Cycloheximide_抗生素,真核生物蛋白质合成抑制剂_66-81-9_Apexbio

抗生素，真核生物蛋白质合成抑制剂
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质量控制
质量控制和MSDS
View current batch:3
3
Purity = 98.20%
COA (Certificate Of Analysis)
HPLC
NMR (Nuclear Magnetic Resonance)
MSDS (Material Safety Data Sheet)
SDF
Naramycin A; Actidione; 3-[2-(3,5-Dimethyl-2-oxocyclohexyl)-2-hydroxyethyl]glutarimide
4-[(2R)-2-[(1S,3S,5S)-3,5-dimethyl-2-oxocyclohexyl]-2-hydroxyethyl]piperidine-2,6-dione
CC1CC(C(=O)C(C1)C(CC2CC(=O)NC(=O)C2)O)C
分子式C15H23NO4分子量281.4
溶解性Soluble to 50 mM in ethanol and to 25 mM in sterile water储存条件Store at 4°C
一般建议为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。

储液可以在零下20℃中保存数月。

运输条件试用装：蓝冰运输。

其他可选规格：常温运输或根据您的要求用蓝冰运输。

生物活性
描述Cycloheximide是一种高度有效的抗生素。

靶点bacteria protein synth esis
IC50
实验操作
Cell experiment: [1]
Cell lines SGBS preadipocytes
Preparation method The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 m inutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
Reacting condition10 μg/ml, 9 hours
Applications Addition of CHX enhanced CD95-induced cleavage of caspase-8 into p43/p41 intermediate and p18 active fragments as well as proteolytic tur nover of the proenzyme form of caspase-8 after 1, 3, 6, and 9 h. In addition, CHX increased cleavage of caspase-3 into the active p20/17 frag ment at these time points. At later time points (24, 48, and 72 h), a decrease in the p55 pro-form of caspase-8 and the p35 pro-form of caspas e-3 was observed. Interestingly, α-APO-1 alone induced caspase-8 and caspase-3 cleavage (3, 6, 9 h) although there is no induction of cell d eath after 24 h. Involvement of caspase-cleavage was confirmed by the use of the caspase inhibitor Z-VAD.fmk, which reduced CD95- and C HX-induced apoptosis. Apoptosis was rescued by ~50% pointing to a potential role of caspase-independent cell death in SGBS preadipocytes .
Animal experiment: [2]
Animal models Sprague Dawley rat pups
Dosage form Intraperitoneal injection, 0.6 mg/kg, 0, 6, 12 or 24 hr
Application The hypoxia-ischemia model was set up using the rat pups. The hypoxia-ischemia control group (HI) and hypoxia-ischemia were treated with cycloheximide treatment group at 0, 6, 12, 24 and 24 hr after HI (HI_0, 6, 12, 24), respectively. Infarct volume, as measured by morphometric analysis of infarct areas with TTC, was significantly reduced by 92% and 61% when cycloheximide was given 0 or 6 hr after HI respectively, b ut showed an insignificant trend in infarct reduction if cycloheximide was administered 12 hr after HI compared to the HI control group, and no protective effect was observed when administration was delayed until 24 hr after HI.
Other notes Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an ex perimental system error and it is normal.
References:
[1] Fischer-Posovszky P, Keuper M, Nagel S, et al. Downregulation of FLIP by cycloheximide sensitizes human fat cells to CD95-induced apoptosis. Experimental cell research, 2 011, 317(15): 2200-2209.
[2] Park W S, Sung D K, Kang S, et al. Therapeutic window for cycloheximide treatment after hypoxic-ischemic brain injury in neonatal rats. Journal of Korean medical science, 20 06, 21(3): 490-494.
产品描述
Cycloheximide是真核生物蛋白合成的抑制剂，广泛用于生物医学研究，抑制真核细胞中蛋白合成。

由于显著的毒性副作用，包括致畸、DNA损伤和其它生殖影
响，cycloheximide通常仅用于体外研究，不适合作为治疗化合物用于人体。

体外实验：Cycloheximide阻断肽酰-tRNA在网织红细胞核糖体上从受位向供位的运动。

这种易位反应依赖于转移酶TF-II和GTP水解。

Cycloheximide对核糖体依赖的TF-II
GTPase活性或肽基转移酶反应没有影响。

在肽基转移酶反应中，核糖体供体位点tRNA上的多肽转移给受体位点tRNA上的氨基酸[1]。

体内实验：在缺血缺氧的新生儿大鼠模型中，cycloheximide在6小时的治疗窗内有效衰减大鼠脑损伤，这些数据支持了以下可能性，即蛋白合成抑制剂，与其它的抗凋亡策略一样，在发育中新生儿大脑的缺氧缺血（HI）事件中可能具有治疗用途，甚至当治疗延迟到初级窒息后的6小时[2]。

临床试验：到目前为止，cycloheximide仍处于临床前开发阶段。

参考文献：
[1] McKeehan W, Hardesty B. The mechanism of cycloheximide inhibition of protein synthesis in rabbit reticulocytes. Biochem Biophys Res Commun. 1969 Aug 15;36(4):625-30.
[2] Park WS, Sung DK, Kang S, Koo SH, Kim YJ, Lee JH, Chang YS, Lee M. Therapeutic window for cycloheximide treatment after hypoxic-ischemic brain injury in neonatal rats. J Korean Med Sci. 2006 Jun;21(3):490-4.。