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Cat. No. M1768
Rapamycin Structure

Sirolimus, Rapamune

Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mM*1mL in DMSO USD 38.4  USD48 In stock
5mg USD 25.6  USD32 In stock
10mg USD 33.6  USD42 In stock
25mg USD 45.6  USD57 In stock
50mg USD 60  USD75 In stock
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Quality Control
Biological Activity

Rapamycin (Sirolimus,Rapamune)is an inhibitor of mTOR.The mammalian target of rapamycin (mTOR) is a kinase responsible for mitogen-induced cell proliferation/survival signaling.In vitro, rapamycin inhibited the proliferation of primary bone marrow cells induced by IL-3, GM-CSF, KL, or a complex mixture of factors present in cell-conditioned media.

Product Citations
Customer Product Validations & Biological Datas
Source BMC Genomics (2017). Additional file 7. Rapamycin (Abmole Bioscience, USA)
Method qRT-PCR
Cell Lines pupa abdomen
Incubation Time 48 h
Results 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.
Source 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).
Method western blot
Cell Lines MDA-MB-231 cells
Concentrations PI3K (10 µM LY294002), Akt (10 µM MK-2206) or mTOR (10 µM rapamycin)
Incubation Time 1h
Results 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.
Source 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).
Method Cell motility assay
Cell Lines MDA-MB-231 cells
Concentrations PI3K (10 μM LY294002), Akt (20 μM MK-2206), mTOR (10 μM rapamycin, Rap), FAK (10 μM PF573228) or Src (10 μM PP2)
Incubation Time 1h
Results "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. "
Source APMIS (2015). Figure 5.Rapamycin was purchased from Abmole (Shanghai, China)
Method mice model bearing cervical cancer
Cell Lines C33A cells
Concentrations 2.5 mg/kg, intra-peritoneal injection
Incubation Time from the 10th day to 37th day
Results 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).
Source APMIS (2015). Figure 4.Rapamycin was purchased from Abmole (Shanghai, China)
Method Cell cycle analysis
Cell Lines C33A cells
Concentrations 5nM
Incubation Time 24 h
Results 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.
Source APMIS (2015). Figure 3.Rapamycin was purchased from Abmole (Shanghai, China)
Method Apoptosis analysis
Cell Lines C33A cells
Concentrations 5nM
Incubation Time 24 h
Results 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).
Source APMIS (2015). Figure 2.Rapamycin was purchased from Abmole (Shanghai, China)
Method MTT assay
Cell Lines HeLa, SiHa, Caski, and C33A cells
Concentrations 0~80nM
Incubation Time 72 h
Results 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).
Cell Experiment
Cell lines HeLa, SiHa, Caski, and C33A cells
Preparation method MTT assay.
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.
Concentrations 0~80nM
Incubation time 72 h
Animal Experiment
Animal models cervical cancer C33A cells tumor bearing mice
Formulation a solution of 0.2%CMC and 0.25% Tween-80 in ddH2O
Dosages 2.5 mg/kg from the 10th day to 37th day
Administration intra-peritoneal injection
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

Chemical Information
Molecular Weight 914.18
Formula C51H79NO13
CAS Number 53123-88-9
Purity 99.18%
Solubility DMSO 80 mg/mL
Storage at -20°C

[1] Ishikawa T, et al. Intern Med. 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.

[2] Kandula P, et al. Transplantation. Impact of Tacrolimus-Sirolimus Maintenance Immunosuppression on Proteinuria and Kidney Function in Pancreas Transplant Alone Recipients.

[3] Maeng M, et al. BMC Cardiovasc Disord. Comparison of zotarolimus-eluting and sirolimus-eluting coronary stents: a study from the Western Denmark Heart Registry.

[4] Zapata G, et al. Ocul Immunol Inflamm. Topical use of rapamycin in herpetic stromal keratitis.

[5] Thuy L Phung, et al. Cancer Cell. Pathological angiogenesis is induced by sustained Akt signaling and inhibited by rapamycin

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Keywords: Rapamycin, Sirolimus, Rapamune supplier, mTOR, inhibitors

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