FuROSemide sodium 是 Na+/K+/2Cl- (NKCC)，NKCC1 和 NKCC2 共转运蛋白的有效的和具有口服活性抑制剂。FuROSemide sodium 也是 GABAA 受体拮抗剂，对含 α6 受体的选择性是含 α1 受体的 100 倍。FuROSemide sodium 用作利尿试剂，用于充血性心力衰竭，高血压和水肿的研究。

Furosemide 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.

Furosemide sodium (500 μM; 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 sodium (10 μM, 30 μM, 100 μM; 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 sodium again[5].

Furosemide sodium (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[1].

41733-55-5

C12H10ClN2NaO5S

352.73

Lasix;Frusemide Sodium

DMSO:135mg/mL (382.7mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years