Results for Chemicals & Small Molecules ( 98591 )
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MS-275, also known as Entinostat, is an inhibitor of histone deacetylases (HDACs) and preferentially inhibits HDAC1 over HDAC3. It does not inhibit HDAC8 (IC50 > 100 µM). It induces cyclin-dependent kinase inhibitor 1A (p21/CIP1/WAF1), slowing cell growth, differentiation, and tumor development in vivo. Recent studies suggest that MS-275 may be particularly useful as an antineoplastic agent when combined with other drugs like adriamycin, inhibitors of PARPs, or inhibitors of Hsp90.
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Cyclopamine inhibits activation of the Hedgehog response pathway by binding to and inhibiting the proto-oncogene Smoothened (SMO). The effects of oncogenic mutations that either activate SMO or inactivate the tumor suppressor Patched (Ptch) can be reversed by cyclopamine treatment. Cyclopamine has also been shown to induce apoptosis in colorectal adenoma cell lines, carcinoma-derived cell lines, and skin basal cell carcinomas and is being investigated as an anti-cancer drug.
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Sorafenib Tosylate, also known as Bay 43-9006, is a novel bi-aryl urea compound that inhibits cell proliferation by targeting receptor tyrosine kinases, including VEGFR-2 and PDGFR-β and their associated signaling cascades of the ERK pathway and angiogenesis. It was originally developed as a Raf kinase inhibitor. It has been shown to have activity against several receptor tyrosine kinases involved in tumorigenesis and angiogenesis. Sorafenib is not active against erbB1, erbB2, ERK-1, MEK-1, EGFR, HER-2, IGFR-1, c-MET, c-yes, PKB, PKA, cdk1/cyclinB, PKC, or pim-1. Sorafenib has been shown to inhibit various nonkinase targets, including adenosine A3, dopamine D1, and muscarine M3 receptors, but at much higher (micromolar) concentrations than kinase targets. It is also the active ingredient in a drug that has been approved in at least one country for use in patients with advanced renal cell cancer. This version is NOT for human use.
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Z-VAD(OMe)-FMK is a cell permeable, irreversible pan-caspase inhibitor and anti-apoptotic agent. It has been shown to inhibit Fas-mediated apoptosis in Jurkat T cells and apoptosis in THP.1 cells induced by diverse stimuli (including cycloheximide, thapsigargin, etoposide and staurosporine). Inhibits caspases 1, 3, 4, and 7.
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Mocetinostat selectively inhibits histone deacetylases (HDACs) 1-3 and 11 at submicromolar concentrations. It blocks cancer cell proliferation in vitro and has significant antitumor activity in vivo. Mocetinostat induces hyperacetylation of histones, causes expression of the tumor suppressor protein p21(WAF1/CIP1), and inhibits proliferation of human cancer cells growing in culture.
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Panobinostat, also known as LBH-589, is a highly active, non-selective HDAC inhibitor. IC50's against HDAC s 1-9 range between 3 - 61 nM except for a slightly higher IC50 value of 248 nM for HDAC 8. Panobinostat inhibits tumor cell proliferation and induces apoptosis in breast cancer and T cell lymphoma cells. In addition to its tumor-suppressive activities, panobinostat induces histone H3K9 and histone H4K8 acetylation and decreases the level of c-Myc expression.
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CI-994 is a histone deacetylase (HDAC) inhibitor that induces histone hyperacetylation. CI-994 inhibited HDAC-1 and HDAC-2 but not GCN5. CI-994 is also a novel antitumor agent, exhibiting activity against pancreatic, colon and mammary tumors. CI-994 inhibited the growth of two non-small cell lung cancer cell lines, A-549 (adenocarcinoma) and LX-1 (squamous cell carcinoma), with an IC50 of 80 µM.