Activators & Inhibitors

Selective inhibitor of class IIa histone deacetylases (HDACs). Exhibits tissue-selective inhibition between members of class II deacetylases in vivo; inhibits HDAC4 and HDAC5 in skeletal muscle and the heart without affecting HDAC3 activity. Displays no inhibition of class I HDAC activity (HDAC1, 2, 3) or expression.

2-Methoxyestradiol (2-MeOE2), an endogenous metabolite of 17β-estradiol (E2), is an inhibitor of microtubule assembly that inhibits the polymerization of tubulin and interferes with mitotic spindle dynamics leading to the blockage of mitosis of human cancer cells which lack estrogen receptors in metaphase. 2-MeOE2 is also an inhibitor of tumor growth and angiogenesis. Study results have shown that 2-MeOE2 induces mammalian cell transformation and genotoxicity in Syrian hamster embryo (SHE) fibroblasts through concentration-dependent inhibition of cell growth. Moreover, 2-MeOE2 has demonstrated anti-proliferative activity against estrogen-responsive breast cancer cell line MCF-7 and subsequent inhibition of the growth of tumors subcutaneously inoculated in mice.

2-Methoxyestradiol (2-MeOE2), an endogenous metabolite of 17β-estradiol (E2), is an inhibitor of microtubule assembly that inhibits the polymerization of tubulin and interferes with mitotic spindle dynamics leading to the blockage of mitosis of human cancer cells which lack estrogen receptors in metaphase. 2-MeOE2 is also an inhibitor of tumor growth and angiogenesis. Study results have shown that 2-MeOE2 induces mammalian cell transformation and genotoxicity in Syrian hamster embryo (SHE) fibroblasts through concentration-dependent inhibition of cell growth. Moreover, 2-MeOE2 has demonstrated anti-proliferative activity against estrogen-responsive breast cancer cell line MCF-7 and subsequent inhibition of the growth of tumors subcutaneously inoculated in mice.

Allosteric and reversible inhibitor of protease-activated receptor 1 (PAR1)-mediated platelet activation (IC50 = 0.26 µM for the inhibition of platelet P-selectin expression on human platelets).

Allosteric and reversible inhibitor of protease-activated receptor 1 (PAR1)-mediated platelet activation (IC50 = 0.26 µM for the inhibition of platelet P-selectin expression on human platelets).

NSC697923 is a cell-permeable and selective inhibitor of the Ub-conjugating enzyme (E2) complex Ubc13-Uev1A. It is believed to act by disrupting formation of the Ubc13:Ub conjugate. Shown to inhibit proliferation and survival of certain B-cell lymphoma cells.

NSC697923 is a cell-permeable and selective inhibitor of the Ub-conjugating enzyme (E2) complex Ubc13-Uev1A. It is believed to act by disrupting formation of the Ubc13:Ub conjugate. Shown to inhibit proliferation and survival of certain B-cell lymphoma cells.

NVP-BEP800 is a novel, fully synthetic, orally bioavailable inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Hsp90. NVP-BEP800 (also known as VER-82576) is a novel ATP-competitive HSP90β inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Heat shock protein 90 (Hsp90). NVP-BEP800 induced robust antitumor responses in tumor xenograft models, including regression in the BT-474 breast cancer model. NVP-BEP800 can radiosensitise tumour cell lines of different entities through destabilisation and depletion of several Hsp90 client proteins, thus causing the depletion of S phase and G2/M arrest, increased DNA damage and repair protraction and, to some extent, apoptosis.

NVP-BEP800 is a novel, fully synthetic, orally bioavailable inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Hsp90. NVP-BEP800 (also known as VER-82576) is a novel ATP-competitive HSP90β inhibitor that binds to the NH(2)-terminal ATP-binding pocket of Heat shock protein 90 (Hsp90). NVP-BEP800 induced robust antitumor responses in tumor xenograft models, including regression in the BT-474 breast cancer model. NVP-BEP800 can radiosensitise tumour cell lines of different entities through destabilisation and depletion of several Hsp90 client proteins, thus causing the depletion of S phase and G2/M arrest, increased DNA damage and repair protraction and, to some extent, apoptosis.