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Azosemide, a sulfonamide loop diuretic, is a potent NKCC1 inhibitor with IC50s of 0.246 μM and 0.197 μM for hNKCC1A and NKCC1B, respectively[1].

Azosemide inhibits the sodium-potassium-chloride-cotransporter human variants hNKCC1A and hNKCC1B[1].

Azosemide shows a smaller AUC (81.9% decrease), shorter terminal half-life (50.9% decrease) and MRT (64.1% decrease), faster CL (454% increase), CLR (853% increase) and CLNR (307% increase) for NARs[2]. Animal Model: Male Sprague-Dawley rats (control rats, weighing 310345 g) and NARs (weighing 220315 g) of 9 weeks of age[2]

[1]. Hampel P, et al. Azosemide is more potent than bumetanide and various other loop diuretics to inhibit the sodium-potassium-chloride-cotransporter human variants hNKCC1A and hNKCC1B. Sci Rep. 2018 Jun 29;8(1):9877. [2]. Kim EJ, et al. Pharmacokinetics and pharmacodynamics of intravenous azosemide in mutant Nagaseanalbuminemic rats. Drug Metab Dispos. 2003 Feb;31(2):194-201.

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