Furosemide is a loop diuretic inhibitor of NKCC (Na+/2Cl-/K+) cotransporter. Furosemide acts as a non-competitive antagonist at GABAA receptors with ~ 100-fold greater selectivity for α6-containing receptors than α1-containing receptors.
Thompson et al (1999) Residues in transmembrane domains I and II determine g-aminobutyric acid type AA receptor subtype-selective antagonism by furosemide. Mol.Pharmacol. 55 993. Gutschmidt et al (1999) Anticonvulsant actions of furosemide in vitro. Neuroscience 91 1471.
Soluble in DMSO (66 mg/ml at 25° C), ethanol (<1 mg/ml at 25° C), water (<1 mg/ml at 25° C), methanol (50 mg/ml), and DMF.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.
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Limmer et alLimmer et al. (PubMed ID 26183401) found that Furosemide increased vasodilator-stimulated phosphoprotein phosphorylation and membrane translocation of NKCC2 via cGkI activation in mice. -SCBT Publication Review
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