Torsemide Chloride Channel inhibitor

Cat.No.S1698

Torsemide (AC-4464, JDL-464) is a pyridyl sulfonylurea with a chemical structure between that of traditional loop diuretics and Cl- channel blockers, used to treat hypertension.
Torsemide  Chloride Channel inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 348.42

Quality Control

Batch: S169801 4-Methylpyridine]30 mg/mL]true]DMSO]1 mg/mL]false]Water]Insoluble]false Purity: 100%
100

Chemical Information, Storage & Stability

Molecular Weight 348.42 Formula

C16H20N4O3S

Storage (From the date of receipt)
CAS No. 56211-40-6 Download SDF Storage of Stock Solutions

Synonyms AC-4464, JDL-464 Smiles CC1=CC(=CC=C1)NC2=C(C=NC=C2)S(=O)(=O)NC(=O)NC(C)C

Solubility

In vitro
Batch:

4-Methylpyridine : 30 mg/mL

DMSO : 1 mg/mL (2.87 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Mechanism of Action

Targets/IC50/Ki
Cl- channel [1]
In vitro
Torsemide inhibits aldosterone secretion by adrenal cells from rats, cows, and guinea pigs stimulated in vitro by potassium, angiotensin, dibutyryl cyclic AMP, ACTH, or corticosterone. [1] This compound's primary site of action is the thick ascending loop of Henle in the nephron, where it promotes excretion of sodium, water, and chloride via interaction with the Na+, K+, 2Cl− cotransporter. It interferes with the secretion of, and receptor ligand binding of, the mineralocorticoid aldosterone in a dose-dependent manner. [2]
In vivo
Torsemide results in elevated levels of circulating angiotensin II and aldosterone (supportive of interference with aldosterone at the receptor level) in dogs with experimental mitral regurgitation whereas furosemide results in elevated levels of angiotensin II, only. [2] This compound increases the BUN and plasma creatinine concentrations in rats, compared with the baseline value. It immediately increases urine volume significantly. [3]
References

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