| Identification | Back Directory | [Name]
GSK-1605786A | [CAS]
886214-18-2 | [Synonyms]
GSK1605786A
GSK-1605786A
GSK 1605786A
CCX282-Bsodium
Traficet-ENsodium
GSK-1605786 sodium
Vercirnon (sodiuM)
LBRWQGMQARTQCO-UHFFFAOYSA-N | [Molecular Formula]
C22H20ClN2NaO4S | [MDL Number]
MFCD28386289 | [MOL File]
886214-18-2.mol | [Molecular Weight]
466.913 |
| Hazard Information | Back Directory | [Uses]
Vercirnon (GSK1605786A) sodium is an orally bioavailable, selective, and potent antagonist of CCR9. Vercirnon sodium inhibits CCR9-mediated Ca2+ mobilization and chemotaxis on Molt-4 cells with IC50 values of 5.4 and 3.4 nM, respectively. Vercirnon sodium is selective for CCR9 over CCR1-12 and CX3CR1-7 (IC50s>10 μM for all). Vercirnon sodium is an equipotent inhibitor of CCL25-directed chemotaxis of both splice forms of CCR9 (CCR9A and CCR9B) with IC50 values of 2.8 and 2.6 nM, respectively[1]. | [in vivo]
Vercirnon (GSK1605786A) sodium (10, 50 mg/kg; s.c.; twice per day; starting at 2 weeks of age until 12 weeks of age) ameliorates the severity of intestinal inflammation in the TNFΔARE mouse model[1]. | Animal Model: | C57BL/6 mice (TNFΔARE Mouse Model of Terminal Ileitis)[1] | | Dosage: | 10, 50 mg/kg | | Administration: | Subcutaneous; twice per day; starting at 2 weeks of age until 12 weeks of age | | Result: | Resulted in complete protection from the severe inflammation associated with TNF- overexpression at 50 mg/kg. A similar protective effect was also noted with a lower dose.
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| [IC 50]
CCR9: 10 nM (IC50) | [References]
[1] Walters MJ, et al. Characterization of CCX282-B, an orally bioavailable antagonist of the CCR9 chemokine receptor, for treatment of inflammatory bowel disease. J Pharmacol Exp Ther. 2010 Oct;335(1):61-9. DOI:10.1124/jpet.110.169714
[2] Bekker P, et al. CCR9 Antagonists in the Treatment of Ulcerative Colitis. Mediators Inflamm. 2015;2015:628340. DOI:10.1155/2015/628340
[3] Zhang J, et al. Biarylsulfonamide CCR9 inhibitors for inflammatory bowel disease. Bioorg Med Chem Lett. 2015 Sep 1;25(17):3661-4. DOI:10.1016/j.bmcl.2015.06.046 |
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