Flavopiridol

Research use only, not for human use.

A potent, ATP-competetive CDKs inhibitor with IC50 of 30, 170, 100 nM for CDk1, 2, 4, respectively.

A potent, ATP-competetive CDKs inhibitor with IC50 of 30, 170, 100 nM for CDk1, 2, 4, respectively; inhibits cell cycle progression in either G1 or G2 in human breast carcinoma cells, induces programmed cell death, promote differentiation, inhibits angiogenic processes and modulates transcriptional events.Blood Cancer Phase 2 Clinical.

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. 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.Flavopiridol (Alvocidib) also inhibits cyclin E1 and induces apoptosis.

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L-868275 | HMR-1275 | Alvocidib | NSC-649890

Cell Cycle/DNA Damage

CDK

CDK1|CDK2|CDK4|CDK6|CDK7

Cancer

Blood cancer

146426-40-6

401.8402

C21H20ClNO5

>98% (HPLC)

10 mM in DMSO

CN1CCC(C(C1)O)C2=C(C=C(C3=C2OC(=CC3=O)C4=CC=CC=C4Cl)O)O

4H-1-Benzopyran-4-one, 2-(2-chlorophenyl)-5,7-dihydroxy-8-[(3S,4R)-3-hydroxy-1-methyl-4-piperidinyl]-

(-20℃)

With Ice Pack

≥ 2 years