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(Synonyms: 苯甲基磺酰氟; Phenylmethylsulfonyl fluoride; Benzylsulfonyl fluoride) 目录号 : GC10477

A nonspecific, irreversible serine protease inhibitor

PMSF Chemical Structure

Cas No.:329-98-6

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10mM (in 1mL DMSO)
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10g
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Sample solution is provided at 25 µL, 10mM.

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实验参考方法

Animal experiment [1]:

Animal models

Adult male mice

Preparation Method

This assay measures analgesic activity. All animals were placed on a 55 ± 1 °C hot plate, and the latency time to either jumping or licking was recorded. The cut-off time was set as 15 s to protect mice from any damage. The antinociceptive effects of a single dose of morphine (10 mg/kg s.c.) and PMSF (60, 120, and 300 mg/kg) were determined.

Dosage form

60, 120, and 300 mg/kg, i.p.

Applications

The results suggest that the administration of the PMSF doses (120 and 300 mg/kg, i.p.) led to significant changes in the analgesic latency time, while administration with PMSF (60 mg/kg i.p.) had no significant difference.

References:

[1]: Akbarabadi E A, Vardanjani H R, Molavinia S, et al. PMSF Attenuates Morphine Antinociceptive Tolerance and Dependence in Mice: Its Association with the Oxidative Stress Suppression[J]. Iranian Journal of Pharmaceutical Research: IJPR, 2021, 20(3): 300.

产品描述

PMSF (Phenylmethanesulfonyl fluoride) is an irreversible serine/cysteine protease inhibitor and PMSF commonly used in the preparation of cell lysates [1,2]. phenylmethylsulfonyl fluoride (PMSF) is also an inhibitor of fatty acid amide hydrolase (FAAH) [3].

Aqueous preparations of PMSF become inactive toward proteases unless promptly brought into contact with protease. Inactivation of PMSF increases with increased pH and temperature. Half-lives of the inhibitor at 25°C are approximately 110,55, and 35 min at pH 7.0, 7.5, and 8.0, respectively. At pH 8, 100 μM PMSF is almost completely inactivated within 1 hr at 25°C or within 22 hr at 4°C. Stock solutions of PMSF in 100% isopropanol are stable at 25°C for months if not longer. Reactivation of PMSF-inhibited chymotrypsin did not occur within 1 week at 25°C at pH 7.0 [4]. PMSF inhibits the acylation of the inositol residue of GPI intermediates in bloodstream form T. brucei. PMSF inhihits the formntion of glycolipid C but does not inhibit fatty acid remodeling in vitro. PMSF inhihits GPI acylation and ethanolamine phosphatp addition in procyclic trypanosomes but not in Hela cells [5].

PMSF has a notable antinociceptive effect at doses 120 and 300 mg/kg. The dose of (60 mg/kg, i.p.) PMSF was considered as a sub-antinociceptive dose. A sub-antinociceptive dose (60 mg/kg) of PMSF could reduce tolerance in both acute and chronic methods of administration. However, alleviation of dependence and suppression of oxidative stress markers occurred in the chronic administration of PMSF [3].

References:
[1]. Tunlid A, Jansson S. Proteases and their involvement in the infection and immobilization of nematodes by the nematophagous fungus Arthrobotrys oligospora[J]. Applied and Environmental Microbiology, 1991, 57(10): 2868-2872.
[2]. Rajakumar A, Brandon H M, Daftary A, et al. Evidence for the functional activity of hypoxia-inducible transcription factors overexpressed in preeclamptic placentae[J]. Placenta, 2004, 25(10): 763-769.
[3]. Akbarabadi E A, Vardanjani H R, Molavinia S, et al. PMSF Attenuates Morphine Antinociceptive Tolerance and Dependence in Mice: Its Association with the Oxidative Stress Suppression[J]. Iranian Journal of Pharmaceutical Research: IJPR, 2021, 20(3): 300.
[4]. James G T. Inactivation of the protease inhibitor phenylmethylsulfonyl fluoride in buffers[J]. Analytical biochemistry, 1978, 86(2): 574-579.
[5]. Güther M L, Masterson W J, Ferguson M A. The effects of phenylmethylsulfonyl fluoride on inositol-acylation and fatty acid remodeling in African trypanosomes[J]. Journal of Biological Chemistry, 1994, 269(28): 18694-18701.

PMSF(苯甲磺酰氟)是一种不可逆的丝氨酸/半胱氨酸蛋白酶抑制剂,PMSF 常用于制备细胞裂解物[1,2]。苯甲基磺酰氟 (PMSF) 也是脂肪酸酰胺水解酶 (FAAH) 的抑制剂[3]

除非立即与蛋白酶接触,否则 PMSF 的水性制剂对蛋白酶失去活性。 PMSF 的失活随着 pH 值和温度的升高而增加。在 25°C 和 pH 7.0、7.5 和 8.0 时,抑制剂的半衰期分别约为 110,55 和 35 分钟。在 pH 8 时,100 μM PMSF 在 25°C 下 1 小时内或在 4°C 下 22 小时内几乎完全失活。 PMSF 的 100% 异丙醇储备溶液在 25°C 下可稳定数月甚至更长。在 25°C 和 pH 7.0 下 1 周内,PMSF 抑制的胰凝乳蛋白酶没有发生再激活 [4]。 PMSF 抑制血流中 GPI 中间体肌醇残基的酰化形成布氏锥虫。 PMSF 抑制糖脂 C 的形成,但不抑制体外脂肪酸重塑。 PMSF 抑制前环锥虫中的 GPI 酰化和乙醇胺磷酸化添加,但不抑制 Hela 细胞[5]

PMSF 在剂量为 120 和 300 mg/kg 时具有显着的镇痛作用。 (60 mg/kg, i.p.) PMSF 的剂量被认为是亚镇痛剂量。亚镇痛剂量 (60 mg/kg) 的 PMSF 可以降低急性和慢性给药方法的耐受性。然而,长期服用 PMSF 可减轻依赖性并抑制氧化应激标志物 [3]

Chemical Properties

Cas No. 329-98-6 SDF
别名 苯甲基磺酰氟; Phenylmethylsulfonyl fluoride; Benzylsulfonyl fluoride
化学名 phenylmethanesulfonyl fluoride
Canonical SMILES C1=CC=C(C=C1)CS(=O)(=O)F
分子式 C7H7FO2S 分子量 174.2
溶解度 ≥ 17.4mg/mL in DMSO 储存条件 Store at RT
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溶解性数据

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1 mM 5.7405 mL 28.7026 mL 57.4053 mL
5 mM 1.1481 mL 5.7405 mL 11.4811 mL
10 mM 0.5741 mL 2.8703 mL 5.7405 mL
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Research Update

PMSF Attenuates Morphine Antinociceptive Tolerance and Dependence in Mice: Its Association with the Oxidative Stress Suppression

Opioids use has been limited due to tolerance and dependence as major unwanted effects. Previous evidence has shown that targeting endocannabinoid signaling can prevent the development of opioid tolerance and dependence. This study was designed to evaluate the effect of phenylmethylsulfonyl fluoride (PMSF), an inhibitor of fatty acid amide hydrolase (FAAH), on morphine antinociceptive tolerance and physical dependence in mice. The antinociceptive effects of PMSF at the doses 60, 120, and 300 mg/kg were investigated. Results showed that PMSF has a notable antinociceptive effect at doses 120 and 300 mg/kg. The dose of (60 mg/kg, i.p.) PMSF was considered as a sub-antinociceptive dose. Morphine tolerance and dependence were induced by twice-daily injection of morphine (10 mg/kg, s.c.) for 10 consecutive days and the last dose on day 11. Tolerance was assessed by the hot-plate test and dependence by naloxone-precipitated morphine withdrawal signs. In the brain, oxidative stress markers include activities of glutathione peroxidase, catalase, superoxide dismutase, and levels of malondialdehyde and glutathione were determined. A sub-antinociceptive dose (60 mg/kg) of PMSF could reduce tolerance in both acute and chronic methods of administration. However, alleviation of dependence and suppression of oxidative stress markers occurred in the chronic administration of PMSF. In conclusion, it seems that PMSF can suppress morphine tolerance and dependence. However, more studies are needed to clarify its mechanism.

Evaluation of phenylmethanesulfonyl fluoride (PMSF) as a tracer candidate mapping acetylcholinesterase in vivo

The availability of phenylmethanesulfonyl fluoride (PMSF), an irreversible cholinesterase inhibitor, for a tracer mapping acetylcholinesterase (AchE) in vivo in brain and other organs was evaluated using [35S]PMSF in mice and rats. [35S]PMSF was well taken up into the brain, heart and muscle, and the radioactivities were trapped in these organs. Pretreatment with non-labeled PMSF decreased 33-40% of the trapped radioactivities in the brain and other organs in mice. However, regional distribution of [35S]PMSF in rat brain did not correlate well with that of AchE activity, suggesting that the selectivity of PMSF toward AchE may be insufficient for use as an in vivo tracer mapping AchE.

Prolyl Endopeptidase-Like Facilitates the α-Synuclein Aggregation Seeding, and This Effect Is Reverted by Serine Peptidase Inhibitor PMSF

The aggregation of α-synuclein (α-Syn) is a characteristic of Parkinson's disease (PD). α-Syn oligomerization/aggregation is accelerated by the serine peptidase, prolyl oligopeptidase (POP). Factors that affect POP conformation, including most of its inhibitors and an impairing mutation in its active site, influence the acceleration of α-Syn aggregation resulting from the interaction of these proteins. It is noteworthy, however, that α-Syn is not cleaved by POP. Prolyl endopeptidase-like (PREPL) protein is structurally related to the serine peptidases belonging to the POP family. Based on the α-Syn-POP studies and knowing that PREPL may contribute to the regulation of synaptic vesicle exocytosis, when this protein can encounter α-Syn, we investigated the α-Syn-PREPL interaction. The binding of these two human proteins was observed with an apparent affinity constant of about 5.7 μM and, as in the α-Syn assays with POP, the presence of PREPL accelerated the oligomerization/aggregation events, with no α-Syn cleavage. Furthermore, despite this lack of hydrolytic cleavage, the serine peptidase active site inhibitor phenylmethylsulfonyl fluoride (PMSF) abolished the enhancement of the α-Syn aggregation by PREPL. Therefore, given the attention to POP inhibitors as potential drugs to treat synucleinopathies, the present data point to PREPL as another potential target to be explored for this purpose.

Phenylmethylsulfonyl fluoride (PMSF) given systemically produces naloxone-reversible analgesia and potentiates effects of beta-endorphin given centrally

Intraperitoneal (IP) injection of the serine proteinase inhibitor phenylmethylsulfonyl fluoride (PMSF) produced dose-dependent analgesia in Sprague-Dawley rats. AD50 was 2.9 +/- 1.4 (S.E.) mg kg-1, the analgesia was antagonized by naloxone but unaffected by atropine. PMSF significantly enhanced the analgesic effect of beta-endorphin (END) given by intracerebroventricular (ICV) infusion in rats, the enhanced END analgesia was naloxone-reversible. In Swiss-Webster mice the 24-hr LD50 value for PMSF was 215 +/- 55 mg kg-1 IP; autonomic and behavioral responses were similar to those seen in rats with ICV END. These results indicate that systemic PMSF can protect central endorphin(s) from enzymatic destruction. The significant analgesia, low toxicity, naloxone reversibility and minimal anticholinesterase effects suggest the use of PMSF as a parenteral analgesic.

Effects of calcium gluconate and PMSF in the treatment of acute intoxication of chicken by TOCP

To examine the efficacy of calcium gluconate (two doses of Ca-Glu 5 mg/kg i.v.) to alleviate the injurious effects of organophosphorus induced delayed neuropathy (OPIDN) in the presence or absence of phenylmethanesulfonyl fluoride (PMSF 90 mg/kg i.m.), 14 groups of four isabrown hens were used. To measure the lymphocyte neuropathy target esterase (LNTE)activity, groups receiving just distilled water (control), groups receiving just Tri-orto-cresyl phosphate (TOCP; 500 mg/kg p.o.) (Positive control), and other groups receiving TOCP and Ca-Glu or PMSF simultaneously or 12 hours later following intoxication by TOCP were used. They were sacrificed 12 and 24 hours after the administration of TOCP. To observe a 28-day time course of neurotoxicity scores and calcium plasma concentration, five groups were used. Regarding free Ca(2+)in the plasma, the positive control produced a characteristic profile time course up and down during 28 days, and some hens with maximum score of neurotoxicity in 28 days. The treatment, which prevented greater oscillation in free Ca(2+) in the plasma, presented a decrease in OPIDN in relation to the positive control. Twelve hours after the administration of TOCP, LNTE was 70-80% inhibited when compared with control, whereas the first decrease in the free Ca(2+) in the plasma was significantly different from the control only 24 hours after the administration of TOCP. In summary, the sooner the Ca-Glu is started, the less severe the neuropathy effects.