BMS-195614

BMS-195614 (BMS 614) is an orally active neutral RARα-selective antagonist with a Ki of 2.5 nM. BMS-195614 restores the expression of Bcl2. BMS-195614 inhibits the transactivation of NF-κB, AP-1 and PPAR. BMS-195614 downregulates the expression of IL-6 and VEGF. BMS-195614 reduces blue light-induced phototoxicity and inhibits cell migration. BMS-195614 modulates inflammation and angiogenesis[1][2][3][4][5].

182135-66-6

BMS 614

12352005

Bcl-2 Family; Interleukin Related; NF-κB; PPAR; RAR/RXR; VEGFR

Reference compound

Apoptosis; Cell Cycle/DNA Damage; Immunology/Inflammation; Metabolic Enzyme/Protease; NF-κB; Protein Tyrosine Kinase/RTK; Vitamin D Related/Nuclear Receptor

Cancer-programmed cell death

Endocrinology; Inflammation/Immunology; Cardiovascular Disease

https://www.medchemexpress.com/bms-195614.html

99.5

DMSO : 30 mg/mL (ultrasonic; warming)

O=C(O)C1=CC=C(NC(C2=CC=C3C(C)(C)CC=C(C4=CC5=CC=CC=C5N=C4)C3=C2)=O)C=C1

C29H24N2O3

448.51

[1]Géhin M, et al. Structural basis for engineering of retinoic acid receptor isotype-selective agonists and antagonists. Chem Biol. 1999;6 (8) :519-529. |[2]Fontaine V, et al. RAR Inhibitors Display Photo-Protective and Anti-Inflammatory Effects in A2E Stimulated RPE Cells In Vitro through Non-Specific Modulation of PPAR or RXR Transactivation. Int J Mol Sci. 2024 Mar 6;25 (5) :3037.|[3]Kurtys E, et al. The combination of vitamins and omega-3 fatty acids has an enhanced anti-inflammatory effect on microglia. Neurochem Int. 2016 Oct;99:206-214.|[4]Inubushi M, et al. Retinoic acid promotes migration of MC3T3‐E1 osteoblast‐like cells via RARα signaling‐mediated upregulation of profilin‐1 expression. Journal of Osaka Dental University, 2019, 53 (2) : 149-156.|[5]Chung SS, et al. Pharmacological activity of retinoic acid receptor alpha-selective antagonists in vitro and in vivo. ACS Med Chem Lett. 2013 May 9;4 (5) :446-450.

Blue Ice

-20°C, 3 years (Powder)

Reference compound1

No Development Reported