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Molsidomine

Cat.No.S4664

Molsidomine (SIN-10, Corvaton, Morsydomine) is an orally active, long acting vasodilating drug. This compound is metabolized in the liver to the active metabolite linsidomine. Linsidomine is an unstable compound that releases nitric oxide (NO) upon decay as the actual vasodilating compound.
Molsidomine Chemical Structure

Chemical Structure

Molecular Weight: 242.23

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 242.23 Formula

C9H14N4O4

Storage (From the date of receipt)
CAS No. 25717-80-0 Download SDF Storage of Stock Solutions

Synonyms SIN-10, Corvaton, Morsydomine Smiles CCOC(=NC1=C[N+](=NO1)N2CCOCC2)[O-]

Solubility

In vitro
Batch:

DMSO : 49 mg/mL (202.28 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : 24 mg/mL

Ethanol : 24 mg/mL

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Calculation results:

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

In vivo
Molsidomine (50, 100, 250 μg/kg) reduces coronary flow while the coronary resistance remains unaffected by this compound. This chemical decreases myocardial oxygen consumption. Heart rate and contractility remains unchanged by it. Stroke volume and cardiac output fall after this agent. The fall in blood pressure after molsidomine follows the reduction in cardiac output as sequel of lowered preload and venous return to the heart[1].
References

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