Inhibition of the formation of vascular hyperpermeability

Details Inhibition of the formation of vascular hyperpermeability Inhibition of the formation of vascular hyperpermeability

A - Human Necessities

61

K

A61K 31/415 (2006.01) A61K 38/17 (2006.01) A61K 38/19 (2006.01) C07K 14/71 (2006.01) A61K 38/00 (2006.01)

Patent

CA 2347916

Vascular hyperpermeability and the subsequent events such as macular edema, retinoblastoma, ocular ischemia, ocular inflammatory disease or infection, choroidal melanoma, edematous side-effects induced by iron chelation therapy, pulmonary edema, myocardial infarction, rheumatoid diseases, anaphylaxis, allergies, hypersensitive reactions, cerebral edema, brain tumor fluid-filled cysts, communicating hydrocephalus, carpal tunnel syndrome, organ damage resulting from a burn, irritation or infection, erythema multiforme, edematous macules and other disorders, brain tumors, tumor effusions, lung or breast carcinomas, ascites, pleural effusions, pericardial effusions, high altitude "sickness", radioanaphylaxis, radiodermatitis, glaucoma, conjunctivitis, choroidal melanoma, adult respiratory distress syndrome, asthma, bronchitis, ovarian hyperstimulation syndrome, polycystic ovary syndrome, menstrual swelling, menstrual cramps, stroke, head trauma, cerebral infarct or occlusion, hyotension, ulcerations, sprains, fractures, effusions associated with synovitis, diabetic complications, hyperviscosity syndrome, liver cirrhosis, microalbuminuria, proteinuria, oliguria, electrolyte imbalance, nephrotic syndrome, exudates, fibroses, keloid, can be inhibited by the administration of a compound that inhibits the enzyme activity of the VEGF tyrosine kinase receptor known as KDR tyrosine kinase. The preferred compound 4,5-dihydro-3-pyridin-4-yl-1(2)H-benzo[g]indazole selectively inhibits the function of KDR tyrosine kinase but do not block the activity of Flt-1 tyrosine kinase which is another VEGE tyrosine kinase receptor.

L'hyperperméabilité vasculaire est généralement le prélude à un certain nombre de désordres physiologiques, souvent délétères, parmi lesquels on peut citer la formation d'oedème, la diapédèse, l'échange aberrant trans-endothélial, l'extravasation, l'exsudation et l'épanchement, le dépôt matriciel (avec souvent une prolifération stromale anormale) et l'hypotension vasculaire. Il est possible d'empêcher l'hyperperméabilité et les désordres qui en découlent en administrant un composé inhibant l'activité enzymatique du récepteur tyrosine kinase du facteur VEGF, dénommé tyrosine kinase KDR. L'administration de composés préférés permet d'inhiber la fonction de la tyrosine kinase KDR sans bloquer l'activité de la tyrosine kinase Flt-1, laquelle constitue un autre récepteur tyrosine kinase du facteur VEGF.

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