Triamterene blocks epithelial Na+ channel (ENaC) in a voltage-dependent manner, which used as a mild diuretic.Target: Sodium ChannelTriamterene blocked rENaC in a voltage-dependent manner, and was 100-fold less potent than amiloride at pH 7.5. At -90 mV and -40 mV, the IC50 values were 5 microM and 10 microM, respectively. The blockage by triamterene, which is a weak base with a pKa of 6.2, was dependent on the extracellular pH. The IC50 was 1 microM at pH 6.5 and only 17 microM at pH 8.5 [1]. Triamterene (TA) is partly eliminated by a first-pass-effect. The main metabolite of TA is OH-TA-ester, which is pharmacologically active [2].
References:
[1]. Busch, A.E., et al., Blockade of epithelial Na+ channels by triamterenes - underlying mechanisms and molecular basis. Pflugers Arch, 1996. 432(5): p. 760-6.
[2]. Gilfrich, H.J., et al., Pharmacokinetics of triamterene after i.v. administration to man: determination of bioavailability. Eur J Clin Pharmacol, 1983. 25(2): p. 237-41.