Rapamycin

53123-88-9

C51H79NO13

914.17

White or off-white powder

Soluble in DMSO, ethanol, methanol, acetone, chloroform, DMF. Practically insoluble in water.

Source: Streptomyces hygroscopicus
Loss on Drying: ≤0.2%
Melting Point: 183-185ºC

-20°C

Spectrum: Filamentous fungi (including AspergillusCandida).

Eukaryotic Cell Culture Applications: Rifampicin was used in IL-2 stimulted T-cells, and found it could disrupt cytokine singnaling, impeding progression through G1/S phase resulting in G1 arrest.
Rapamycin was able to impair human omental and subcutaneous adipocyte differentiation in primary culture. Human preadipocytes in primary culture differentiate into adipocytes without any clonal expansion, unlike 3T3-L1 preadipocytes. Preadipocytes were grown with 100nM Rapamycin added to the differentiation medium. Rapamycin can interrupt adipogenesis independently from its antiproliferative effect. It inhibited the accumulation in intracellular lipid and it inhibited the induction of GPDH activity, a marker for adipogenesis. The pathway regulating human adipocyte differentiation has not been defined. Multiple signaling pathways regulated by mTOR may be operating in the preadipocyte (Bell et al, 2000).
Rapamycin can be used to probe functions of proteins in Rapamycin-based ligand-mediated colocalization systems for bioengineering. It is important to make sure the purity of the Rapamycin derivatives you are using are free of contaminating Rapamycin (Edwards and Wandless, 2007).

Cancer Applications: Rapamycin is able to inhibit growth of a number of tumor cell lines including mammary, colon 26, B16 3 melanocarcinoma, and EM ependymoblastoma.
Rapamycin suppresses the immune system by preventing T-cell and B-cells from responding to Interleukin 2 (IL-2), a cytokine that would otherwise induce cell proliferation. It does this in a similar mechanism to how it blocks cancer cell proliferation. One might think its action as an immunosuppressive would be detrimental to its use as an anti-cancer agent but it seems to be the contrary. The evidence suggests that in terms of tumor growth, its anti-cancer activities are dominant over its immunosuppressive effects (Law, 2005).
Endothelial cells in growing tumors have chronic Akt activation, resulting in abnormal tumor blood vessels, that are abnormal in structure and function. Rapamycin may affect tumor growth by acting as an Akt inhibitor and could be used as an angiogenesis inhibitor to inhibit tumor growth and tumor vascular permeability. Angiogenic regulators are involved in the development of blood vessels, and disruption is thought to cause pathological blood vessels (Phung et al, 2006).