Licensed by Pfizer Catalog No.S1039 Synonyms: AY 22989，NSC-2260804
Molecular Weight(MW): 914.18
Rapamycin (Sirolimus) is a specific mTOR inhibitor with IC50 of ~0.1 nM HEK293 cells.
Cited by 63 Publications
12 Customer Reviews
Protein blots showing MYC expression in naive and persister cells after 3 d of treatment with 2 uM AKT inhibitor MK-2206 (AKTi) or 10 nM mTOR inhibitor rapamycin (Rapa).
Nat Genet 2014 46(4), 364-70. Rapamycin (Sirolimus) purchased from Selleck.
Cooperative Effects of AR and mTOR Inhibition In Vitro and In Vivo (A) In vitro response of Pten null;Ar+ murine (CaP8) and human (LNCaP) prostate cancer cells to AR knockdown (sh-AR) or pharmacological inhibition of AR (MDV3100, 10 nM) with and without rapamycin (R: 1 nM) treatment (Sc, control sh oligo). (B and D) In vivo response to treatments with castration, MDV3100, rapamycin, or their combinations as measured by cell proliferation (Ki67+cells) and (C and D) tumor burden in Pb-Cre+;-PtenL/L and Pb-Cre+;PtenL/L:ArL/Y mutants. Scale bars represent 2 mm (C), 200 mm (D), and 75 mm (D, inset). Error bars represent mean ±SD.
Cancer Cell 2011 19(6), 792-804. Rapamycin (Sirolimus) purchased from Selleck.
48 hours after addition of rapamycin(150 nM), the cells were imaged as described in Figure A to detect formation of punctuated GFP-LC3 structure. Quantification represented the ratio of GFP-LC3 punctuated positive cell to the total cell counted(Figure B).
Cell Res 2012 22(6), 1003-21. Rapamycin (Sirolimus) purchased from Selleck.
H4-LC3-GFP cells were treated with 1 nM IFNA2 for the indicated periods in the presence of 200 nM rapamycin. Images of the cells were collected using an ArrayScan HCS 4.0 Reader. Representative cells are shown. The average spot intensity in 500 cells from each indicated sample was determined. Data are displayed as means ?SD of the spot intensity per cell (below). RLU, relative leight unit.
Autophagy 2015 11(4), 617-28. Rapamycin (Sirolimus) purchased from Selleck.
Rheb Induces Phospho-eIF2a Independent of mTORC1 and Promotes Phospho-eIF2a Predominantly through PERK (A) Western blotting of indicated proteins of HEK293 expressing cDNAs of myc (control) or myc-Rheb WT were grown in DMEM with serum (+) or without serum (-) or pretreated with the inhibitors rapamycin (250 nM) or DMSO (0.5%, control). (B) Western blotting of indicated proteins in HEK293 cells expressing myc or myc-Rheb and pretreated with rapamycin or DMSO as in (A). (C) Western blotting of indicated proteins in HEK293 cells expressing myc or myc-Rheb and pretreated with inhibitors of MAPK (PD98059, 50 mM) or PI3K (wortmannin, 100 nM), rapamycin, or DMSO.
Cell Rep 2015 10.1016/j.celrep.2015.01.014. Rapamycin (Sirolimus) purchased from Selleck.
Autophagy induced by PL-0N and PL may restrict LPS-induced inflammatory responses in RAW264.7 cells. LPS induced autophagy in RAW264.7 cells. Cells were incubated with 1 mM 3-MA or 10 uM Rapamycin in the absence or presence of LPS (1 ug/mL) for 16 h. Then immunofluorescence for LC3 was visualized using a Zeiss LSM 710 confocal microscope.
Biochem Pharmacol 2015 95(3), 156-69. Rapamycin (Sirolimus) purchased from Selleck.
Inhibition of mTOR activity may be responsible for sorafenib-induced down-regulation of survivin. H1299 cells were treated with the indicated concentration of RAD001 or Rapamycin for 48 h. Then H1299 cells were incubated with or without 5 μM sorafenib, with or without 5 μM RAD001, and with or without 2 μM rapamycin for 48 h. The indicated protein levels were determined by Western blot analysis. β-Actin protein levels were measured as loading controls.
Biochem Pharmacol 2011 82, 216-226. Rapamycin (Sirolimus) purchased from Selleck.
Rapamycin (RPM) inhibits OA-induced lipogenesis. Male SD rats were divided into three groups, and then treated as follows for seven days: group I (control; Ctrl), normal diet + vehicle; group II (OA), 1% OA diet + vehicle; group III (OA + RPM), 1% OA diet + RPM. (A) Hepatic TG concentrations were determined using the serum triglyceride determination kit. (B) Fixed liver sections were subjected to HE and Oil Red O staining as well as immunohistochemistry assays with SREBP-1 antibody. Representative microphotographs of liver specimens from all groups of rats are shown. (C) The levels of mRNA of the indicated genes involved in lipogenesis were determined by real-time PCR. Each bar represents the mean ±SE of the results obtained from six rats. * P < 0.05, ** P < 0.01, *** P < 0.001.
J Lipid Res 2011 52, 1617-1625. Rapamycin (Sirolimus) purchased from Selleck.
Immunophilins participate in SOCE activation by CN-dependent but also CN-independent signaling pathways. Fura-2 loaded platelets were suspended in HBS and subsequently incubated at 37oC for 30 min with rapamycin (500 nM). Once incubation time was over, platelets were stimulated with TG (200 nM) in a calcium free-HBS (EGTA 100 μM was added as indicated the by arrowhead) and 4 min later CaCl2 (300 µM) was added to visualized calcium entry. Changes in fura-2 fluorescence were monitored using the 340/380nm ratio and calibrated in terms of [Ca2+]c . Traces are representative of four to six independent experiments. *,**, *** represents p < 0.05, p < 0.01 and p <0.001, respect control platelets.
Biochim Biophys Acta 2013 1833(3), 652-62. Rapamycin (Sirolimus) purchased from Selleck.
Rapamycin inhibits growth-dependent TCTP induction. Cells were serum-starved for 24h and restimulated with 20% FBS for the indicated times in the presence or absence of rapamycin. The graph shows the relative TCTP signal, corrected for the loading control.
2011 Dr.Ulrich Bommer of University of Wollongong. Rapamycin (Sirolimus) purchased from Selleck.
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Choose Selective mTOR Inhibitors
|Description||Rapamycin (Sirolimus) is a specific mTOR inhibitor with IC50 of ~0.1 nM HEK293 cells.|
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||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. |
Immunoblotting for the mTOR kinase assay:HEK293 cells are plated at 2-2.5×105 cells/well of a 12-well plate and serum-starved for 24 hours in DMEM. Cells are treated with increasing concentrations of Rapamycin (0.05-50 nM) for 15 minutes at 37 °C. Serum is added to a final concentration of 20% for 30 minutes at 37 °C. Cells are lysed, and cell lysates are separated by SDS-PAGE. Resolved proteins are transferred to a polyvinylidene difluoride membrane and immunoblotted with a phosphospecific primary antibody against Thr-389 of p70 S6 kinase. Data are analyzed using ImageQuant and KaleidaGr
-  Edwards SR, et al. J Biol Chem, 2007, 282(18), 13395-13401.
-  Barbet NC, et al. Mol Biol Cell, 1996, 7(1), 25-42.
-  Takeuchi H, et al. Cancer Res, 2005, 65(8), 3336-3346.
|In vitro||DMSO||20 mg/mL (21.87 mM)|
|In vivo||Add solvents individually and in order:
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT00062712||Completed||Kidney Transplantation||National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)|National Institutes of Health Clinical Center (CC)||June 9, 2003||Phase 2|
|NCT01814059||Terminated||Eosinophilic Gastroenteritis|Eosinophilic Esophagitis||National Institute of Allergy and Infectious Diseases (NIAID)|National Institutes of Health Clinical Center (CC)||March 7, 2013||Phase 1|
|NCT01303965||Active, not recruiting||Multiple Myeloma||Sherif S. Farag|Celgene Corporation|Indiana University||February 7, 2011||Phase 1|Phase 2|
|NCT02891603||Not yet recruiting||Graft Vs Host Disease|GVHD||H. Lee Moffitt Cancer Center and Research Institute||April 30, 2017||Phase 1|Phase 2|
|NCT02423915||Recruiting||Leukemia|Lymphoma||M.D. Anderson Cancer Center|National Cancer Institute (NCI)|Targazyme, Inc.|Cancer Prevention Research Institute of Texas||July 30, 2015||Phase 1|Phase 2|
|NCT01182883||Withdrawn||Brain Stem Neoplasms|Glioma|Pinealoma||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||July 28, 2010||Phase 1|
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