41733-55-5
Chemical Structure
Furosemide sodium
- CAS No.: 41733-55-5
- Formula:C12H10ClN2NaO5S
- Molecular Weight:352.73
IUPAC Name: sodium 4-chloro-2-((furan-2-ylmethyl)amino)-5-sulfamoylbenzoate
InChIKey: DLFCAVBMDSKMEY-UHFFFAOYSA-M
SMILES: O=C(C1=CC(S(=O)(N)=O)=C(C=C1NCC2=CC=CO2)Cl)O[Na]
Biological Activity: Furosemide sodium is an orally active GABAA receptor antagonist. Furosemide sodium inhibits carbonic anhydrase, the sodium-chloride cotransporter, sodium reabsorption, tubuloglomerular feedback, and GABA-induced chloride flux. Furosemide sodium can be used as a diuretic reagent. Furosemide sodium is applied in the research of hepatic necrosis, sepsis-associated acute kidney injury, hypoalbuminemia-related fluid retention, and congestive heart failure[1][2][3][4][5][6][7][8][9].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
Furosemide sodium | 99.87% | Furosemide sodium is an orally active GABAA receptor antagonist. Furosemide sodium inhibits carbonic anhydrase, the sodium-chloride cotransporter, sodium reabsorption, tubuloglomerular feedback, and GABA-induced chloride flux. Furosemide sodium can be used as a diuretic reagent. Furosemide sodium is applied in the research of hepatic necrosis, sepsis-associated acute kidney injury, hypoalbuminemia-related fluid retention, and congestive heart failure. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
|
|
Furosemide sodium (Standard) | 99.97% | Furosemide (sodium) (Standard) is the analytical standard of Furosemide (sodium). This product is intended for research and analytical applications. 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. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
References
- [1]. Tucker BJ, et al. Effect of furosemide administration on glomerular and tubular dynamics in the rat. Kidney international. 1984 Aug;26(2):112-21.
- [2]. Mitchell JR, et al. Hepatic necrosis caused by furosemide. Nature. 1974 Oct 11;251(5475):508-11.
- [3]. Das PK, et al. Furosemide Stress Test and Renal Resistive Index for Prediction of Severity of Acute Kidney Injury in Sepsis. Cureus. 2023 Aug;15(8):e44408.
- [4]. Kelly MR, et al. Pharmacokinetics of orally administered furosemide. Clin Pharmacol Ther. 1974 Feb;15(2):178-86.
- [5]. Inoue M, et al. Mechanism of furosemide resistance in analbuminemic rats and hypoalbuminemic patients. Kidney international. 1987 Aug;32(2):198-203.
- [6]. McCurley JM, et al. Furosemide and the progression of left ventricular dysfunction in experimental heart failure. Journal of the American College of Cardiology. 2004 Sep 15;44(6):1301-7.
- [7]. Korpi ER, et al. Furosemide interactions with brain GABAA receptors. British journal of pharmacology. 1997 Mar;120(5):741-8.
- [8]. Cataliotti A, et al. Brain natriuretic peptide enhances renal actions of furosemide and suppresses furosemide-induced aldosterone activation in experimental heart failure. Circulation. 2004 Apr 06;109(13):1680-5.
- [9]. Duchin KL, et al. Effect of furosemide on renal autoregulation. Kidney Int. 1977 Dec;12(6):379-86. [Content Brief]
