. This finding confirms that the metabolism of 2OHOA at C17:1 n-9 is necessary to enhance its antitumor activity. Conversely, no changes were observed in these signaling proteins in non-tumor cell lines after any of the treatments (Figure 19A-19C).Although 2OHOA has antiproliferative activity when its metabolism at C17:1 n-9 is inhibited, the formation of the C17:1n-9 metabolite has a major impact on the mechanism of action of 2OHOA, enhancing its antiproliferative effect, and confirms that 2OHOA is also a prodrug that gives rise to an active 17:1 n-9 metabolite. Example 7: In vivo tests with 2OHOA and C17:1n-9. 7.1 Analysis of the fatty acid composition in plasma of rats after 24 hours of treatment with 2OHOA The pharmacokinetic profile of 2OHOA and its C17:1 n-9 metabolite was studied in animal plasma. In this case, rats were used as the experimental animal model. Rats have a larger blood volume than mice, making them the most suitable model for studying the effect of continuous administration of the maximum tolerated dose of 2OHOA (2 g / kg) defined in preclinical studies. For this study, 2 g of 2OHOA sodium salt / kg were administered orally to 12-14 week old rats for 15 days. Plasma samples were then collected at different time points (0, 1, 2, 3, 4, 6, 8, and 24 h) on days 1 (acute treatment) and 15 (chronic treatment). Finally, the fatty acid profile of the plasma samples was analyzed using gas chromatography. Analysis of the chromatograms revealed the detection of 2OHOA and C17:1 n-9 fatty acids in the plasma samples collected after the acute treatment (administration of cenAnn / zznz / E / YiAi on day 1) (Figure 20A). The two compounds, 2OHOA and C17:1 n-9, showed a very similar pharmacokinetic profile in rat plasma after acute treatment (Figure 20B). A significant increase in the levels of 2OHOA and C17:1n-9 was observed, reaching a maximum plasma concentration 2 hours after administration of 2OHOA (26.23 ± 5.79 nmol of 2OHOA / ml of plasma and 60.47 ± 6.53 nmol of C17:1 n-9 / ml of plasma). A subsequent decrease in the plasma levels of 2OHOA and C17:1 n-9 occurred, reaching minimum values ​​at 24 hours (2.80 ± 0.69 and 14.03 ± 2.20 nmol / ml of plasma, respectively). However, baseline levels were not reached, especially in the case of C17:1 n-9 (1.22 ± 0.33 and 8.45 ± 2.52 nmol / mL of plasma, respectively). C17:1 n-9 metabolite levels after chronic treatment were higher than those of 2OHOA (Figure 21B). The differences between the two compounds were significant before 2OHOA administration (0 hours; 1.22 ± 0.33 nmol of 2OHOA / ml of plasma, compared to 8.45 ± 2.52 nmol of C17:1 n9 / plasma), after 8 hours (7.12 ± 1.56 nmol of 2OHOA / ml of plasma, compared to 23.31 ± 5.18 nmol of C17:1 η-9 / plasma) and after 24 hours (2.80 ± 0.69 nmol of 2OHOA / ml plasma, compared to 14.03 ±2.21 nmol of C17:1 η-9 / plasma). 7.2. Analysis of the fatty acid composition of xenographic tumors from immunodeficient mice. To study the effects of C17:1 n-9 formation, a product of 2OHOA metabolism via oxidation, the levels of this metabolite were detected and analyzed in animal models, compared to those of 2OHOA, in a xenogeneic tumor model in immunocompromised mice. For this purpose, U-118 MG glioblastoma cells were injected into immunocompromised mice, and one week later, the mice were treated orally daily for 42 days with 2OHOA sodium salt (200 mg / kg) for 42 days. After treatment, the mice were euthanized, the tumors were removed, and the lipids were processed by gas chromatography to detect the fatty acids 2OHOA and C17:1 n-9. The fatty acid 2OHOA was not detected in xenographic tumors of mice treated with this compound, as no peak was observed in the retention time corresponding to 2OHOA (Figure 22A).However, the 2OHOA metabolite, the fatty acid C17:1n-9 (0.25 ± 0.04 nmol C17:1 η-9 / g tissue), was detected in the tumors of mice treated with 2OHOA (Figure 22B). 7.3. Correlation between tumor volume and the amount of the C17:1n-9 metabolite. We investigated whether there was a correlation between the levels of the C17:1 n-9 metabolite present in tumors and tumor volume, as an indicator of the relationship between the incorporation and metabolism of 2OHOA and the compound's efficacy in tumors. The graphs obtained showed a negative correlation between the amount of C17:1 n-9 present in the tumors and their volume (Figure 23). A coefficient of determination (r) of -0.8248 and a p-value of 0.0001 were obtained for tumors of mice treated with 2OHOA between the amount of C17:1 n-9 and tumor volume. That is, the smaller the tumor volume, the greater the amount of the C17:1 n-9 metabolite detected in it. These results demonstrate that the C17:1 n-9 metabolite has marked antitumor activity and that 2OHOA is an effective prodrug of this compound. 7.4. Analysis of fatty acid composition in human patients with advanced glioma after treatment with 2OHOA The detection and quantification of the fatty acids 2OHOA and C17:1 n-9 were carried out in plasma samples from 8 patients who responded, or did not respond, to treatment with 12 g / day of 2OHOA sodium salt for at least one 3-week cycle in the 2OHOA clinical phase l / lIA (MIN-001-1203). Plasma samples were obtained at different time points (0, 2, 4, 6, 8 hours and after 8, 15, 21, and 28 days after 2OHOA treatment) and subsequently submitted for fatty acid analysis using gas chromatography. 2OHOA and its metabolite C17:1n-9 were detected in all patient plasma samples analyzed (Figure 24A). A very similar pharmacokinetic profile was observed in all patients, both those who showed a clinical response (responders) and those who did not (non-responders) (Figure 24B). Both compounds reached peak levels 4 hours after administration with 2OHOA. Analyzing the results of all patients, responders and non-responders, values ​​of 53.08 ± 6.52 nmol of 2OHOA / ml of plasma and 122.80 ± 10.61 nmol of C17:1 n-9 / ml of plasma were obtained 4 hours after the first dose of the drug (Figure 24C). Subsequently, the levels of 2OHOA and C17:1n-9 gradually decreased until 8 hours after treatment (25.39 ± 3.99 and 92.89 ± 9.39 nmol / ml of plasma, respectively).At 8 days of treatment (192 hours), a significant increase in the plasma concentrations of both compounds was observed (25.39 ± 3.99 nmol / ml of 2OHOA plasma and 141.10 ± 16.35 nmol / ml of C17:1n-9 plasma). The compounds 2OHOA and C17:1n-9 accumulated in the patients' plasma over time, as observed after 15 days (360 hours) of treatment with 2OHOA (184.70 ± 25.60 and 366.9 ± 72.47 nmol / ml of 2OHOA and C17:1n-9 plasma, respectively) (Figure 24C). It is worth noting that, similar to what occurred in cells and animals, plasma levels of the metabolite C17:1 n-9 in all patients were higher than those of 2OHOA (Figure 14B), being significantly higher from 8 hours after 2OHOA administration (Figure 24C). C17:1 n-9 levels were observed to be 3.66 and 2.20 times higher than those of 2OHOA in patients who had been treated with 2OHOA for 8 and 15 days, respectively (92.89 ± 9.39 and 311.10 ± 37).38 and nmol of C17:1 n-9 / ml of plasma compared to 25.39 ± 3.99 and 141.10 ± 16.35 nmol of 2OHOA / ml of plasma, respectively). Finally, after 21 days of treatment with 2OHOA, the levels of C17:1 n-9 were 1.90 times higher than those of 2OHOA (366.9 ± 72.47 nmol of C17:1 n-9 / ml of plasma compared to 184.70 ± 25.60 nmol of 20H0A / ml of plasma, respectively).

Claims

1. A pharmaceutically or nutraceutically acceptable salt or ester of a compound selected from the group consisting of: a compound of formula (II): COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (H) and a compound of formula (III): COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)^^ (III); wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and wherein a+3b+c+3 is an even integer.

2. A salt or an ester according to claim 1, wherein c is 0.3 or 6 and m=0.

3. A salt or ester of a compound of formula (II), according to claim 1, wherein: a=6, b=1 and c=6; oa=6, b=2 and c=3; oa=6, b=3 and c=0; oa=3, b=3 and c=3; oa=2, b=4 and c=3; oa=2, b=5 and c=0.

4. A salt or ester of formula (III), according to claim 1, wherein a=1, b=3, c=0 and m=0.

5. A salt or ester according to any of claims 1 to 4, wherein said pharmaceutically or nutraceutically acceptable salt is a sodium salt.

6. A salt or ester according to any of claims 1 to 5, for use as a medicament.

7. A salt or ester according to any one of claims 1 to 5, for use in the induction of neuroregeneration and in the prevention and / or treatment of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease.

8. A salt or ester for use according to claim 7, wherein the prevention and / or treatment or induction of neuroregeneration is characterized by the administration of a compound of formula (I), or a pharmaceutically acceptable salt or ester thereof: cenAnn / zznz / E / YiAi COOH-CHOH-(CH2)a-(CH=CH-CH2MCH2)c-CH3 (l) wherein the values ​​of a, b and c are equal to the values ​​of a, b and c of the compound of formula (II) or of the compound of formula (III); and wherein said compound of formula (I) is metabolized to produce a therapeutically effective amount of a compound of formula (II) or of a compound of formula (III).

9. A salt or ester for use according to claim 7, characterized in that said compound is administered before, after, or in conjunction with a compound of formula (I) or a pharmaceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; and a+3b+c+3 is an even integer; and wherein said values ​​of a, b, and c are equal to or different from the values ​​of a, b, and c of the compound of formula (II) or of the compound of formula (III).

10. A pharmaceutical or nutraceutical composition comprising at least a first compound selected from the group consisting of: a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (II): COOH-(CH2)a-(CH=CH-CH2) / >-(CH2)c-CH3 (H) and a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (III): COOH-(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)fM.mr(CH2)c-CH3 (III); wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b - 1); and a+3b+c+3 is an even integer; and at least one pharmaceutically or nutraceutically acceptable excipient.

11. Pharmaceutical or nutraceutical composition according to claim 10, further comprising a second compound of formula (I), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2MCH2)c-CH3 (i) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14 and a+3b+c+3 is an even integer; and wherein said values ​​of a, b and c of the second compound are equal to or different from the values ​​of a, b and c of the at least first compound.

12. Pharmaceutical or nutraceutical composition according to any of claims 10 or 11, wherein c is 0, 3 or 6 and m=0.

13. Pharmaceutical or nutraceutical composition according to any of claims 10 or 11, wherein at least the first compound is a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (II), wherein: a=6, b=1 and c=6; oa=6, b=2 and c=3; oa=6, b=3 and c=0; oa=3, b=3 and c=3; oa=2, b=4 and c=3; oa=2, b=5 and c=0.

14. Pharmaceutical or nutraceutical composition according to any of claims 10 or 11, wherein the at least first compound is a pharmaceutically or nutraceutically acceptable salt or ester of a compound of formula (III), wherein a=1, b=6, c=0 and m=0.

15. Pharmaceutical or nutraceutical composition according to any of claims 10 to 14, wherein the pharmaceutically acceptable salt is a sodium salt.

16. Pharmaceutical composition according to any of claims 10 to 15, for use as a medicament.

17. Pharmaceutical composition according to any of claims 10 to 15, for use in the induction of neuroregeneration and in the prevention and / or treatment of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease.

18. Nutraceutical composition according to any of claims 10 to 15, for use in the prevention of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease.

19. An in vitro method for determining the efficacy of a therapeutic or preventive treatment for a disease or pathology with a compound of formula (I), or with a pharmaceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2MCH2)c-CH3 (l) in a subject, wherein said method comprises determining in vitro in a biological sample from said subject, the amount of a compound: of formula (II): COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (H) or of formula (III): COOH -(CH2)a-(CH=CH-CH2)nr(CH2)3-(CH=CH-CH2)fW(CH2)c-CH3 (III) or of its carboxylate anion, or of a derivative formed therefrom in vivo or in vitro, wherein said amount is related to the efficacy of the treatment for said disease or pathology; and where a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; m is an integer between 0 and (b -1); and where a+3b+c+3 is an even integer.

20. Method according to claim 19, wherein c is 0.3 or 6 and m=Q.

21. Method according to claim 19, wherein said method comprises determining in vitro in a biological sample of said subject, the amount of a compound of formula (II): COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (II) or of its carboxylate anion, or of a derivative formed from the same in vivo or in vitro, and wherein: a=6, b=1 and c=6; oa=6, b=2 and c=3; oa=6, b=3 and c=0; oa=3, b=3 and c=3; oa=2, b=4 and c=3; oa=2, b=5 and c=0.

22. Method according to claim 19, wherein said method comprises determining in vitro in a biological sample of said subject, the amount of a compound of formula (III): COOH -(CH2)a-(CH=CH-CH2)m-(CH2)3-(CH=CH-CH2)ÍW(CH2)c-CH3 (III) or of its carboxylate anion, or of a derivative formed from the same in vivo or in vitro, and wherein a=1, b=6, c=0 and m=0.

23. Method according to any of claims 19 to 22, wherein the pharmaceutically acceptable salt is a sodium salt.

24. A compound of formula (II): COOH -(CH2)a-(CH=CH-CH2)í,-(CH2)c-CH3 (H) where: a=6, b=1 and c=6; oa=6, b=2 and c=3; oa=6, b=3 and c=0; oa=3, b=3 and c=3; oa=2, 5=4 and c=3; or a=2, b=5 and c=0.

25. A compound according to claim 24 for use as a medicament.

26. A compound according to claim 24 for use in the induction of neuroregeneration and in the prevention and / or treatment of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease.

27. A compound for use according to claim 26, wherein the prevention and / or treatment or induction of neuroregeneration is characterized by the administration of a compound of formula (I), or a pharmaceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2HCH2)c-CH3 (i) wherein the values ​​of a, b and c are equal to the values ​​of a, b and c of the compound of formula (II) or of the compound of formula (III); and wherein said compound of formula (I) is metabolized to produce a therapeutically effective amount of a compound of formula (II) or of a compound of formula (III).

28. A compound for use according to claim 26, characterized in that said compound is administered before, after, or in conjunction with a compound of formula (I) or a pharmaceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14; and a+35+c+3 is an even integer; and wherein said values ​​of a, b, and c are equal to or different from the values ​​of a, b, and c of the compound of formula (II).

29. A pharmaceutical or nutraceutical composition comprising at least a first compound of formula (II): COOH -(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (H) wherein a=6, b=1 and c=6; oa=6, b=2 and c=3; oa=6, b=3 and c=0; oa=3, b=3 and c=3; oa=2, b=4 and c=3; oa=2, b=5 and c=0; and at least one pharmaceutically or nutraceutically acceptable excipient.

30. Pharmaceutical or nutraceutical composition according to claim 29, further comprising a second compound of formula (I), or a pharmaceutically or nutraceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (i) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14 and a+3b+c+3 is an even integer; and wherein said values ​​of a, b and c of the second compound are equal to or different from the values ​​of a, b and c of the at least first compound.

31. Pharmaceutical composition according to any of claims 29 or 30, for use as a medicament.

32. Pharmaceutical composition according to any of claims 29 or 30, for use in the induction of neuroregeneration and in the prevention and / or treatment of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease.

33. Nutraceutical composition according to any of claims 29 or 30, for use in the prevention of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease; a cancer; a neoplasm; an inflammatory disease; a cardiovascular disease; a pathology of the skin and subcutaneous tissue; a metabolic pathology; neuropathic pain; paralysis; sleep disorders; a digestive pathology; a musculoskeletal and connective tissue disease; a genitourinary pathology; and a metabolic disease.

34. A compound of formula (III): COOH -(CH2)a+r(CH=CH-CH2)Mr(CH2)c-CH3 (III); wherein a=1, b=Q, c=0 and m=0, for use in the induction of neuroregeneration and in the prevention and / or treatment of a selected disease or pathology from the group consisting of: a neurological or neurodegenerative disease, neuropathic pain, and paralysis. cenAnn / zznz / E / YiAi 35. A pharmaceutical composition comprising at least a first compound of formula (III): COOH -(CH2)a+r(CH=CH-CH2)Mj-(CH2)c-CH3 (III); wherein a=1, b=6, c=0 and m=0, and at least one pharmaceutically acceptable excipient, for use in the induction of neuroregeneration and in the prevention and / or treatment of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease, neuropathic pain and paralysis.

36. A pharmaceutical composition for use according to claim 35, further comprising a second compound of formula (I), or a pharmaceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2)b-(CH2)c-CH3 (I) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14 and a+3b+c+3 is an even integer; and wherein said values ​​of a, b, and c of the second compound are equal to or different from the values ​​of a, b, and c of the at least first compound.

37. A nutraceutical composition comprising at least a first compound of formula (III): COOH -(CH2)a+r(CH=CH-CH2W(CH2)c-CH3 (III); wherein a=1, b=6, c=0 and m=Q, and at least one nutraceutically acceptable excipient, for use in the prevention of a disease or pathology selected from the group consisting of: a neurological or neurodegenerative disease, neuropathic pain and paralysis.

38. A nutraceutical composition for use according to claim 37, further comprising a second compound of formula (I), or a nutraceutically acceptable salt or ester thereof: COOH-CHOH-(CH2)a-(CH=CH-CH2HCH2)c-CH3 (l) wherein a is an integer between 1 and 14; b is an integer between 1 and 7; c is an integer between 0 and 14 and a+3b+c+3 is an even integer; and wherein said values ​​of a, b and c of the second compound are equal to or different from the values ​​of a, b and c of the at least first compound.