BMS CCR2 22 is a potent, specific and high affinity CC-type chemokine receptor 2 (CCR2) antagonist. It has excellent binding affinity (binding IC50 of 5.1 nM) and potent functional antagonism (calcium flux IC50 of 18 nM and chemotaxis IC50 of 1 nM)[1][2].

BMS CCR2 22 is a potent, specific and high affinity CC-type chemokine receptor 2 (CCR2) antagonist. BMS CCR2 22 (Compound 22) has binding affinity for wild-type and E291A mutants with IC50 values of 7.5 nM and 3.7 nM, respectively[1]. It has excellent binding affinity (binding IC50 of 5.1 nM) and potent functional antagonism (calcium flux IC50 of 18 nM and chemotaxis IC50 of 1 nM)[1][2]. BMS CCR2 22 inhibits the internalization of hMCP1_AF647 with an IC50 value of approximately 2 nM[2]. BMS CCR2 22 prevents both the binding and the internalization of fluorescently labeled hMCP-1_AF647 internalization in human monocytes. The addition of BMS CCR2 22 (0.1-10 μM; 24 h), cenicriviroc (CVC) or a combination of both BMS CCR2 22 and MVC to human aortic endothelial cells (HAoECs) prior to MCP-1 stimulation do not alter E-selectin, ICAM-1, or CD99 cell surface expression. Incubation of HAoECs with BMS CCR2 22 before MCP-1 significantly increases VCAM-1 and PECAM1 cell surface levels (from 72.8 to 160% and from 97.2 and 127%, respectively)[3].

445479-97-0

C28H34F3N5O4S

593.66

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years