11 results about "Interferon alfa" patented technology

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.

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.

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 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.

The present invention discloses compounds according to Formula (I) wherein X1, X2, Y, R1, L1, R 2, R 3, Cy and the subscript n 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, transplant 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, IL-17 and / or IL-23, respiratory diseases, endocrine diseases, metabolic diseases, cardiovascular diseases, dermatological diseases, and / or abnormal angiogenesis associated diseases by administering a compound of the invention.

This disclosure relates to methods and compositions for the treatment of SLE. Specifically, this disclosure relates to methods including the administration of type I IFN receptor inhibitors.

This invention provides methods for treating acute respiratory distress syndrome (ARDS), including ARDS associated with respiratory viral infections. [Solution] Administer plasma kallikrein (pKal) inhibitors such as anti-pKal antibodies as inhibitors of the contact activation pathway. Immunomodulators such as IL-6R inhibitors, antiviral agents such as lopinavir, ritonavir, interferon beta, umfenovir, and remdesivir, antimalarial agents such as chloroquine, and / or inhibitors of the contact activation pathway such as C1 inhibitors, pKal inhibitors, and bradykinin receptor antagonists may be administered to the patient as additional therapeutic agents.