Laniquidar is a non-competitive P-gp inhibitor with an IC50 of 0.51 μM. Laniquidar binds to the P-gp transporter with high affinity and exhibits low activity as a substrate. Laniquidar is applicable to epilepsy-related research [1].
In Vivo, 11C]laniquidar (20-100 MBq; i.v.; single dose) shows low cerebral uptake in healthy Wistar rats, which is significantly increased by cyclosporine A pretreatment but unaffected by valspodar, and exhibits relatively low in vivo plasma metabolism[1].
In Vitro, Laniquidar potently inhibits purified P-glycoprotein with an IC50 of 0.51 μM, acts primarily as an inhibitor rather than a substrate, and has higher P-gp binding affinity than verapamil[1].
References:
[1]. Luurtsema G, et al. Evaluation of [11C]laniquidar as a tracer of P-glycoprotein: radiosynthesis and biodistribution in rats. Nucl Med Biol. 2009;36(6):643-649.
In Vivo, 11C]laniquidar (20-100 MBq; i.v.; single dose) shows low cerebral uptake in healthy Wistar rats, which is significantly increased by cyclosporine A pretreatment but unaffected by valspodar, and exhibits relatively low in vivo plasma metabolism[1].
In Vitro, Laniquidar potently inhibits purified P-glycoprotein with an IC50 of 0.51 μM, acts primarily as an inhibitor rather than a substrate, and has higher P-gp binding affinity than verapamil[1].
References:
[1]. Luurtsema G, et al. Evaluation of [11C]laniquidar as a tracer of P-glycoprotein: radiosynthesis and biodistribution in rats. Nucl Med Biol. 2009;36(6):643-649.