54 results about "Interferon alfa" patented technology

Provided are methods for treating cancer using local administration of certain CpG oligonucleotides (CpG ODN) and systemic administration of a checkpoint inhibitor such as an anti-PD-1 antibody, an anti-PD-L1 antibody, and / or an anti-CTLA-4 antibody. In preferred embodiments, the CpG ODN are selected based on their propensity to induce high amounts of interferon alpha (IFN-α) and T-cell activation relative to interleukin-10 (IL-10) and B-cell activation. In certain embodiments, the methods further include pretreatment with radiotherapy, to potentiate the combination immunotherapy.

Provided herein, inter alia, are novel compositions and solid forms of Compound 1 useful for the prevention and / or treatment of allergic diseases, inflammatory diseases, metabolic diseases, autoinflammatory diseases, autoimmune diseases, proliferative diseases, transplant rejection, diseases involving impairment of cartilage renewal, congenital cartilage malformations, and / or intermediates associated with IFN [alpha], interferon ("interferon disease", etc. In particular type I or type III interferon disease), diseases associated with excessive secretion of IL-12 and / or IL-23. # imgabs0 #

The present invention discloses compounds according to Formula I:wherein R1a, R1b, R1c, R2a, W1, W2, X1, X2, X3, Y, and Z are as defined herein.The present invention relates to compounds, methods for their production, pharmaceutical compositions comprising the same, and methods of treatment using the same, for the prophylaxis and / or treatment of inflammatory diseases, autoinflammatory diseases, autoimmune diseases, proliferative diseases, fibrotic diseases, transplantation rejection, diseases involving impairment of cartilage turnover, congenital cartilage malformation, diseases involving impairment of bone turnover, diseases associated with hypersecretion of IL-6, diseases associated with hypersecretion of TNFα, interferons, IL-12 and / or IL-23, respiratory diseases, endocrine and / or metabolic diseases, cardiovascular diseases, dermatological diseases, and / or abnormal angiogenesis associated diseases by administering the compound of the invention.

The invention relates to a recombinant human interferon alpha1b solution as well as a preparation method and application thereof, and belongs to the technical field of pharmaceutical preparations. The technical problems that in the prior art, the production cost is increased and the risk of blood virus infection exists due to the fact that the recombinant human alpha interferon spray is prepared from human albumin are solved. The recombinant human interferon alpha 1b solution comprises recombinant human interferon alpha 1b, gelatin, a pH regulator, a surfactant, a bacteriostatic agent and water, and further comprises one or more of an antioxidant, a thickening agent and an osmotic pressure regulator. The recombinant human interferon alpha1b solution is good in product quality and good in stability, can be stored for at least 24 months at the temperature of 2-8 DEG C under the dark condition, and can be stably stored for 3 months under the common indoor condition; the compound can be applied to preparation of medicines for treating or preventing diseases (herpes simplex, herpangina of children, hand-foot-and-mouth disease and respiratory diseases) caused by virus infection.

The present invention relates to the field of biomedicine. Disclosed herein is interferon-based method and pharmaceutical combination for treating cancer. In particular, the present invention relates to an interferon-based method for treating cancer, comprising i) intermittently administering an interferon-based therapeutic agent, and ii) administering an additional anticancer agent, preferably, Gemcitabine, to a subject, wherein said additional anti-cancer agent is administered after the first administration of said intermittent administration of an interferon-based therapeutic agent. The present invention also relates to a pharmaceutical combination for use in said method.

The application discloses CpG-containing oligodeoxynucleotide (ODN) with the function of regulating the body's immune capacity and application thereof. The oligodeoxynucleotide in the application is different from the design concept of traditional A-type CpG ODN in sequence and structure, embodies the complex drug-making rule and overcomes the problem of traditional A-type CPG in drug-making. The oligodeoxynucleotide has excellent activity of regulating the body's immune function in vitro and in vivo, can stimulate the production of I, II and III type interferons, regulates the Th1 type immune response, and inhibits the Th2 type and Th17 type inflammatory response. Therefore, the oligodeoxynucleotide can prevent and treat allergic diseases caused by Th2 type immune response, including allergic rhinitis, atopic dermatitis, asthma, chronic obstructive pulmonary disease, eosinophil and Th17 related diseases, can prevent and treat the infection and spread of respiratory or non-respiratory pathogenic microorganisms including viruses, bacteria, fungi and parasites, can improve the immune level of the elderly and immunodeficient population, can convert "cold tumor" into "hot tumor", improve the effect of cancer immunotherapy, can prevent and treat central nervous system diseases related to immune dysfunction such as Alzheimer's disease, and can be applied to other diseases related to immune dysfunction.

Therapeutic methods and pharmaceutical compositions for treating a myeloproliferative neoplasm (MPN), including polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis, are described. In certain embodiments, the invention includes therapeutic methods of treating a MPN using a combination of a compound of Formula (I) or Formula (II) with a therapeutic agent selected from the group consisting of a JAK inhibitor, an IDH inhibitor, a PD-1 inhibitor, a PD-L1 inhibitor, a PD-L2 inhibitor, an interferon, a PI3K inhibitor, an AKT inhibitor, an mTOR inhibitor, a nucleoside analog, and combinations thereof.

The invention provides an application of dihydroergomine in preparation of a product for treating and / or preventing glioblastoma, and belongs to the technical field of medicines. Researches find that dihydroergomine is specifically combined with an RING structural domain of TRIM47, inhibits the activity of E3 ubiquitin linker enzyme of TRIM47, blocks the TRIM47 from inhibiting activation of STAT1 through ubiquitination modification of STAT1, and promotes activation of interferon on STAT1, so that tumor cell apoptosis is promoted, proliferation and migration are inhibited, and finally tumor growth is inhibited. Dihydroergomine has good anti-glioblastoma activity, has low toxicity to normal cells, and provides more choices and possibilities for treatment of glioblastoma.

The invention discloses a method for screening interferon pathways activated by intervention of glioblastoma, and relates to the technical field of biological medicines. The invention provides a new application of Atopaxar in treatment of glioma, and the clinical application range of the medicine is widened; meanwhile, clear molecular mechanism evidence is provided, and it is proved that the cGAS-STING-1 type interferon pathway is activated to achieve the anti-tumor effect; the invention proposes that Atopaxar has good blood brain barrier penetrating power, solves the bottleneck problem of a traditional immune agonist in central nervous system tumor treatment, and provides a new target spot and strategy for precise immunotherapy of glioblastoma.

The invention discloses a process for synergistically inhibiting melanoma by carrying low-dose paclitaxel on nanoparticles based on immunoregulation. According to the invention, hyaluronic acid functionalized albumin nanoparticles are combined with low-dose paclitaxel, the tumor targeting property of the drug is improved by utilizing a nanotechnology, and meanwhile, the tumor immune microenvironment is regulated and the anti-tumor immune effect is enhanced by activating an STING pathway. Through the combination, the treatment effect of the medicine is improved, the side effect of the medicine is remarkably reduced, and a new strategy is provided for tumor treatment. High-efficiency delivery of low-dose paclitaxel is realized through the nano-carrier, the drug dosage is reduced, the toxicity is reduced, meanwhile, the antitumor activity of the paclitaxel is retained, a new thought is provided for clinical application of traditional chemotherapeutic drugs, the tolerance and life quality of patients are expected to be improved, polarization of M1 type macrophages is promoted by activating an STING pathway, and the antitumor activity of the paclitaxel is improved. Interferon and other inflammatory factors are released, CD8 + T cells are recruited and activated, and therefore the anti-tumor effect is achieved.

The present invention relates to a dry powder formulation of interferon beta and a method for preparing the same, and more particularly, to a dry powder formulation of interferon beta in the form of spherical particles having high morphological integrity prepared by spray drying a liquid composition containing interferon beta, and a method for preparing the dry powder formulation of interferon beta.

The invention relates to the technical field of medicines, and particularly discloses application of interferon alpha combined with stiripentanol in virus infection resistance. As an antiviral drug, interferon alpha has the problems of limited curative effect, remarkable side effect, narrow applicable crowd, inconvenience in medication and the like clinically. The invention finds that the accumulation of host lactic acid in the later stage of virus infection is a key negative factor, and lactic acid directly inhibits the antiviral activity of interferon alpha and induces inflammatory storm. Through combined use of a lactic dehydrogenase inhibitor stiripentol (Stiripentol, STP), lactic acid production is reduced, a lactic acid-mediated antiviral inhibition-inflammation promotion effect is reversed, and the antiviral activity of interferon alpha is enhanced and side effects are reduced. Experiments prove that the combined therapy can effectively inhibit virus replication and inflammatory factor expression, and a new strategy is provided for broad-spectrum antiviral therapy.

A pharmaceutical composition including an active ingredient, wherein the active ingredient includes at least a first drug conjugate having a structure shown by the following formula: Z-(linker-[R]m)n. In the formula, Z is a drug compound, R is a sugar, and m and n are independently an integer from 1 to 6. The drug compound Z is a first drug compound X selected from the group consisting of Tenofovir, Tenofovir diisoproxil, Tenofovir alafenamide, Entecavir, Telbivudine, Adefovir, Adefovir dipivoxil, Lamivudine, Interferon-α-2A, Interferon-α-2B, Selgantolimod, BI-82 and Zosuquidar, and the sugar R is selected from the group consisting of a monosaccharide, a disaccharide, a trisaccharide, a tetrasaccharide, an oligosaccharide, and a polysaccharide.

This invention provides an application of type I interferon signaling pathway inhibitors in the preparation of drugs for treating age-related cataracts. By inhibiting type I interferon receptors, it can precisely intervene in the aging mechanism of lens epithelial cells, block the transmission of aging signals, and directly improve lens transparency, exhibiting higher therapeutic efficacy and targeting. The use of IFNAR inhibitors can effectively reverse the aging phenotype caused by STEAP3 deficiency, restore the proliferative capacity of lens epithelial cells, thereby maintaining lens transparency, significantly reducing surgical risks, and providing patients with an early intervention opportunity, delaying the onset and progression of cataracts. IFNAR inhibitors, through precise intervention in specific signaling pathways, have more significant therapeutic effects, and due to their targeting, have fewer side effects and are safer. They can not only improve existing cataracts but also play a preventive and delaying role in the early stages of cataracts. For patients with mild cataracts, the use of type I interferon receptor inhibitors can avoid premature surgical treatment, reducing patient dependence on surgery and also reducing the costs and risks associated with surgery.

The present disclosure relates to methods and compositions for local expression of IL-12 in mucosal tissues, preferably in combination with an IFN-1 activator / inducer, for use in cancer immunotherapy.SOLUTION: The present invention solves the unmet need in the art for effective local expression of IL-12 using derivatized chitosan polyplexes reversibly coated with polyanion-containing block copolymers for potent transfection of mucosal tissues present in or proximal to tumors.SELECTED DRAWING: Figure 6

This invention discloses compounds of formula I, wherein X1, X2, and R 1 and R 2 As defined herein, this invention relates to compounds for the prevention and / or treatment of the following diseases, methods of their preparation, pharmaceutical compositions comprising them, and methods of treatment using them: inflammatory diseases, autoinflammatory diseases, autoimmune diseases, proliferative diseases, fibrotic diseases, transplant rejection, diseases involving impaired cartilage turnover, congenital cartilage malformations, diseases involving impaired bone turnover, diseases associated with excessive IL-6 secretion, diseases associated with excessive secretion of TNFα, interferon, IL-12, IL-17, and / or IL-23, respiratory diseases, endocrine diseases, metabolic diseases, cardiovascular diseases, skin diseases, and / or diseases associated with abnormal angiogenesis, wherein the methods are carried out by administering the compounds of the invention.

The present disclosure relates to compounds of formula (IA') as STING (stimulator of interferon genes) agonists for use in the treatment of, for example, cancer, obesity, liver injury, glycolipid metabolism, and viral infections. The synthesis and characterization of exemplary compounds and their pharmacological data are disclosed herein (e.g., pages 128-286; Examples 1-54; Tables 1, 2a, 2b, and 3). An exemplary compound is, for example, Example 1: (E)-N-(5-carbamoyl-1-(4-(5-carbamoyl-2-(4-ethyl-2-methyloxazole-5-carboxamide)-7-(3-hydroxypropoxy)-1H-benzo[d]imidazol-1-yl)but-2-en-1-yl)-7-methoxy-1H-benzo[d]imidazol-2-yl)-4-ethyl-2-methyloxazole-5-carboxamide (Compound 9). TIFF2022543086000329.tif89128

The present invention is directed to methods for treating or preventing neuroinflammation in a subject by administering an effective amount of a single-domain antibody (sdAb) comprising SEQ ID NO:1. The method is applicable to subjects with multiple sclerosis, including secondary progressive, primary progressive, and relapsing-remitting forms. Administration may be intravenous, subcutaneous, or intrathecal, with dosage regimens including daily administration, loading and maintenance doses, or continuous infusion. The method may be initiated upon first clinical signs of central nervous system demyelination and contin- ued for at least 14 days. The sdAb may be co-administered with a pharmaceutically acceptable excipient such as mannitol, sucrose, or polysorbate 80, and optionally combined with disease-modifying therapies including interferon-β, glatiramer acetate, fingolimod, or ocrelizumab. The invention provides a targeted approach for modulating neuroinflammatory processes in neurological disorders.

Provided herein are methods for treating a brachyury-associated cancer or neoplasm, e.g., chordoma, with a type I interferon in a subject in need thereof. The methods further include treating the brachyury-associated cancer or neoplasm with interferon alpha or interferon beta by injection of interferon protein into a subject in need thereof, wherein the interferon can be an interferon polypeptide or an interferon nucleic acid formulated for expression.

This invention relates to the field of biomedicine, specifically to the combined application of interferon-alpha (IFN-α) and NF-κB signaling pathway inhibitors, particularly the application of interferon-alpha combined with bortezomib in the preparation of drugs for the prevention and / or treatment of viral infections. Host-produced lactate is a key microenvironmental factor driving the shift of IFN-α from "anti-inflammatory" to "pro-inflammatory." Lactic acid, in conjunction with IFN-α, excessively activates the NF-κB signaling pathway, thereby triggering a cytokine storm. Based on this novel mechanism, this invention creatively proposes the combined use of IFN-α and bortezomib. This combination effectively blocks lactate / IFN-α-induced NF-κB overactivation, retaining the potent antiviral activity of IFN-α while completely reversing its side effect of exacerbating inflammation in the later stages of viral infection, achieving a dual effect of "antiviral" and "inflammatory control."

The invention discloses application of piperlongumine in treating and preventing lung injury, and belongs to the technical field of medicines. Aiming at the technical bottlenecks of limited treatment means and high case fatality rate of the existing acute lung injury (ALI) / acute respiratory distress syndrome (ARDS), the invention discovers that piperlongumine can specifically inhibit cGAS-STING signal channel activation for the first time, and expression release of inflammatory factors IFN-beta, IL-6 and TNF-alpha is reduced by regulating phosphorylation of a downstream interferon regulatory factor 3 (IRF3). In-vitro experiments prove that piperlongumine inhibits ISD-induced inflammatory response in a dose-dependent manner, and in-vivo experiments show that piperlongumine can significantly relieve LPS-induced mouse acute lung tissue inflammatory cell infiltration, reduce serum IL-6 and TNF-alpha levels, and improve lung tissue pathological injury. According to the invention, the medicinal application of piperlongumine is expanded, a new lung injury treatment scheme based on natural active compounds is provided, and the piperlongumine can be widely applied to prevention and treatment of acute lung injury and related inflammatory lung diseases.

Disclosed herein are compositions and methods for modulating IFN-γ-mediated signaling by completely or partially agonizing the downstream signal transduction mediated through at least one of the IFN-γ receptors. More particularly, the disclosure provides novel IFN-γ polypeptide variants with reduced binding affinity to at least one of its receptors. The disclosure also provides compositions and methods useful for producing such molecules, as well as methods for the treatment of health diseases associated with the perturbation of signal transduction mediated by IFN-γ.

Compositions and methods for treating cancer are provided. In particular, the compositions comprise an anti-neoplastic agent and either an interferon type I agonist or an interferon type II agonist, or a combination of an interferon type I agonist and an interferon type II agonist.

The present disclosure provides interferon (IFN) receptor antagonists. The IFN receptor antagonists disclosed herein comprise an anchoring moiety, an IFN masking moiety, an IFN moiety, and a separating moiety, such as a targeting moiety that recognizes an antigen associated with a cell expressing a type 1 interferon receptor and anchors the IFN receptor antagonist to such cell. The disclosure further provides pharmaceutical compositions comprising the IFN receptor antagonists, and methods of using the IFN receptor antagonists in inhibition of IFN signaling, including methods of treatment. Also disclosed are nucleic acids encoding the IFN receptor antagonists, recombinant cells expressing the IFN receptor antagonists, and methods of producing the IFN receptor antagonists.

The invention relates to the technical field of medicines, and particularly discloses a pharmaceutical composition based on an IRF7-PTEN signal axis and application of the pharmaceutical composition in spinal cord injury. According to the application, a plurality of spinal cord injury single cell sequencing data sets are integrated, and the interferon regulatory factor 7, namely IRF7, is screened and verified to be a key hub gene for regulating and controlling apoptosis of astrocytes. Knock-down IRF7 significantly inhibits astrocyte apoptosis induced by etoposide, and rotation IRF7 can reverse the effect. In mechanism, the IRF7 promotes cell apoptosis by negatively regulating a PTEN pathway, and the PTEN inhibitor SF1670 can block the IRF7 overexpression mediated apoptosis promoting effect. On the basis, the invention provides a pharmaceutical composition taking the signal axis as a target spot, and the active ingredient of the pharmaceutical composition can be an IRF7 inhibitor or a PTEN inhibitor; the invention also discloses application of the inhibitor in preparation of drugs for treating spinal cord injury. The application provides a new target spot and an effective intervention strategy for treatment of spinal cord injury.

The present invention is directed to methods for treating or preventing neuroinflammation in a subject by administering an effective amount of a single-domain antibody (sdAb) comprising SEQ ID NO:1. The method is applicable to subjects with multiple sclerosis, including secondary progressive, primary progressive, and relapsing-remitting forms. Administration may be intravenous, subcutaneous, or intrathecal, with dosage regimens including daily administration, loading and maintenance doses, or continuous infusion. The method may be initiated upon first clinical signs of central nervous system demyelination and continued for at least 14 days. The sdAb may be co-administered with a pharmaceutically acceptable excipient such as mannitol, sucrose, or polysorbate 80, and optionally combined with disease-modifying therapies including interferon-β, glatiramer acetate, fingolimod, or ocrelizumab. The invention provides a targeted approach for modulating neuroinflammatory processes in neurological disorders.

The present invention provides interferon-beta (IFN-β) for use in the treatment of viral-induced COPD exacerbations in patients treated with systemic corticosteroids, wherein the IFN-β is administered by inhalation, for example by use of a nebulizer.

Methods of preparing mesenchymal stromal cells (MSCs) through co-stimulation with interferon gamma (IFNγ) and tumor necrosis factor alpha (TNFα), and methods for using the co-stimulated MSCs to treat conditions associated with exocrine glands. Co-treatment of MSCs with IFNγ and TNFα significantly enhances their trophic secretome, preserves their immunomodulatory capacity compared to untreated MSCs, and maximizes their therapeutic efficacy. The MSCs may be allogeneic to the recipient.

The invention provides a traditional Chinese medicine composition for improving immunity and a preparation method thereof. Comprising 20-30 parts of rhodiola rosea, 15-25 parts of lucid ganoderma, 10-20 parts of boschniakia rossica, 20-30 parts of fructus lycii and 500-1000 parts of Baijiu. The preparation method comprises the following steps: 1, cleaning the traditional Chinese medicines, airing, crushing into 20-40-mesh particles, and putting into a closed container; step 2, adding Baijiu, soaking for 30 days, and shaking for 1-2 times every day to promote dissolution of effective components; 3, medicine residues are filtered after soaking is completed, the obtained medicine liquid is the final product, the immunity of the composition is enhanced through the multi-target-point synergistic effect, salidroside in the rhodiola rosea can adjust the hypothalamus-pituitary-adrenal axis and relieve the stress reaction, and ganoderan can activate macrophages and T lymphocytes and promote interferon secretion, so that the immunity of the composition is improved. The phenylethanoid glycoside component of the boschniakia rossica has anti-oxidation and anti-inflammatory effects, and the lycium barbarum polysaccharide can improve the level of serum immune globulin. The composition is free of obvious toxic and side effects, and slight dry mouth possibly occurs to a few people with fire excess from yin deficiency and can be relieved after reduction.