- AGN 194310
- SR 11302
- AC 261066
- AC 55649
- TTNPB (Arotinoid Acid)
- CD 2314
| BMS 453RAR agonist |

Sample solution is provided at 25 µL, 10mM.
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Cell Stem Cell.2017 Nov 20. pii: S1934-5909(17)30375-2.Quality Control & MSDS
- View current batch:
- Purity = 98.00%
- COA (Certificate Of Analysis)
- MSDS (Material Safety Data Sheet)
- Datasheet
Chemical structure


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| Cas No. | 166977-43-1 | SDF | Download SDF |
| Chemical Name | (E)-4-(2-(5,5-dimethyl-8-phenyl-5,6-dihydronaphthalen-2-yl)vinyl)benzoic acid | ||
| Canonical SMILES | OC(C1=CC=C(C=C1)/C=C/C2=CC=C3C(C)(C)CC=C(C4=CC=CC=C4)C3=C2)=O | ||
| Formula | C27H24O2 | M.Wt | 380.48 |
| Solubility | Soluble in DMSO | Storage | Store at -20°C |
| Physical Appearance | A crystalline solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
BMS 453 is a synthetic RAR (retinoic acid receptor) antagonist [1]. The retinoic acid receptors (RARα, RARβ, RARγ) belong to steroid nuclear receptor superfamily and the expressions of retinoid receptor RARα and RARβ are correlated with the antiproliferative effects of retinoids.In normal breast cells, BMS453 inhibited the cell proliferation without significantly apoptosis. BMS 453 blocked the G1/S transition of the cell cycle with an increase in the amount of cells in G0/G1 and a decrease in the amount of cells in S phase. Also, BMS453 increased active TGFβ activity by 33-fold, which show BMS453 induces conversion of latent TGFβ to active TGFβ. TGFβ mediates the anti-proliferative effect of BMS453 in breast cells [1]. BMS 453 transrepresses AP-1 but does not activate RAR-dependent gene expression. In normal breast cells (HMEC and 184) and T47D breast cancer cells, BMS453 inhibited the growth of T47D breast cancer cells and normal breast cells (HMEC and 184). Breast cancer cells were resistant to BMS453 and normal human breast cells were most sensitive to BMS453. BMS453 may suppress growth by inhibiting transcription factors such as AP-1 [2].References:[1]. Yang L, Ostrowski J, Reczek P, et al. The retinoic acid receptor antagonist, BMS453, inhibits normal breast cell growth by inducing active TGFbeta and causing cell cycle arrest. Oncogene, 2001, 20(55): 8025-8035.[2]. Yang L, Munoz-Medellin D, Kim HT, et al. Retinoic acid receptor antagonist BMS453 inhibits the growth of normal and malignant breast cells without activating RAR-dependent gene expression. Breast Cancer Res Treat, 1999, 56(3): 277-291.


