Vercirnon (GSK1605786A) sodium is an orally bioavailable, selective, and potent CCR9 antagonist. It effectively inhibits CCR9-mediated calcium mobilization and chemotaxis in Molt-4 cells, exhibiting IC50 values of 5.4 nM and 3.4 nM, respectively. Demonstrating high selectivity, Vercirnon sodium does not significantly affect CCR1-12 or CX3CR1-7, with IC50 values exceeding 10 µM for these receptors. Additionally, it inhibits CCL25-directed chemotaxis equally well in both CCR9 splice variants, CCR9A and CCR9B, with IC50 values of 2.8 nM and 2.6 nM, respectively.

CCR9:10 nM (IC50)

Vercirnon (GSK-1605786) sodium inhibits chemotaxis of primary CCR9-expressing cells to CCL25 with an IC 50 of 6.8 nM. Vercirnon sodium inhibits CCL25-Induced Chemotaxis of retinoic acid (RA)-Cultured Human T Cells. Vercirnon sodium inhibits RA-cultured cell CCL25-medidated chemotaxis in 100% human AB serum resulted in an IC 50 of 141 nM. Vercirnon sodium is a potent inhibitor of CCL25-induced mouse and rat thymocyte chemotaxis with IC 50 values of 6.9 nM and 1.3 nM, respectively[1].

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.