Rapamycin (Sirolimus)是一种选择性的mTOR抑制剂，IC50为~0.1 nM。
Rapamycin (Sirolimus)是一种选择性的mTOR抑制剂，IC50为~0.1 nM。Rapamycin作用于HEK293细胞，抑制内源性mTOR活性，IC50为~0.1 nM,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2 nM和 1 μM, 而对U373-MG细胞没有作用活性，IC50>25 μM。
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|数据来源||BMC Genomics (2017). Additional file 7. Rapamycin (Abmole Bioscience, USA)|
|实验结果||We performed injection experiments involving several inhibitors of the insulin signaling pathway. It was observed that the development of follicles was clearly delayed and the follicles showed abnormalities (Additional file 7), and the expressions of marker genes, like Cyp18a1 and early chorion gene, were up-regulated at choriogenic stages.|
|数据来源||Oncotarget (2016). Figure 11. Inhibitors of PI3K (LY294002), Akt (MK-2206), Src (PP2), FAK (PF573228) and mTOR (rapamycin) were purchased from Abmole Bioscience (Houston, TX, USA).|
|浓度||PI3K (10 µM LY294002), Akt (10 µM MK-2206) or mTOR (10 µM rapamycin)|
|实验结果||As shown in Figure 11. Pretreating MDA-MB-231 cells with the specific inhibitors of PI3K (10 µM LY294002), Akt (10 µM MK-2206) and mTOR (10 µM rapamycin) completely abolished the LSS-induced MT1-MMP expression, indicating that the PI3K/Akt/mTOR pathway is required for LSS-induced MT1-MMP expression.|
|数据来源||Oncotarget (2016). Figure 1. Inhibitors of PI3K (LY294002), Akt (MK-2206), Src (PP2), FAK (PF573228) and mTOR (rapamycin) were purchased from Abmole Bioscience (Houston, TX, USA).|
|方法||Cell motility assay|
|浓度||PI3K (10 μM LY294002), Akt (20 μM MK-2206), mTOR (10 μM rapamycin, Rap), FAK (10 μM PF573228) or Src (10 μM PP2)|
|实验结果||"Notably, inhibitors of PI3K (LY294002), Akt (MK-2206) and mTOR (rapamycin) markedly decreased the LSS-induced wound closure activity. However, pretreatment with inhibitors of FAK (PF573228) and Src (PP2) has no effect on the LSS-induced cell motility (Figure 1B). It is suggested that PI3K, Akt and mTOR might be participated LSS-induced cell motility in an FAK and Src-independent manner. "|
|数据来源||APMIS (2015). Figure 5.Rapamycin was purchased from Abmole (Shanghai, China)|
|方法||mice model bearing cervical cancer|
|浓度||2.5 mg/kg, intra-peritoneal injection|
|处理时间||from the 10th day to 37th day|
|实验结果||MicroRNA-218 increased tumor sensitivity to Rapamycin in vivo.Compared to the parental controls, both microRNA-218 overexpression and Rapamycin notably suppressed tumor growth (Fig. 5A, p = 0.023 and p = 0.015, respectively); moreover, the combination of microRNA- 218 overexpression and Rapamycin further enhanced this suppressive effects (Fig. 5A, p < 0.001). In addition, Rapamycin notably suppressed the tumor weights of C33A xenografts (Fig. 5B, p = 0.0019), which was also enhanced by the combined therapy (Fig. 5B, p = 0.0423). As shown in Fig. 5C and D, the single treatment with microRNA-218 or Rapamycin notably downregulated the expression of cyclin D1 (the cell cycle related marker) and upregulated cleaved-caspase-3 (the apoptosis marker).|
|数据来源||APMIS (2015). Figure 4.Rapamycin was purchased from Abmole (Shanghai, China)|
|方法||Cell cycle analysis|
|实验结果||Rapamycin induced G1 phase arrest and upregulated the cell cycle related proteins (cyclin D1 and CDK4) in C33A cells, which was further enhanced by the overexpression of microRNA-218. Consistently, in the other three cervical cancer cell lines, Rapamycin also induced G1 phase arrest and this effect was further enhanced by the overexpression of microRNA-218.|
|数据来源||APMIS (2015). Figure 3.Rapamycin was purchased from Abmole (Shanghai, China)|
|实验结果||Compared to the negative control, Rapamycin induced notable apoptosis and upregulated the apoptosis related proteins like cleaved caspase-3 and cleaved PRAP in C33A cells, which was further enhanced by the overexpression of microRNA-218 (Fig. 3A and B). Consistently, similar effects of microRNA-218 on apoptosis were detected in the other three cervical cell lines (Fig. 3C).|
|数据来源||APMIS (2015). Figure 2.Rapamycin was purchased from Abmole (Shanghai, China)|
|细胞系/动物模型||HeLa, SiHa, Caski, and C33A cells|
|实验结果||As the MTT assay shown, overexpression of microRNA-218 notably increased cellular sensitivity to Rapamycin in the four cervical cancer cell lines (Fig. 2A–D, IC50 = 31 nM, 27 nM, 19 nM, and 13 nM for the parental HeLa, SiHa, Caski, and C33A cells, IC50 = 8.5 nM, 6.2 nM, 5 nM, and 3.6 nM for HeLa, SiHa, Caski, and C33A cells with microRNA-218 overexpression, p = 0.045, 0.032, 0.018, and 0.009 respectively).|
|细胞系||HeLa, SiHa, Caski, and C33A cells|
In brief, 2*103 cells/well were seeded into 96-well plates and routinely cultured overnight. Then, these cells were treated with Rapamycin for 72 h. Next, 5 µL MTT (5 mg/ mL; Sigma-Aldrich) and 200 µL DMSO were sequentially added into each well and the absorbance was measured at the wavelength of 570 nm.
|动物模型||cervical cancer C33A cells tumor bearing mice|
|配制||a solution of 0.2%CMC and 0.25% Tween-80 in ddH2O|
|剂量||2.5 mg/kg from the 10th day to 37th day|
|动物 A (mg/kg) = 动物 B (mg/kg) ×||动物 B的Km系数|
例如，依据体表面积折算法，将化合物用于小鼠的剂量20 mg/kg 换算成大鼠的剂量，需要将20 mg/kg 乘以小鼠的Km系数（3），再除以大鼠的Km系数（6），得到化合物用于大鼠的等效剂量为10 mg/kg。
|溶解性（25°C）||DMSO 80 mg/mL|
固体粉末： -20°C 冷藏长期储存
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.0939 mL||5.4694 mL||10.9388 mL|
|5 mM||0.2188 mL||1.0939 mL||2.1878 mL|
|10 mM||0.1094 mL||0.5469 mL||1.0939 mL|
Retrospective Comparison of Midterm Clinical and Angiographic Outcomes after the Implantation of Paclitaxel- and Sirolimus-Eluting Stents for de novo Coronary Complex Lesions in Nonrandomized Japanese Patients.
Ishikawa T, et al. Intern Med. 2012;51(19):2695-701. PMID: 23037458.
Impact of Tacrolimus-Sirolimus Maintenance Immunosuppression on Proteinuria and Kidney Function in Pancreas Transplant Alone Recipients.
Kandula P, et al. Transplantation. 2012 Oct 3. PMID: 23037007.
Comparison of zotarolimus-eluting and sirolimus-eluting coronary stents: a study from the Western Denmark Heart Registry.
Maeng M, et al. BMC Cardiovasc Disord. 2012 Oct 2;12(1):84. PMID: 23031197.
Topical use of rapamycin in herpetic stromal keratitis.
Zapata G, et al. Ocul Immunol Inflamm. 2012 Oct;20(5):354-9. PMID: 23030354.
Pathological angiogenesis is induced by sustained Akt signaling and inhibited by rapamycin
Thuy L Phung, et al. Cancer Cell. 2006 Aug;10(2):159-70. PMID: 16904613.
MTI-31 (LXI-15029) 是一种新型的低毒性 mTORC1/mTORC2 抑制剂，对 mTOR 结合亲和力和选择性超过相关 PI3K 家族同种型的 5000 倍。MTI-31 在细胞试验中抑制 mTORC1 和 mTORC2 功能的浓度为 ≤120 nM。
mTOR inhibitor-1 is a potential ATP-competitive inhibitor of mTOR which could inhibit cell growth and proliferation.
L-亮氨酸（L-leucine）又称白氨酸，是人体必须的八种氨基酸之一，可激活 mTOR 信号通路。
LY303511 hydrochloride 是LY294002的一种结构类似物，可增强SHEP-1神经母细胞瘤细胞的TRAIL敏感性。