2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Biological activity
Description
Target:
In Vivo
In Vitro
BMS453 (1 μM; 11 hours; 184 and HMEC cells) treatment inhibits the proliferation of normal breast cell growth without significantly inducing apoptosis[2]. BMS453 (1 μM; 5 days; 184 and HMEC cells) treatment inhibits normal breast cell proliferation by causing G1 arrest[2]. BMS453 (1 μM; 24-72 hours; 184 cells) treatment induces Rb hypophosphorylation and decrease CDK2 kinase activity. BMS453 increases total p21 protein levels and CDK2-bound p21 protein, but does not change CDK4-bound p21[2]. BMS453 inhibits breast cell growth predominantly through the induction of active TGFβ[2]. Cell Proliferation Assay[2] Cell Line: Normal human mammary epithelial cells (184 and HMEC) Concentration: 1 μM Incubation Time: 11 hours Result: Inhibited 3H-thymidine uptake in normal breast cells (184 and HMEC) by 40 %. Cell Cycle Analysis[2] Cell Line: Normal human mammary epithelial cells (184 and HMEC) Concentration: 1 μM Incubation Time: 5 days Result: Increased the proportion of cells in G0/G1 phase and decreased the proportion of cells in S phase. Western Blot Analysis[2] Cell Line: 184 cells Concentration: 1 μM Incubation Time: 24 hours, 48 hours, 72 hours Result: Induced Rb hypophosphorylation and decrease CDK2 kinase activity.
Kinase Assay
Cell Assay
Animal Administration
References
[1]. J Y Chen, et al. RAR-specific agonist/antagonists which dissociate transactivation and AP1 transrepression inhibit anchorage-independent cell proliferation. EMBO J. 1995 Mar 15;14(6):1187-97.
[2]. L Yang, et al. The retinoic acid receptor antagonist, BMS453, inhibits normal breast cell growth by inducing active TGFbeta and causing cell cycle arrest. Oncogene. 2001 Nov 29;20(55):8025-35.
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