For research use only. Not for therapeutic Use.
BMS CCR2 22 is a potent, specific and high affinity CC-type chemokine receptor 2 (CCR2) antagonist with 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 (Compound 22) has binding affinity for wild-type and E291A mutants with IC50 values of 7.5 nM and 3.7 nM, respectively[1].
BMS CCR2 22 prevents both the binding and the internalization of fluorescently labeled hMCP-1_AF647 internalization in human monocytes. BMS CCR2 22 inhibits the internalization of hMCP1_AF647 with an IC50 value of approximately 2 nM[2].
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].
| Catalog Number | I010705 |
| CAS Number | 445479-97-0 |
| Synonyms | N-[2-[[(1S,2R)-2-[(4-methylsulfanylbenzoyl)amino]cyclohexyl]amino]-2-oxoethyl]-2-(propan-2-ylcarbamoylamino)-5-(trifluoromethyl)benzamide |
| Molecular Formula | C28H34F3N5O4S |
| Purity | ≥95% |
| InChI | InChI=1S/C28H34F3N5O4S/c1-16(2)33-27(40)36-21-13-10-18(28(29,30)31)14-20(21)26(39)32-15-24(37)34-22-6-4-5-7-23(22)35-25(38)17-8-11-19(41-3)12-9-17/h8-14,16,22-23H,4-7,15H2,1-3H3,(H,32,39)(H,34,37)(H,35,38)(H2,33,36,40)/t22-,23+/m0/s1 |
| InChIKey | IBPXYDUJQWENPM-XZOQPEGZSA-N |
| SMILES | CC(C)NC(=O)NC1=C(C=C(C=C1)C(F)(F)F)C(=O)NCC(=O)NC2CCCCC2NC(=O)C3=CC=C(C=C3)SC |
| Reference | [1]. Cherney RJ, et al. Discovery of disubstituted cyclohexanes as a new class of CC chemokine receptor 2 antagonists. J Med Chem. 2008 Feb 28;51(4):721-4. [2]. Kredel S, et al. High-content analysis of CCR2 antagonists on human primary monocytes. J Biomol Screen. 2011 Aug;16(7):683-93. [3]. D’Antoni ML, et al. Cenicriviroc inhibits trans-endothelial passage of monocytes and is associated with impaired E-selectin expression. J Leukoc Biol. 2018 Dec;104(6):1241-1252. |
