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- B5a27f09ee3aadf41118e4b03ca9cfa97 NCIT_P378 "NCI" @default.
- B5a27f09ee3aadf41118e4b03ca9cfa97 type Axiom @default.
- B5a27f09ee3aadf41118e4b03ca9cfa97 annotatedProperty IAO_0000115 @default.
- B5a27f09ee3aadf41118e4b03ca9cfa97 annotatedSource NCIT_C29062 @default.
- B5a27f09ee3aadf41118e4b03ca9cfa97 annotatedTarget "The sodium salt of a synthetic lipid-lowering agent with potential antineoplastic activity. Fluvastatin competitively inhibits hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses through the suppression of MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Through the inhibition of mevalonate synthesis, statins, like fluvastatin, have been shown to inhibit the production of dolichol, geranylpyrophosphate (GPP) and farnesylpyrophosphate (FPP) and the isoprenylation of the intracellular G-proteins Ras and Rho, which may result in antiangiogenic, apoptotic, and antimetastatic effects in susceptible tumor cell populations." @default.