PMSF (Phenylmethanesulfonyl fluoride) is an irreversible inhibitor of serine proteinases, which is associated with the development of the delayed organophosphorus neuropathy. It has a role in a lot of cellular repair and regeneration processes in many kinds of tissues. PMSF is a long acting Neuropathy Target Esterase (NTE) inhibitor. NTE is a protection was related to inhibition of the putative target of organophosphate-induced delayed polyneuropathy (OPIDP). PMSF can increase NTE inhibition to more than 90%. PMSF also acts as an active site directed reagent for γ-glutamyl transpeptidase.

99%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

Phenylmethylsulfonyl fluoride; Benzylsulfonyl fluoride

white powder

Ethanol：15mg/mL(86.11mM)
DMSO：35mg/ml(200.93 mM)

cysteine protease ，chymotrypsin

Although human trypsin is less susceptible to inhibition by PMSF, PMSF rapidly inactivates purified chymotrypsin from human pancreas. PMSF also rapidly inhibits acetylcholinesterase from human red cells. As an inhibitor of phosphatidylinositol-specific phospholipase C, PMSF treatment 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, PMSF produces a transient inhibition of contraction by both carbachol and potassium. PMSF has been shown to inhibit the addition of ethanolamine phosphate to glycosylphosphatidylinositol (GPI) intermediates in Trypanosoma brucei. PMSF also inhibits the acylation of the inositol residue of GPI intermediates in bloodstream form T. brucei. PMSF inhibits ethanolamine phosphate addition and inositol acylation for procyclic forms of T. brucei but not for mammalian HeLa cells. PMSF 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.

Intraperitoneal injection of PMSF produces dose-dependent analgesia in Sprague-Dawley rats. PMSF significantly enhances the analgesic effect of beta-endorphin (END) in rats. Mice receiving i.p. injections of PMSF 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 PMSF (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 PMSF 12 hours prior to PSP causes complete protection in organophosphorus ester-induced delayed neuropathy (OPIDN) in hens, but PMSF administered 4 hours after PSP potentiates its neurotoxic effects. Pretreatment with PMSF (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 PMSF inhibits tri-ortho-cresyl phosphate (TOCP)-induced neurofilament (NF) degradation, and protects hens against the development of organophosphate-induced delayed neuropathy (OPIDN). Administration of PMSF enhances the characteristic cannabimimetic effects of Δ(9)-tetrahydrocannabinol (THC) or anandamide (AEA) in ICR mice, by inhibiting the enzyme fatty acid amide hydrolase.

[1] Turini P, et al. J Pharmacol Exp Ther, 1969, 167(1), 98-104.
[2] Pinsky C, et al. Life Sci, 1982, 31(12-13), 1193-1196.
[3] Sekar MC, et al. Cell Calcium, 1984, 5(3), 191-203.