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PMSF Serine Protease inhibitor

Cat.No.S3025

PMSF (Phenylmethylsulfonyl Fluoride, Benzylsulfonyl fluoride) is an irreversible serine/cysteine protease inhibitor.
PMSF  Serine Protease inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 174.19

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Quality Control

Batch: Purity: 99.91%
99.91

Solubility

In vitro
Batch:

DMSO : 35 mg/mL (200.93 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 35 mg/mL

Water : Insoluble

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In vivo
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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.
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Chemical Information, Storage & Stability

Molecular Weight 174.19 Formula

C7H7FO2S

Storage (From the date of receipt)
CAS No. 329-98-6 Download SDF Storage of Stock Solutions

Synonyms Phenylmethylsulfonyl Fluoride, Benzylsulfonyl fluoride Smiles C1=CC=C(C=C1)CS(=O)(=O)F

Mechanism of Action

Targets/IC50/Ki
cysteine protease
chymotrypsin
In vitro
Although human trypsin is less susceptible to inhibition by PMSF, this compound rapidly inactivates purified chymotrypsin from human pancreas. It also rapidly inhibits acetylcholinesterase from human red cells. As an inhibitor of phosphatidylinositol-specific phospholipase C, treatment with this chemical at 2 mM almost completely inhibits carbachol-stimulated inositol incorporation into phosphatidylinositol (PI) of longitudinal smooth muscle of guinea pig ileum, while it has no effect on potassium-stimulated inositol incorporation. In contrast to its specific inhibition of carbachol-stimulated phosphoinositide turnover, this agent produces a transient inhibition of contraction by both carbachol and potassium. It has been shown to inhibit the addition of ethanolamine phosphate to glycosylphosphatidylinositol (GPI) intermediates in Trypanosoma brucei. This inhibitor also inhibits the acylation of the inositol residue of GPI intermediates in bloodstream form T. brucei. It inhibits ethanolamine phosphate addition and inositol acylation for procyclic forms of T. brucei but not for mammalian HeLa cells. This compound is the more reactive inactivator of mouse acetylcholinesterase (AChE), as the 8-fold higher BSF concentration is necessary to achieve even a 6-fold slower inactivation than that using PMSF.
In vivo
Intraperitoneal injection of PMSF produces dose-dependent analgesia in Sprague-Dawley rats. This compound significantly enhances the analgesic effect of beta-endorphin (END) in rats. Mice receiving i.p. injections of this chemical exhibit cannabinoid effects that include antinociception, hypothermia and immobility with ED50 of 86 mg/kg, 224 mg/kg and 206 mg/kg, respectively. Pretreatment with an inactive dose of this compound (30 mg/kg) enhances the effects of anandamide on tail-flick response (antinociception), spontaneous activity and mobility by 5-, 10- and 8-fold, respectively. Administration of this chemical 12 hours prior to PSP causes complete protection in organophosphorus ester-induced delayed neuropathy (OPIDN) in hens, but it administered 4 hours after PSP potentiates its neurotoxic effects. Pretreatment with this compound (30 mg/kg, i.p.) prior to an injection of 1 or 10 mg/kg 3H-anandamide results 5 minutes later in enhanced brain levels of anandamide compared to those obtained with 3H-anandamide plus vehicle injection. Pretreatment with it inhibits tri-ortho-cresyl phosphate (TOCP)-induced neurofilament (NF) degradation, and protects hens against the development of organophosphate-induced delayed neuropathy (OPIDN). Administration of this chemical enhances the characteristic cannabimimetic effects of Δ(9)-tetrahydrocannabinol (THC) or anandamide (AEA) in ICR mice, by inhibiting the enzyme fatty acid amide hydrolase.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/7518442/
  • [5] https://pubmed.ncbi.nlm.nih.gov/9399986/
  • [6] https://pubmed.ncbi.nlm.nih.gov/10591511/

Clinical Trial Information

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

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT04062786 Unknown status
Scheduled Heart Surgery|Valve Replacement|Coronary Artery Bypass
University Hospital Strasbourg France
February 21 2019 --
NCT03300323 Unknown status
Peri-operative Fluid Management
St George''s Healthcare NHS Trust
October 2017 Not Applicable
NCT02569008 Completed
Post Cardiac Surgery
St George''s University of London
January 2014 Not Applicable

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