Nuclear retinoic acid receptors (RARs) are transcriptional regulators with roles in cell proliferation and differentiation. BMS 453 is a synthetic retinoid that acts as an agonist of RARβ and an antagonist of RARα and RARγ.¹ It has been shown to inhibit the proliferation of normal breast cells via the induction of TGF-β activity, causing G₁ arrest.² BMS 453 binding to RARα and RARγ can induce a transrepression of phorbol ester-induced AP-1 activity (IC₅₀s = ~0.1 nM in HeLa and MCSF-7 cells), which also correlates with reduced cell proliferation.¹ BM 453 has been used to trigger the differentiation of mouse embryonic stem cells (mES) in a study of RARβ-induced mES cell adipogenesis.³

≥98%

Store at -20℃

BMS 189453;

1.Chen, J.Y.,Penco, S.,Ostrowski, J., et al. RAR-specific agonist/antagonists which dissociate transactivation and AP1 transrepression inhibit anchorage-independent cell proliferation. EMBO Journal 14(6), 1187-1197 (1995).

2.Yang, L.,Ostrowski, J.,Reczek, P., et al. The retinoic acid receptor antagonist, BMS453, inhibits normal breast cell growth by inducing active TGFß and causing cell cycle arrest. Oncogene 20(55), 8025-8035 (2001).

3.Monteiro, M.C.,Wdziekonski, B.,Villageois, P., et al. Commitment of mouse embryonic stem cells to the adipocyte lineage requires retinoic acid receptorβand active GSK3. Stem Cells Dev. 18(3), 457-463 (2009).