Rapamycin 53123-88-9

简要描述：Rapamycin 53123-88-9
作用于HEK293细胞，抑制内源性mTOR活性，IC50为~0.1nM,而iRap和AP21967 作用时，IC50分别为~5 nM 和~10 nM。Rapamycin处理酿酒酵母，诱导细胞周期停在G1/S期，且抑制翻译。

产品型号：abs810030
厂商性质：生产厂家
更新时间：2026-04-30
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生化试剂

其它生化试剂植物提取物碳水化合物生物缓冲剂荧光探针与染料表面活性剂酶&辅酶&酶底物蛋白质组学动植物激素小分子化合物生化检测试剂盒逆行示踪剂抗生素核苷&核苷酸多肽

品牌	absin	货号	abs810030
规格	5mg	供货周期	现货
主要用途	作用于HEK293细胞,抑制内源性mTOR活性	应用领域	化工,生物产业,农林牧渔,制药/生物制药,综合

Rapamycin 53123-88-9

产品描述
描述	Rapamycin (Sirolimus)是一种特定的 mTOR 抑制剂，在 HEK293细胞中，IC50 为 ~0.1nM。 Rapamycin作用于HEK293细胞，抑制内源性mTOR活性，IC50为~0.1nM,而iRap和AP21967 作用时，IC50分别为~5 nM 和~10 nM。Rapamycin处理酿酒酵母，诱导细胞周期停在G1/S期，且抑制翻译。Rapamycin显著抑制T98G和U87-MG细胞活力，这种作用具有剂量依赖性，IC50分别为2nM和1μM，而对U373-MG细胞没有作用活性，IC50>25μM。Rapamycin(100 nM) 作用于对Rapamycin敏感的U87-MG和T98G细胞，通过抑制mTOR功能，而诱导细胞周期停在G1期，也诱导自噬而不是凋亡。在体内，Rapamycin 处理，特定阻断mTOR下游靶点，如p70S6K磷酸化和激活，和PHAS-1/4E-BP1导致的eIF4E抑制释放，完quan阻断跖肌重量和纤维尺寸的肥厚增高。短期Rapamycin处理,即使按最di剂量0.16 mg/kg处理, 强抑制p70S6K活性, 与提高的肿瘤细胞死亡和Eker肾脏肿瘤坏死相关。Rapamycin作用于CT-26移植瘤模型，通过降低VEGF产量，及阻断VEGF诱导的内皮细胞信号，而抑制转移性肿瘤生长和血管新生。Rapamycin每天按4mg/kg剂量处理C6移植瘤，显著降低肿瘤生长，和肿瘤血管通透性。
纯度	>98 %
储存/保存方法	Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.
基本信息
别名	雷帕霉素；Sirolimus；AY 22989；NSC-2260804
外观	Lyophilized powder
可溶性/溶解性	DMSO ：20 mg/mL (21.87 mM)
生物活性
靶点	mTOR
In vitro(体外研究)	Rapamycin inhibits endogenous mTOR activity in HEK293 cells with IC50 of ~0.1 nM, more potently than iRap and AP21967 with IC50 of ~5 nM and ~10 nM, respectively. In Saccharomyces cerevisiae, Rapamycin treatment induces a severe G1/S cell cycle arrest and inhibition of translation initiation to levels below 20% of control. Rapamycin significantly inhibits the cell viability of T98G and U87-MG in a dose-dependent manner with IC50 of 2 nM and 1 μM, respectively, while displaying little activity against U373-MG cells with IC50 of >25 μM despite the similar extent of the inhibition of mTOR signaling. Rapamycin (100 nM) induces G1 arrest and autophagy but not apoptosis in Rapamycin-sensitive U87-MG and T98G cells by inhibiting the function of mTOR.
In vivo(体内研究)	Treatment with Rapamycin in vivo specifically blocks targets known to be downstream of mTOR such as the phosphorylation and activation of p70S6K and the release of inhibition of eIF4E by PHAS-1/4E-BP1, leading to complete blockage of the hypertrophic increases in plantaris muscle weight and fibre size. Short-term Rapamycin treatment, even at the lowest dose of 0.16 mg/kg, produces profound inhibition of p70S6K activity, which correlates with increased tumor cell death and necrosis of the Eker renal tumors. Rapamycin inhibits metastatic tumor growth and angiogenesis in CT-26 xenograft models by reducing the production of VEGF and blockage of VEGF-induced endothelial cell signaling. Rapamycin treatment at 4 mg/kg/day significantly reduces tumor growth of C6 xenografts, and tumor vascular permeability.
参考文献
参考文献	[1] Edwards SR, et al. J Biol Chem, 2007, 282(18), 13395-13401. [2] Barbet NC, et al. Mol Biol Cell, 1996, 7(1), 25-42. [3] Takeuchi H, et al. Cancer Res, 2005, 65(8), 3336-3346.

研究领域
研究领域	CancerCell cycleCell cycle inhibitorsOther CardiovascularHeartCardiogenesisTranscription factors/regulators Cell CycleCell Cycle InhibitorsOther EpigeneticsDNA / RNADNA Damage & RepairDNA Damage ResponseDNA Damage Recognition MetabolismTypes of diseaseObesity NeuroscienceDevelopment NeuroscienceProcesses Drug DiscoverySmall Molecule DrugLead Compound Discovery

Rapamycin 53123-88-9 温馨提示：本产品仅作科研实验使用，不支持临床等研究

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Rapamycin 53123-88-9

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