Home Immunology & Inflammation ROS inhibitor (S)-Methylisothiourea sulfate

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(S)-Methylisothiourea sulfate ROS inhibitor

Cat.No.S3631

(S)-Methylisothiourea sulfate is a potent inhibitor of inducible NO synthase (iNOS).
(S)-Methylisothiourea sulfate ROS inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 139.19

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Quality Control

Batch: S363101 Water]27 mg/mL]false]DMSO]Insoluble]false]Ethanol]Insoluble]false Purity: 99.66%
99.66

Solubility

In vitro
Batch:

Water : 27 mg/mL

DMSO : Insoluble
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 139.19 Formula

C2H6N2S.1/2 H2SO4

 Storage (From the date of receipt)
CAS No. 867-44-7 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles CSC(=N)N.CSC(=N)N.OS(=O)(=O)O

Mechanism of Action

Targets/IC50/Ki
iNOS
In vitro
S-Methylisothiourea sulfate (SMT) is at least 10- to 30-fold more potent as an inhibitor of inducible NOS (iNOS) in immunostimulated cultured macrophages (EC50, 6 microM) and vascular smooth muscle cells (EC50, 2 microM) than NG-methyl-L-arginine (MeArg) or any other NOS inhibitor yet known. The effect of SMT on iNOS activity can be reversed by excess L-arginine in a concentration-dependent manner. SMT is a competitive inhibitor of iNOS activity at the L-arginine site. SMT (up to 1 mM) does not inhibit the activity of xanthine oxidase, diaphorase, lactate dehydrogenase, monoamine oxidase, catalase, cytochrome P450, or superoxide dismutase. SMT is equipotent with MeArg in inhibiting the endothelial, constitutive isoform of NOS in vitro.
In vivo
Treatment of the mice with S-methylisothiourea sulfate (SMT), a potent inhibitor of inducible NO synthase (NOS), prevents the elevation of serum NO levels and concomitantly reduces the enhanced response to pentylenetetrazole. Therapeutic administration of SMT (5 mg/kg, i.p., given 2 hr after LPS, 10 mg/kg, i.p.) attenuates the rises in plasma alanine and aspartate aminotransferases, bilirubin, and creatinine and also prevents hypocalcaemia when measured 6 hr after administration of LPS. SMT (1 mg/kg, i.p.) improves 24-hr survival of mice treated with a high dose of LPS (60 mg/kg, i.p.). SMT is beneficial to myocardial contractility in this model of endotoxemia.
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT05770284 Recruiting
Liver Diseases
Institute of Liver and Biliary Sciences India
 March 15 2023 Not Applicable
NCT02858362 Terminated
Duchenne Muscular Dystrophy
Summit Therapeutics
 June 2016 Phase 2

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