Furosemide

54-31-9

330.74

DMSO : >= 100 mg/mL (302.35 mM); H2O : 0.1 mg/mL (0.30 mM; Need ultrasonic)

Membrane Transporter/Ion Channel; Neuronal Signaling; Membrane Transporter/Ion Channel

Furosemide is a potent and orally active inhibitor of Na⁺/K⁺/2Cl^- (NKCC) cotransporter, NKCC1 and NKCC2^[1]. Furosemide is also a GABA_A receptors antagonist and displays 100-fold selectivity for alpha6-containing receptors than alpha1-containing receptors. Furosemide acts as a loop diuretic and used for the study of congestive heart failure, hypertension and edema^[2]. IC50 & Target: IC50: NKCC1 and NKCC2^[1]
IC50: GABA_A receptors^[2] In Vitro: Furosemide (500 uM; 72-96 hours) significantly changes the proliferation rates in MKN45 cells (the poorly differentiated human gastric adenocarcinoma cell line). however, it has no effects on MKN28 cells (the moderately differentiated human gastric adenocarcinoma cell line). The growth rate of MKN45 cells is larger than that of MKN28 cells^[4].
Furosemide (10 uM, 30 uM, 100 uM; 45 min exposure) significantly decreases cation channel activity and [Ca(2+)](i) in human erythrocytes drawn from healthy individuals. Tert-butylhydroperoxide similarly enhances the non-selective cation channels activity, increases [Ca(2+)](i) and triggered cell membrane scrambling, however, the effects is significantly blunted by furosemide again^[5].
In Vivo: Furosemide (intraperitoneal injection; 100 mg/kg; single dose) is injected after kanamycin (KM) (1000 mg/kg) to creat a deaf mouse model in C57BL/6 mouse. After injection, hearing loss and cochlear hair cell damage are evaluated on day 1, day 2 and day 3, respectively. The hearing is markedly deteriorated even from the next day (Day-1 group), OHCs (outer hair cell) morphology of apical, middle and basal turns are disorganized in mice on day3^[3].