BMS-192364 is targeting the Gα-RGS interaction to produce an inactive Gα-RGS complex. BMS-192364 reduces urinary bladder contraction and exert RGS-agonist properties by increasing the action of GAPs on Gq proteins. BMS-192364 inhibits calcium flux.

BMS-193885 is a selective neuropeptide Y1 receptor antagonist (Ki=3.3 nM) that competitively blocks the receptor to inhibit NPY-mediated appetite regulation signaling pathways, reduce food intake and inhibit weight gain. BMS-193885 has good blood-brain barrier penetration

BMS-1 is an inhibitor of the PD-1/PD-L1 protein/protein interaction (IC50 between 6 and 100 nM).

BMS-1001 is an orally active human PD-L1/PD-1 immune checkpoint inhibitor. BMS-1001 exhibits low-toxicity in cells. The IC50 value of BMS-1001 in a homogeneous time-resolved fluorescence (HTRF) binding assay is 2.25 nM.

BMS-191095 is a selective activator of mitochondrial ATP-sensitive potassium (mitoKATP) channels. BMS-191095 inhibits human platelet aggregation by opening mitochondrial K(ATP) channels.

BMS 191011 (BMS-A) is a potent BKCa channel opener (large-conductance Ca2+-activated potassium channel). BMS-191011 shows neuroprotective activities in rodent models of stroke.

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

BMS-199264 hydrochloride is an inhibitor of F1F0 ATP hydrolase (IC50=0.5 μM) without inhibitory effect on F1F0 ATP synthase. BMS-199264 hydrochloride selectively inhibits ATP decline during ischemia to reduces cardiac necrosis. BMS-199264 hydrochloride also enhances the

BMS-1166 is a potent PD-1/PD-L1 immune checkpoint inhibitor. BMS-1166 induces dimerization of PD-L1 and blocks its interaction with PD-1, with an IC50 of 1.4 nM. BMS-1166 antagonizes the inhibitory effect of PD-1/PD-L1 immune checkpoint on