Cell Death Dis. 2014 Mar 20;5:e1134.
|Source||Cell Death and Disease (2014) 5, e1134. Figure 5. ARRY-162 were obtained from AbMole BioScience, HongKong, China,|
|Method||Flow cytometric enumeration of propidium iodide staining|
|Cell Lines||U266, OPM2, RPMI8226, OCIMY1|
|Incubation Time||72 hours|
|Results||It was clear that LBH589 was found to be synergistic with MAPK and FAK inhibitors in all HMCL.|
|Cell lines||A549 and H460 human lung cancer cell lines|
|Preparation method||Cells were collected and seeded in 96-well plates at a density of 5×103 cells/well. Human lung cancer A549 cells or H460 cells were untreated or treated with indicated concentration of perifosine (0.3–10 μM), in the presence or absence of MEK-162 (1 μM); for 24 or 72 h, cell growth was tested by MTT assay.|
|Incubation time||24 or 72 h|
|Animal models||A549 lung cancer xenograft|
|Formulation||Formulated in 30% Captisol|
|Dosages||2.5 mg/kg, once daily|
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo
Jianli Zhang,et,al. Tumor Biol. 2015;36:5699–5706.
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