Rapamycin **
產品名稱：Rapamycin
產品貨號：LC R-5000
產品規格：1 G
Trusted Worldwide: more than 10,000 vials of our rapamycin have been shipped to more than 2,500 laboratories worldwide since 2002.
Immunosuppressant, related to FK-506, but without calcineurin inhibitory activity even when complexed to FK-506 binding protein. Selectively blocks signaling that leads to p70 S6 kinase activation (IC50 = 50 pM). Terada, N., et al. "Failure of rapamycin to block proliferation once resting cells have entered the cell cycle despite inactivation of p70 S6 kinase." J. Biol. Chem. 268: 12062-12068 (1993). Fingar, D.C., et al. "Dissociation of pp70 ribosomal protein S6 kinase from insulin-stimulated glucose transport in 3T3-L1 adipocytes." J. Biol. Chem. 268: 3005-3008 (1993). Price, D.J., et al. "Rapamycin-induced inhibition of the 70-kilodalton S6 protein kinase." Science 257: 973-977 (1992). Chung, J., et al. "Rapamycin-FKBP specifically blocks growth-dependent activation of and signaling by the 70 kd S6 protein kinases." Cell 69: 1227-1236 (1992).
Lymphokine-induced cell proliferation at the G1 phase is inhibited and apoptosis in a murine B cell line is induced by rapamycin. Rapamycin arrests the Saccharomyces cerevisiae cell cycle irreversibly in the G1 phase. Morice, W.G. ,et al. "Rapamycin-induced inhibition of p34cdc2 kinase activation is associated with G1/S-phase growth arrest in T lymphocytes." J. Biol. Chem. 268: 3734-3738 (1993). Kay, J.E., et al. "Inhibition of T and B lymphocyte proliferation by rapamycin." Immunology 72: 544-549 (1991). Heitman, J., et al. "Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast." Science 253: 905-909 (1991).
Rapamycin extended median and maximal lifespan of both male and female mice when fed late in life. Harrison, D.E., et al. "Rapamycin fed late in life extends lifespan in genetically heterogeneous mice." Nature 460: 392-395 (2009).
Rapamycin has shown activity in slowing cellular and organismal aging. Rapamycin abolished nuclear blebbing, delayed the start of cellular senescence, and improved the degradation of progerin in Hutchinson-Gilford progeria syndrome fibroblast cells. It also reduced the formation of insoluble progerin aggregates and resulted in clearance through autophagic mechanisms in normal fibroblasts. Cao, K., et al. "Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells." Sci. Transl. Med. 3: 89ra58 (2011).
Due to a different mechanism of action than FK506 and other immunosuppressants, rapamycin may prove to be important in organ transplant patient therapy. Fewer side effects than the standard anti-rejection treatments have been observed. Proliferation of activated T cells, but not apoptosis, is blocked by rapamycin. The induction of apoptosis of rejection-causing T cells reduces the tendency towards transplant rejection. Schwarz, C. and Oberbauer, R. "The future role of target of rapamycin inhibitors in renal transplantation." Curr Opin Urol. 12: 109-113 (2002). Wells, A.D. et al. "Requirement for T-cell apoptosis in the induction of peripheral transplantation tolerance." Nat. Med. 5: 1303-1307 (1999). Li, Y., et al. "Blocking both signal 1 and signal 2 of T-cell activation prevents apoptosis of alloreactive T cells and induction of peripheral allograft tolerance." Nat. Med. 5: 1298-1302 (1999).
We have had one lot of Selleck Chemical's rapamycin analyzed by a highly experienced and expert clinical analytical laboratory that specializes in rapamycin analyses. Using liquid chromatography - mass spectrometry, they found a purity of 96.7% (cis plus trans) for a lot of Selleck's rapamycin. In contrast, we have proven our rapamycin to be greater than 99% in purity for every lot, no exceptions.
Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 200 mg/mL; soluble in ethanol at 50 mg/mL; very poorly soluble in water; maximum solubility in plain water is estimated to be about 5-20 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A
