PET scans using the Pgp substrate (R)-[11C]NSC 657799 in FVB wild-type mice pretreated intravenously with Encequidar (HM30181) (at doses of 10 or 21 mg/kg) did not demonstrate significant increases in (R)-[11C]NSC 657799 brain uptake compared to vehicle-treated animals^[1].

Encequidar primarily inhibits P-gp in the intestinal endothelium, offering potential benefits by avoiding widespread P-gp inhibition, especially in the brain, which could trigger adverse effects. Encequidar (HM30181) enhances the oral bioavailability of co-administered NSC 125973 by over 12-fold in rats^[2].

Encequidar demonstrates comparable potency to the reference Pgp inhibitor tariquidar in blocking rhodamine 123 efflux from CCRF-CEM T cells (IC50, tariquidar: 8.2±2.0 nM, Encequidar: 13.1±2.3 nM) ^[1].

Encequidar (HM30181) exhibits high selectivity for mP-gp, with a potency 20-50 times greater than that of tariquidar, another third-generation P-gp inhibitor^[2].