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In vitro study data: Mirogabalin was not metabolized by CYP but was metabolized by UGT1A3, UGT1A4, UGT1A9, UGT2B4, UGT2B7 and UGT2B17.
Mirogabalin was secreted from the kidney and was suggested to be a substrate for OAT1, OAT3, OCT2, MATE1, and MATE2-K.
Mirogabalin did not inhibit or induce major human CYP molecular species, and did not inhibit activities of drug transporters (OAT1, OAT3, OCT1, OCT2, OATP1B1, OATP1B3, MATE1, and MATE2-K). Mirogabalin also did not inhibit activities of P-glycoprotein (P-gp) or breast cancer resistance protein (BCRP).
In clinical study data: Co-administration of probenecid (500 mg) with TARLIGE (15 mg) increased the Cmax and AUClast of TARLIGE by 29% and 76%, respectively.
Co-administration of cimetidine (400 mg) with TARLIGE (15 mg) increased the Cmax and AUClast of TARLIGE by 17% and 44%, respectively.
Co-administration of TARLIGE with ethanol or lorazepam had no notable effect on the pharmacokinetics of TARLIGE or these drugs. Co-administration of TARLIGE in with these drugs decreased attention and balance-function more profoundly than monotherapy with TARLIGE.
Co-administration of TARLIGE with tramadol had no notable effect on the pharmacokinetics of TARLIGE or tramadol.