54-31-9
54-31-9
Chemical Structure
Furosemide
- CAS No.: 54-31-9
- Formula:C12H11ClN2O5S
- Molecular Weight:330.74
IUPAC Name: 4-chloro-2-((furan-2-ylmethyl)amino)-5-sulfamoylbenzoic acid
InChIKey: ZZUFCTLCJUWOSV-UHFFFAOYSA-N
SMILES: O=C(O)C1=CC(S(=O)(N)=O)=C(Cl)C=C1NCC2=CC=CO2
Biological Activity: Furosemide is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide selectively antagonizes GABAA receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide can be used in research on congestive heart failure, hypertension, and edema[1][2][3][4][5][6][7][8][9][10][11][12][13][14].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Furosemide | 99.83% | Furosemide is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide selectively antagonizes GABAA receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide can be used in research on congestive heart failure, hypertension, and edema. | ||||||||||||||||||||
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Furosemide (Standard) | 99.95% | Furosemide (Standard) is the analytical standard of Furosemide (HY-B0135). This product is intended for research and analytical applications. Furosemide is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide selectively antagonizes GABAA receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide can be used in research on congestive heart failure, hypertension, and edema. | ||||||||||||||||||||
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Furosemide solution | Furosemide solution is mainly composed of Furosemide (HY-B0135). Furosemide is a potent and orally active inhibitor of Na+/K+/2Cl- (NKCC) cotransporter, NKCC1 and NKCC2. Furosemide is also a GABAA receptors antagonist and displays 100-fold selectivity for α6-containing receptors than α1-containing receptors. Furosemide acts as a loop diuretic and used for the study of congestive heart failure, hypertension and edema. | |||||||||||||||||||||
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Furosemide-d5 | 99.85% | Furosemide-d5 is the deuterated-labeled Furosemide (HY-B0135). Furosemide is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide selectively antagonizes GABAA receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide can be used in research on congestive heart failure, hypertension, and edema. | ||||||||||||||||||||
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Structural Analogs
-
Similarity Score 0.90
HY-B0135AFurosemide sodium -
Similarity Score 0.84
HY-W208353Furosemide impurity 1 -
Similarity Score 0.71
HY-W140611Furosemide impurity 7 -
Similarity Score 0.69
HY-174066SI-W052 -
Similarity Score 0.65
HY-Z8151Furosemide impurity 3 -
Similarity Score 0.64
HY-174166AqF026 -
Similarity Score 0.63
HY-43670RChlorthalidone impurity (Standard) -
Similarity Score 0.63
HY-43670AChlorthalidone impurity ammonium -
Similarity Score 0.63
HY-W042301RXipamide (Standard) -
Explore the MedChemAI to find more analogs
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]
- [10]. Orlov SN, et al. NKCC1 and NKCC2: The pathogenetic role of cation-chloride cotransporters in hypertension. Genes & diseases. 2015 Jun;2(2):186-196.
- [11]. Limmer F, et al. Regulation of the Na(+)-K(+)-2Cl(-) cotransporter by cGMP/cGMP-dependent protein kinase I after furosemide administration. The FEBS journal. 2015 Oct;282(19):3786-98.
- [12]. Suki WN, et al. Acute treatment of hypercalcemia with furosemide. N Engl J Med. 1970;283(16):836-840.
- [13]. Osmanovic E, et al. The Effect of Furosemide on Arterial Blood Pressure, Blood Glucose Levels and Incidence of Heart Arrhythmias. American Journal of Internal Medicine. 2017;5(3):41-45.
- [14]. Tenzing D, et al. Effect of furosemide in the treatment of high-altitude pulmonary edema. BMC Pulm Med. 2024 Mar 4;24(1):109.
