bms182874 hydrochloride

BMS 182874 hydrochloride is a nonpeptide endothelin (El) receptor antagonist.

The BMS-582949 hydrochloride (BMS-582949 HCl) is a highly specific p38α MAPK inhibitor (IC50: 13 nM).

BMS-823778 hydrochloride is a potent, selective, and orally active inhibitor of 11β-HSD1 (11β-Hydroxysteroid Dehydrogenase Type 1), demonstrating an IC50 (half maximal inhibitory concentration) of 2.3 nM against the human form of the enzyme.

BMS 182874 is an orally effective and highly selective endothelin receptor ETA antagonist with an IC50 value of 0.150 μM for ETA and a Ki value of 0.055 μM for ETA.BMS 182874 is able to reduce arterial pressure in a rat hypertension model induced by Deoxycorticosterone acetate. BMS 182874 was able to reduce Deoxycorticosterone-induced arterial pressure in a rat model of hypertension and can be used to study cardiovascular disease.

Motixafortide (BKT140 4-fluorobenzoyl) is an antagonist of CXCR4 (IC50: 1 nM). BMS-1166 hydrochloride is an inhibitor of PD-1/PD-L1 interaction (IC50: 1.4 nM). BMS-1166 rivalries the inhibitory effect of PD-1/PD-L1 immune checkpoint on T cell activation.

BMS-345541 hydrochloride is a selective IKK inhibitor (IKK2 and IKK1 with IC50 of 0.3 μM and 4 μM,respectively).

BMS-199264 hydrochloride potently inhibits the ATP hydrolase activity of mitochondrial F1F0 ATP synthase.

BMS-599626 Hydrochloride (AC480 Hydrochloride) is an orally bioavailable inhibitor of the HER1, HER2 and HER4 tyrosine kinases (IC50 =22, 32 and 190 nM, respectively) with potential antineoplastic activity. BMS-599626 Hydrochloride inhibits human epidermal growth factor receptors (HER) HER1, HER2 and HER4, thereby inhibiting the proliferation of tumor cells that overexpress these receptors.

BMS-1001 hydrochloride is an orally active inhibitor of human PD-1/PD-L1 immune checkpoint with low-toxicity in cells.BMS-1001 alleviates the inhibitory effect of the soluble PD-L1 on the T-cell receptor-mediated activation of T-lymphocytes. BMS-1001 is capable of alleviating the PD-1/PD-L1 immune checkpoint-mediated exhaustion of Jurkat T-lymphocytes.