|Source||Chin J Integr Med (2015). Figure 5. CYC116|
|Method||Flow Cytometry Detection of Apoptosis|
|Cell Lines||RPMI8226 Cell|
|Incubation Time||24 h|
|Results||For treatment with matrine or CYC116 alone, early apoptosis rates were 1.91% and 2.38%, respectively. However, the early apoptosis rate following combined drug treatment was 9.25%, indicating a synergistic effect of matrine and CYC116 on the induction of apoptosis in MM cells.|
|Cell lines||HeLa, MCF7, MV4-11 and A2780 cells line|
|Preparation method||Cell Viability Assay.
Inhibition of cell growth was measured by a standard MTT (thiazolyl blue; 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay using a panel of tumor cell lines.Briefly: cells were seeded (2,500–5,000 cells/well) in 96-well plates and allowed to attach for ~ 24 h. Cells were incubated with test compounds for 96 h in DMEM medium containing 10% fetal bovine serum. Cells were treated with a range of compound concentrations in triplicate to generate dose-response curves. The compound concentration required to inhibit 50% of cell growth (IC50) was determined using nonlinear regression analysis.
|Concentrations||0~10 μ M|
|Incubation time||96 h|
|Animal models||Murine P388/D1 Leukemia Model (1) / Murine NCI-H460 non-small cell lung cancer xenograft model (2)|
|Dosages||45 or 67mg/kg twice daily on days 1-3 and 7-9(1) / 75 and 100mg/kg once daily starting on day 1 and for 5 days(2)|
|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.
An integrated pharmacokinetic-pharmacodynamic model for an Aurora kinase inhibitor.
Kamei et al. J Pharmacokinet Pharmacodyn. 2010 Aug;37(4):407-34. PMID: 20694801.
Discovery of N-phenyl-4-(thiazol-5-yl)pyrimidin-2-amine aurora kinase inhibitors.
Wang S, et al. J Med Chem. 2010 Jun 10;53(11):4367-78. PMID: 20462263.
|Related Aurora Kinase Products|
SNS-314 is a potent and selective inhibitor of Aurora A, Aurora B and Aurora C with IC50 of 9 nM, 31 nM, and 3 nM, respectively.
GSK1070916 is a reversible and ATP-competitive inhibitor of Aurora B/C with IC50 of 3.5 nM/6.5 nM. It displays >100-fold selectivity against the closely related Aurora A-TPX2 complex.
PHA-680632 is potent inhibitor of Aurora A, Aurora B and Aurora C with IC50 of 27 nM, 135 nM and 120 nM, respectively. It has 10- to 200-fold higher IC50 for FGFR1, FLT3, LCK, PLK1, STLK2, and VEGFR2/3.
MK-5108 (VX-689) is a highly selective Aurora A inhibitor with IC50 of 0.064 nM and is 220- and 190-fold more selective for Aurora A than Aurora B/C, while it inhibits TrkA with less than 100-fold selectivity.
PF-03814735 is a novel, potent and reversible inhibitor of Aurora A/B with IC50of 0.8 nM/5 nM, is less potent to Flt3, FAK, TrkA, and minimally active to Met and FGFR1.
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