In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Rapamycin was used as a kind of original antifungal antibiotic, which is produced by Streptomyces hygroscopicus. Now it has been used in the prevention of transplant rejection because of its immunosuppressive effect. It also exhibits activity against several transplantable tumors and slightly activity to inactive against leukemias. The immunosuppressive effect of Rapamycin is exerted by inhibiting the activation and proliferation of T cells. Rapamycin binds to FK-binding protein 12 (FKBP12) and forms the rapamycin-FKBP12 complex, which regulates an enzyme that plays an important role in the progression of the cell cycle.
1. Sehgal, Suren N. "Rapamune®(RAPA, rapamycin, sirolimus): mechanism of action immunosuppressive effect results from blockade of signal transduction and inhibition of cell cycle progression." Clinical biochemistry 31.5 (1998): 335-340.
2. Sehgal, S. N., H. Baker, and Claude Vézina. "Rapamycin (AY-22,989), a new antifungal antibiotic. II. Fermentation, isolation and characterization." The Journal of antibiotics 28.10 (1975): 727-732.
- 1. Zhao F, Wang J, et al. "Neuroprotection by Walnut-derived Peptides through Autophagy Promotion via Akt/mTOR Signaling Pathway against Oxidative Stress in PC12 Cells." J Agric Food Chem. 2020;10.1021/acs.jafc.9b08252. PMID:32090563
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|Physical Appearance||A solid|
|Storage||Desiccate at -20°C|
|Synonyms||Sirolimus,(-)-Rapamycin, AY-22989, WY-090217, Antibiotic AY22989|
|Solubility||≥45.709mg/mL in DMSO, ≥58.9 mg/mL in EtOH with ultrasonic,insoluble in H2O|
|Canonical SMILES||O[[email protected]]1[[email protected]](OC)C[[email protected]](C[[email protected]@H](C)[[email protected]](CC([[email protected]](C)/C=C(C)/[[email protected]]([[email protected]@H](OC)C([[email protected]@H](C[[email protected]@H](/C=C/C=C/C=C(C)/[[email protected]@H](OC)C[[email protected]@H]2CC[[email protected]@H](C)[[email protected]@](C(C(N3[[email protected]]4CCCC3)=O)=O)(O)O2)C)C)=O)O)=O)OC4=O)CC1|
|Shipping Condition||Evaluation sample solution: ship with blue ice. All other available sizes: ship with RT, or blue ice upon request.|
|General tips||For obtaining a higher solubility, please warm the tube at 37°C and shake it in the ultrasonic bath for a while. Stock solution can be stored below -20°C for several months.|
Hepatocyte growth factor (HGF)-induced lens epithelial cells (LECs)
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
10 ng/ml, 72h
Using cell proliferation, cell viability and flow cytometric apoptosis assays, we found that rapamycin potently not only suppressed proliferation but also induced the apoptosis of LECs in a dose-dependent manner under HGF administration. Further investigation of the underlying mechanism using siRNA transfection revealed that rapamycin could promote apoptosis of LECs via inhibiting HGF-induced phosphorylation of AKT/mTOR, ERK and JAK2/STAT3 signaling molecules. Moreover, the forced expression of AKT, ERK and STAT3 could induce a significant suppression of apoptosis in these cells after treatment of rapamycin.
8 mg/kg every other day, intraperitoneal injection
Rapamycin, a specific inhibitor of the mechanistic target of rapamycin (mTOR) signaling pathway, robustly enhances survival and attenuates disease progression in a mouse model of Leigh syndrome. Administration of rapamycin to these mice, which are deficient in the mitochondrial respiratory chain subunit Ndufs4 [NADH dehydrogenase (ubiquinone) Fe-S protein 4], delays onset of neurological symptoms, reduces neuroinflammation, and prevents brain lesions. Although the precise mechanism of rescue remains to be determined, rapamycin induces a metabolic shift toward amino acid catabolism and away from glycolysis, alleviating the buildup of glycolytic intermediates. This therapeutic strategy may prove relevant for a broad range of mitochondrial diseases.
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.
1. Tian F, Dong L, Zhou Y et al. Rapamycin-Induced Apoptosis in HGF-Stimulated Lens Epithelial Cells by AKT/mTOR, ERK and JAK2/STAT3 Pathways. Int J Mol Sci. 2014 Aug 11;15(8):13833-48.
2. Johnson SC1, Yanos ME, Kayser EB et al. mTOR inhibition alleviates mitochondrial disease in a mouse model of Leigh syndrome. Science. 2013 Dec 20;342(6165):1524-8.
|Description||Rapamycin (Sirolimus, AY-22989, WY-090217) is a specific inhibitor of mTOR with IC50 of ~0.1 nM.|
Quality Control & MSDS
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