Rapamycin | CAS 53123-88-9 | Immunosuppressive Antibiotic | AG Scientific, Inc.

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Rapamycin, Immunosuppressive Antibiotic

  • CAS: 53123-88-9
  • Formula: C51H79NO13
  • MW: 914.2 Da
  • Appearance: White powder
  • Purity: 99%




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Rapamycin (also known as Sirolimus) is macrocyclic lactone produced by the bacterium Streptomyces hygroscopicus isolated from soil samples from Easter Island. Rapamycin is an antifungal agent with immunosuppressive properties. Rapamycin has antirejection properties without the side effects associated with other antirejection agents. Rapamycin binds to a specific protein, Target of Rapamycin (TOR). TOR is serine/threonine kinase. TOR (mTOR) forms two major complexes: mTORC1,and mTORC2. The mTORC1 consists of mTOR, Raptor, mLST8, FKBP38, PRAS40, and Deptor, and through specific binding of rapamycin to FKBP12, rapamycin inhibits the activity of mTORC1 leading to a decrease in protein synthesis, increased autophagy and inhibition of cell growth. Recent studies and investigation in mice have demonstrated the potential of Rapamycin to slow aging. Rapamycin is being tested in dogs for its anti-aging properties.

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SynonymsRAPA, Rapamune, Sirolimus, AY-22989, NSC-226080
Product #R-1018
CAS #53123-88-9
Chemical Name(3S,6R,7E,9R,10R,12R,14S,15E,17E,19E,21S,23S,26R,27R,34AS)-9,10,12,13,14,21,22,23,24,25,26,27,32,33,34,34A-HEXADECAHYDRO-9,27-DIHYDROXY-3-[(1R)-2-[(1S,3R,4R)-4-HYDROXY-3-METHOXYCYC LOHEXYL]-1-METHYLETHYL]-10,21-DIMETHOXY-6,8,12,14,20,26-HEXAMETHYL-23,27-E
MW914.2 Da
AppearanceWhite powder
SolubilityClear colorless solution at 50 mg/mL in Ethanol or DMSO
Melting Point183-184°C
Storage Temp-20°C.
Therapeutic AreaAutoimmune Diseases, Infectious Diseases
UseRapamycin is a member of the macrolide immunosuppressant family and a FRAP inhibitor is used to prevent rejection in organ transplantation

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Merck Index13.8202.2001
MDL NumberMFCD00867594

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GHS Pictograms
HandlingHygroscopic! Protect from light and moisture! Warning! Irritant, harmful!

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Certificate of Analysis 1R-1018, E1381J.pdf
Certificate of Analysis 2R-1018, E1381H.pdf
Certificate of Analysis 3R-1018, E1381G.pdf
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CitationsLamichhane, Tek N., et al. "Lack of tRNA-i6A modification causes mitochondrial-like metabolic deficiency in S. pombe by limiting activity of cytosolic tRNATyr, not mito-tRNA." RNA (2016).
Lamichhane, Tek N., et al. "Lack of tRNA modification isopentenyl-A37 alters mRNA decoding and causes metabolic deficiencies in fission yeast." Molecular and cellular biology (2013): MCB-00278.
Dengjel, Jorn, et al. "Identification of autophagosome-associated proteins and regulators by quantitative proteomic analysis and genetic screens." Molecular & Cellular Proteomics (2012): mcp-M111.
Yan, Hongbo, Yunying Zhao, and Linghuo Jiang. "The putative transcription factor CaRtg3 is involved in tolerance to cations and antifungal drugs as well as serum-induced filamentation in Candida albicans." FEMS yeast research 14.4 (2014): 614-623.
Feng, Jinrong, et al. "Genetic interactions between protein phosphatases CaPtc2p and CaPph3p in response to genotoxins and rapamycin in Candida albicans." FEMS yeast research 13.1 (2013): 85-96.
Cokol, Murat, et al. "Systematic exploration of synergistic drug pairs." Molecular systems biology 7.1 (2011): 544.
Feng, Jinrong, et al. "CaTip41 regulates protein phosphatase 2A activity, CaRad53 deactivation and the recovery of DNA damage-induced filamentation to yeast form in Candida albicans." FEMS yeast research 16.2 (2016): fow009.
Jiang, Linghuo, et al. "The putative ABC transporter encoded by the orf19. 4531 plays a role in the sensitivity of Candida albicans cells to azole antifungal drugs." FEMS yeast research 16.3 (2016).
Gong, Xuan, et al. "Activating the translational repressor 4E-BP or reducing S6K-GSK3 activity prevents accelerated axon growth induced by hyperactive mTOR in vivo." Human molecular genetics 24.20 (2015): 5746-5758.
Cao, Jiumei, et al. "Rapamycin inhibits CaCl2-induced thoracic aortic aneurysm formation in rats through mTOR-mediated suppression of proinflammatory mediators." Molecular medicine reports 16.2 (2017): 1911-1919.
Pelicano, Helene, et al. "Mitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potential." Breast cancer research 16.5 (2014): 434.
Pan, Sunlei, et al. "Folic acid delays development of atherosclerosis in low-density lipoprotein receptor-deficient mice." Journal of cellular and molecular medicine 22.6 (2018): 3183-3191.

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