RS-1269 is a highly potent, selective CCR4 antagonist, inhibits [125I]CCL17 binding to human CCR4 with IC50 of 27.7 nM.
RS-1269 also has strong affinity to displace the CCL17 binding with IC50 of 27.0 nM in CCR4-expressing CHO cells.
RS-1269 displays no competitive displacement in the binding of [125I]CCL3 (MIP-1α) to CCR1 and [125I]CCL2 (MCP-1) to CCR2b.
RS-1269 dose-dependently inhibited CCL17-induced migration of Th2 cells with IC50 of 5.5 nM.
Orally administered RS-1269 (30 mg/kg) ameliorates ovalbumin-induced ear swelling in mice.
RS-1269 also inhibited LPS-induced TNF-α production in vivo.
