摘要:
The present invention relates to a pharmaceutical composition for preventing or treating autophagy-related diseases, angiogenic diseases or hypermelanosis, comprising: (a) a pharmaceutically effective amount of an indatraline derivative or a pharmaceutically acceptable salt thereof; and a pharmaceutically acceptable carrier. The composition of the present invention effectively induces autophagy of cells, and thus is very effective for preventing or treating autophagy-related diseases. In addition, the composition of the present invention inhibits angiogenesis through the mechanism of inhibiting angiogenesis, invasion and metastasis and inhibits melanogenesis, and thus can also be effective for preventing or treating angiogenic diseases or melanin-related diseases.
摘要:
The present disclosure relates to bisphenyl compounds that are useful for inhibiting the ADP-ribosyl cyclase (ADPR-cyclase). More particularly, the disclosed compounds can be used for treatment and prevention of hypertension, hypertensive cardiac hypertrophy, diabetes, and diabetic nephropathy, in which pathogenesis ADPR-cyclase is involved. The compounds and compositions of the invention can be used for treatment and prevention of cardiovascular disease and related disease states, particularly, hypertension or diabetes related disorders, such as, hypertensive cardiac hypertrophy, diabetic nephropathy, and the like.
摘要:
Provided is a pharmaceutical composition for inhibiting angiogenesis, comprising a therapeutically effective amount of a compound represented by Formula 1: (I) wherein R1 through R13 and X are as defined in the specification. Compounds used as an active ingredient in the pharmaceutical composition of the present invention bind to QP-C to provide effective prevention of angiogenesis and can be effectively used for prevention and/or treatment of angiogenesis-related diseases or disorders. Further, the active compounds of the present invention inhibit biological functions of QP-C, which consequently leads to inhibition of angiogenic responses without the risk of cellular apoptosis, thus significantly improving safety of the drug.