2,3-Butanedione-2-monoxime, a non-competitive inhibitor of myosin ATPase, inhibits the ATPase rate of myosin-V and non-muscle myosin-II but not of kinesin or dynein.
2,3-Butanedione-2-monoxime also acts as a reactivator of phosphorylated acetylcholinesterase by removing the phosphate group from the enzyme[1].
In vitro, 2,3-Butanedione-2-monoxime (50mM; 6h or 48h) decreased protein secretion in C. cinerea[2]. 2,3-Butanedione-2-monoxime (50mM; 2h or 4h) resulted in Golgi aggregation but did not alter ER localization in C. cinerea[2]. 2,3-Butanedione-2-monoxime (30mM; 10min; 37℃) decreased accumulated sarcoplasmic reticulum (SR) Ca2+ in Canine ventricular myocytes in the absence of efflux inhibitors[3].
In vivo, 2,3-Butanedione-2-monoxime (5-200mg/kg; i.v.; once) dose-dependently reduced blood pressure in Male spontaneously hypertensive (SHR) and age-matched Wistar-Kyoto (WKY) rat, with a greater antihypertensive effect in SHR rats[4]. 2,3-Butanedione-2-monoxime (0-205mg/kg; i.p.; once) dose-dependently suppressed clonic and tonic-clonic seizures induced by picrotoxin (PTX) in adult mice[5].
References:
[1] Ostap, E Michael. “2,3-Butanedione monoxime (BDM) as a myosin inhibitor.” Journal of muscle research and cell motility vol. 23,4 (2002): 305-8.
[2] Hashimoto, Kohsuke et al. “The myosin ATPase inhibitor, 2,3-butanedione 2-monoxime, prevents protein secretion by the basidiomycete Coprinopsis cinerea.” Biotechnology letters vol. 33,4 (2011): 769-75.
[3] Phillips, R M, and R A Altschuld. “2,3-Butanedione 2-monoxime (BDM) induces calcium release from canine cardiac sarcoplasmic reticulum.” Biochemical and biophysical research communications vol. 229,1 (1996): 154-7.
[4] Xiao, Y F, and J J McArdle. “Effects of 2,3-butanedione monoxime on blood pressure, myocardial Ca2+ currents, and action potentials of rats.” American journal of hypertension vol. 8,12 Pt 1 (1995): 1232-40. doi:10.1016/0895-7061(95)00251-0
[5] Brightman, T et al. “2,3-Butanedione monoxime protects mice against the convulsant effect of picrotoxin by facilitating GABA-activated currents.” Brain research vol. 678,1-2 (1995): 110-6.
2,3-Butanedione-2-monoxime是一种肌球蛋白ATP酶的非竞争性抑制剂，可抑制肌球蛋白-V和非肌肉肌球蛋白-II的ATP酶速率，但对驱动蛋白和动力蛋白无抑制作用。
2,3-Butanedione-2-monoxime还可作为磷酸化乙酰胆碱酯酶的再活化剂，通过去除酶上的磷酸基团使其恢复活性[1]。
体外实验中，50mM的2,3-Butanedione-2-monoxime处理6小时或48小时，抑制灰盖拟鬼伞菌（C. cinerea）中的蛋白质分泌[2]。50mM的2,3-Butanedione-2-monoxime处理2小时或4小时，会导致灰盖拟鬼伞菌细胞中高尔基体聚集，但不改变内质网的定位[2]。在无外排抑制剂存在的情况下，30mM的2,3-Butanedione-2-monoxime在37°C下处理10分钟，降低了犬心室肌细胞中的肌浆网（SR）钙含量[3]。
体内实验中，2,3-Butanedione-2-monoxime（5-200mg/kg；i.v.；once）剂量依赖性降低雄性自发性高血压（SHR）和同龄Wistar-Kyoto（WKY）大鼠血压，其中SHR大鼠降压效果更明显[4]。2,3-Butanedione-2-monoxime (0-205mg/kg；i.p.；once)剂量依赖性地抑制了成年小鼠中由PTX诱导的阵挛性和强直-阵挛性发作[5]。