Furosemide sodium (Frusemide Sodium) is a potent and orally active inhibitor of Na+/K+/2Cl- (NKCC) cotransporter, NKCC1 and NKCC2. Furosemide sodium is also a GABAA receptors antagonist and displays 100-fold selectivity for α6-containing receptors than α1-containing receptors. Furosemide sodium acts as a loop diuretic and used for the study of congestive heart failure, hypertension and edema.

NKCC:, GABAA receptor:

Furosemide sodium, at a concentration of 500 µM administered over 72-96 hours, significantly alters the proliferation rates of MKN45 cells, a poorly differentiated human gastric adenocarcinoma cell line, while exhibiting no impact on MKN28 cells, a moderately differentiated counterpart, with MKN45 cells displaying a higher growth rate [4]. Additionally, exposures to Furosemide sodium at concentrations of 10 µM, 30 µM, and 100 µM for 45 minutes substantially reduce cation channel activity and intracellular Ca(2+) levels in human erythrocytes from healthy individuals. Conversely, Tert-butylhydroperoxide increases non-selective cation channel activity and intracellular Ca(2+) concentrations, promoting cell membrane scrambling, which is notably mitigated by Furosemide sodium [5].

Furosemide sodium (intraperitoneal injection; 100 mg/kg; single dose) is administered following kanamycin (KM) (1000 mg/kg) to establish a deaf mouse model in C57BL/6 mice. This regimen leads to the evaluation of hearing loss and cochlear hair cell damage on days 1, 2, and 3 post-injection. Marked deterioration in hearing is observed as early as the next day (Day-1 group), with the morphology of outer hair cells (OHCs) within the apical, middle, and basal turns of the cochlea becoming disorganized by day 3[1].