Ridaforolimus (Deforolimus, AP23573, MK-8669)
|CAS No.: 572924-54-0||Request for quotation|
Ridaforolimus, was formerly known as Deforolimus, it is an inhibitor of mammalian target of rapamycin.
Ridaforolimus used to treat HT-1080 cells induces a dose-dependent inhibition of both S6 and 4E-BP1 phosphorylation, with IC50 of 0.2 nM and 5.6 nM, respectively, and leads to a decrease in cell size, an increase in the proportion of cells in the G1 phase of the cell cycle, and inhibition of glucose uptake. Ridaforolimus shows antiproliferative activity a variety of cell lines with EC50 of 0.2-2.3 nM. Ridaforolimus is a potent and selective inhibitor of VEGF production in a dose-dependent manner. Ridaforolimus treatment causes growth suppression in human NSCLC cell lines with IC30 values of 2.45-8.83 nM, with the exception of H157 with IC30 of >20 nM. Ridaforolimus treatment causes dephosphorylation of p70S6KThr389 in A549, H1703 and H157 cells, except H1666 that may express a resistant variant of mTORC1, and causes increased phosphorylation of pAKTser473 and pAKTThr308 in A549 and H1703 cells. Ridaforolimus, when combined with the MEK inhibitors CI-1040 or PD0325901, exhibits dose-dependent synergism in lung cancer cell lines, which is associated with the suppression of proliferation rather than enhancement of cell death, involving the inhibition of ribosomal biogenesis by 40% within 24 hours and a decreased polysome/monosome ratio.
Ridaforolimus may act as a regulator of protein synthesis, cell proliferation, cell cycle progression and cell survival.
|Appearance||Off-white Crystalline powder||Standard Packing||500mg/bag or per customer request|
|Purity (HPLC)||95%||Inventory||Normally we have Ridaforolimus in stock|
|Melting point||95-98 °C (lit.)|
|Ridaforolimus physical parameters|
|Solubility||Soluble in DMSO, Methanol|
|Certificate of Analysis||Ridaforolimus (Deforolimus, AP23573, MK-8669) COA|
|Literature||Ridaforolimus (Deforolimus, AP23573, MK-8669) literature|
|MSDS||Ridaforolimus (Deforolimus, AP23573, MK-8669) MSDS|
|1.||J. Nemunaitis et al: Clinical Oncology 25(6) 2013, 336–342. Oral ridaforolimus (40 mg QDx5/wk) is feasible to combine with standard doses of bevacizumab, although careful patient selection would be needed to mitigate the risk of bowel perforation-related adverse events. Combination therapy produced prolonged stable disease in several heavily pretreated patients.|
|2.||Christine M. Hartford et al: Clin Cancer Res 2009;15(4) Deforolimus was well tolerated on the schedule tested in this trial with toxicity and pharmacokinetic profiles that were similar to that of other mTOR inhibitors. Additional phase II studies are needed to determine if deforolimus is superior to other mTOR inhibitors in terms of efficacy. The change in serum cholesterol as a potential biomarker of activity should be studied further. Full text|
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