Torsemide - CAS 56211-40-6
Catalog number: 56211-40-6
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Torsemide is a pyridine-sulfonyl urea type loop diuretic with an IC50 of 2.7 ± 0.17 μM.
AC-4464, JDL-464; AC 4464, JDL 464; AC4464, JDL464
Canonical SMILES:
1.Loop Diuretics in the Treatment of Hypertension.
Malha L1, Mann SJ2. Curr Hypertens Rep. 2016 Apr;18(4):27. doi: 10.1007/s11906-016-0636-7.
Loop diuretics are not recommended in current hypertension guidelines largely due to the lack of outcome data. Nevertheless, they have been shown to lower blood pressure and to offer potential advantages over thiazide-type diuretics. Torsemide offers advantages of longer duration of action and once daily dosing (vs. furosemide and bumetanide) and more reliable bioavailability (vs. furosemide). Studies show that the previously employed high doses of thiazide-type diuretics lower BP more than furosemide. Loop diuretics appear to have a preferable side effect profile (less hyponatremia, hypokalemia, and possibly less glucose intolerance). Studies comparing efficacy and side effect profiles of loop diuretics with the lower, currently widely prescribed, thiazide doses are needed. Research is needed to fill gaps in knowledge and common misconceptions about loop diuretic use in hypertension and to determine their rightful place in the antihypertensive arsenal.
2.Torsemide versus furosemide in heart failure patients: insights from Duke University Hospital.
Mentz RJ1, Buggey J, Fiuzat M, Ersbøll MK, Schulte PJ, DeVore AD, Eisenstein EL, Anstrom KJ, OʼConnor CM, Velazquez EJ. J Cardiovasc Pharmacol. 2015 May;65(5):438-43. doi: 10.1097/FJC.0000000000000212.
Furosemide has historically been the primary loop diuretic in heart failure patients despite data suggesting potential advantages with torsemide. We used the Duke Echocardiography Lab Database to investigate patients admitted with heart failure to Duke Hospital from 2000 to 2010 who were discharged on either torsemide or furosemide. We described baseline characteristics based on discharge diuretic and assessed the relationship with all-cause mortality through 5 years. Of 4580 patients, 86% (n = 3955) received furosemide and 14% (n = 625) received torsemide. Patients receiving torsemide were more likely to be female and had more comorbidities compared with furosemide-treated patients. Survival was worse in torsemide-treated patients [5-year Kaplan-Meier estimated survival of 41.4% (95% CI: 36.7-46.0) vs. 51.5% (95% CI: 49.8-53.1)]. After risk adjustment, torsemide use was no longer associated with increased mortality (hazard ratio 1.16; 95% CI: 0.
3.Optimization and Validation of a Sensitive Method for HPLC-PDA Simultaneous Determination of Torasemide and Spironolactone in Human Plasma using Central Composite Design.
Subramanian V, Nagappan K, Sandeep Mannemala S. Acta Chim Slov. 2015;62(3):633-41.
A sensitive, accurate, precise and rapid HPLC-PDA method was developed and validated for the simultaneous determination of torasemide and spironolactone in human plasma using Design of experiments. Central composite design was used to optimize the method using content of acetonitrile, concentration of buffer and pH of mobile phase as independent variables, while the retention factor of spironolactone, resolution between torasemide and phenobarbitone; and retention time of phenobarbitone were chosen as dependent variables. The chromatographic separation was achieved on Phenomenex C(18) column and the mobile phase comprising 20 mM potassium dihydrogen ortho phosphate buffer (pH-3.2) and acetonitrile in 82.5:17.5 v/v pumped at a flow rate of 1.0 mL min(-1). The method was validated according to USFDA guidelines in terms of selectivity, linearity, accuracy, precision, recovery and stability. The limit of quantitation values were 80 and 50 ng mL(-1) for torasemide and spironolactone respectively.
4.Heritability of metoprolol and torsemide pharmacokinetics.
Matthaei J1, Brockmöller J1, Tzvetkov MV1, Sehrt D1, Sachse-Seeboth C1, Hjelmborg JB2, Möller S2, Halekoh U2, Hofmann U3, Schwab M3,4, Kerb R3. Clin Pharmacol Ther. 2015 Dec;98(6):611-21. doi: 10.1002/cpt.258. Epub 2015 Oct 19.
Genetic variation in the pharmacokinetics of metoprolol and torsemide due to polymorphisms in CYP2D6, CYP2C9, and OATP1B1 has been extensively studied. However, it is still unknown how much of the variation in pharmacokinetics of these two clinically important drugs in total is due to genetic factors. Metoprolol and torsemide were intravenously administered to 44 monozygotic and 14 dizygotic twin pairs. Metoprolol area under the curve (AUC) varied 4.7-fold and torsemide AUC 3.5-fold. A very high fraction of AUC variations, 91% of metoprolol and 86% of torsemide, were found to be due to additive genetic effects. However, known genetic variants of CYP2D6, -2C9, and OATP1B1 explained only 39%, 2%, and 39% of that variation, respectively. Comparable results for genetically explained variation in pharmacokinetics and pharmacodynamics have been found for other substrates of these enzymes earlier. These findings indicate that a substantial fraction of the heritable variability in the pharmacokinetics of metoprolol and torsemide remains to be elucidated.
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CAS 56211-40-6 Torsemide

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