Description |
Flavopiridol Hydrochloride is a broad inhibitor of CDK, competing with ATP to inhibit CDKs including CDK1, CDK2, CDK4 with IC50s of 30, 170, 100 nM, respectively.
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Target |
CDK1/Cyc B1:30 nM (IC50)
CDK2/Cyc E:170 nM (IC50)
CDK4/Cyc D1:100 nM (IC50)
MAP:19000 nM (IC50)
PKC:14000 nM (IC50)
EGFR:22000 nM (IC50)
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In Vitro |
Flavopiridol (2 μM) robustly induces a distinct pattern of ER stress in CLL cells that contributes to cell death through IRE1-mediated activation of ASK1 and possibly downstream caspases[1]. Flavopiridol results in potent upregulation of a number of PRGs in treatments lasting 4-24 h. Flavopiridol has and immediate and long-term effect on the expression of several PRGs. In serum starved cells re-stimulated with serum, flavopiridol also inhibits the expression of these genes, but subsequently, JUNB, GADD45B and EGR1 are upregulated in the presence of flavopiridol[2].
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Cell Assay |
The cells treated with flavopiridol are washed after 4 hours with PBS and resuspended in regular growth medium (RPMI 1640) supplemented with 10% human serum and antibiotics for the remainder of the incubation time. In the case of flavopiridol/chloroquine samples, chloroquine is re-added in the fresh media after flavopiridol is washed at 4 hours. For all the other conditions, cells are incubated with the respective drugs for 24 hours continuously.
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Boiling Point | 603.6ºC at 760 mmHg |
Flash Point | 318.8ºC |
Exact Mass | 437.079681 |
PSA | 94.14000 |
LogP | 4.04450 |
Vapour Pressure | 2.03E-15mmHg at 25°C |
Storage condition | -20℃ |