Bumetanide sodium is a potent loop diuretic that acts as a blocker for the sodium-potassium-chloride cotransporter (NKCC). It selectively inhibits NKCC1 and NKCC2, with IC50 values of 0.68 μM and 4.0 μM for hNKCC1A and hNKCC2A, respectively [1] [2].

Bumetanide sodium effectively inhibits the major human splice variants of NKCCs, specifically hNKCC1A and hNKCC2A. It demonstrates dose-dependent inhibition of ^86Rb^+ uptake in NKCC1A-expressing oocytes, ranging from 0.03 to 100 μM over 5 minutes. Additionally, Bumetanide sodium targets the NKCC2 isoform B in HEK-293 cells, achieving an IC50 value of 0.54 μM.

Bumetanide sodium (7.6-30.4 mg/kg; i.v.) reduces the decline in apparent diffusion coefficients (ADC) ratios in the cortex and striatum by 40-67%, indicating decreased edema formation [3], and decreases infarct size [3]. It has varying half-lives—21.4 min, 53.8 min, and 137 min—after intravenous doses of 2 mg/kg, 8 mg/kg, and 20 mg/kg, respectively, in rats [4].