Ridaforolimus (MK-8669) is a potent and selective mTOR inhibitor; inhibits ribosomal protein S6 phosphorylation with an IC₅₀ of 0.2 nM in HT-1080 cells^[1].

Treatment of HT-1080 fibrosarcoma cells with Ridaforolimus results in a dose-dependent inhibition of phosphorylation of both S6 and 4E-BP1, with IC₅₀s of 0.2 and 5.6 nM, respectively, and EC₅₀s of 0.2 and 1.0 nM, respectively. In HT-1080 cells, the EC₅₀ for inhibition of cell proliferation (0.5 nM) is similar to the EC₅₀s for inhibition of S6 and 4E-BP1 phosphorylation. Exposure to Ridaforolimus reduces the proliferation of cell lines representing a variety of tumor types. Administration of Ridaforolimus to tumor cells in vitro elicit dose-dependent inhibition of mTOR activity with concomitant effects on cell growth and division. Ridaforolimus exhibits a predominantly cytostatic mode of action, consistent with the findings for other mTOR inhibitors. Potent inhibitory effects on vascular endothelial growth factor secretion, endothelial cell growth, and glucose metabolism^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Ridaforolimus inhibits tumor growth in mice bearing PC-3 (prostate), HCT-116 (colon), MCF7 (breast), PANC-1 (pancreas), or A549 (lung) xenografts. Ridaforolimus inhibits tumor growth in a dose-dependent manner, with 0.3 mg/kg being the lowest dose that inhibits tumor growth significantly and 3 and 10 mg/kg doses achieving maximum inhibition^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

990.21

C₅₃H₈₄NO₁₄P

572924-54-0

Room temperature in continental US; may vary elsewhere.

*该产品在溶液状态不稳定，建议您现用现配，即刻使用。

DMSO : ≥ 44 mg/mL (44.44 mM)

* “≥” means soluble, but saturation unknown.

请根据产品在不同溶剂中的溶解度，选择合适的溶剂配制储备液；该产品在溶液状态不稳定，建议您现用现配，即刻使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.5 mg/mL (2.52 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.52 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 2.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.5 mg/mL (2.52 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.52 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Rivera VM, et al. Deforolimus (AP23573; MK-8669), a potent mTOR inhibitor, has broad antitumor activity and can be optimally administered using intermittent dosing regimens. Mol Cancer Ther. 2011 Jun;10(6):1059-71.

  [2]. Brandt M, et al. mTORC1 Inactivation Promotes Colitis-Induced Colorectal Cancer but Protects from APC Loss-Dependent Tumorigenesis. Cell Metab. 2018 Jan 9;27(1):118-135.e8.

Cells are treated with 10-fold serial dilutions of Ridaforolimus (1,000 to 0.0001 nM) or vehicle (ethanol). Following 72 hours culture at 37°C, the plates are aspirated and stored at -80°C for proliferation analysis^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Mice: Animals selected with tumors in the proper size range are assigned to various treatment groups. Ridaforolimus, at dosages of 3 and 10 mg/kg, is administered i.p. on 2 different treatment schedules: (a) daily, 5 continuous days every other week and (b) once weekly. The control group is untreated^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Rivera VM, et al. Deforolimus (AP23573; MK-8669), a potent mTOR inhibitor, has broad antitumor activity and can be optimally administered using intermittent dosing regimens. Mol Cancer Ther. 2011 Jun;10(6):1059-71.

  [2]. Brandt M, et al. mTORC1 Inactivation Promotes Colitis-Induced Colorectal Cancer but Protects from APC Loss-Dependent Tumorigenesis. Cell Metab. 2018 Jan 9;27(1):118-135.e8.