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Pan-cdk inhibitor
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Flavopiridol is a potent and selective inhibitor of cyclin-dependent kinases (CDKs) with IC50 values of ~41 nM for CDK1, CDK2, CDK4, CDK6 and 300 nM for CDK7, respectively [1].
CDKs are a family of protein kinases regulating the cell cycle and play an important role in transcription, mRNA processing, and cell differentiation.
Analysis of the crystal structure suggested flavopiridol binded to the ATP-binding pocket of CDK2. In MCF-7 breast cancer cells, flavopiridol reduced the mRNA level of cyclin D1 protein and cyclin D3 protein [1]. In 23 human tumor cell models, flavopiridol significantly inhibited human bone marrow colony formation between 10 and 100 ng/ml [2].
In prostate cancer xenograft PRXFI369, flavopinidol (10 mg/kg/day) had antitumor activity of optimal test/control (T/C) of 33% and a growth delay of 30 days. Also, it reduced tumor volume by 85%. In prostate cancer xenograft PRXFI337, the optimal T/C was 27% and the growth delay was 17 days [2].
[1]. Senderowicz AM. The cell cycle as a target for cancer therapy: basic and clinical findings with the small molecule inhibitors flavopiridol and UCN-01. Oncologist, 2002, 7 Suppl 3: 12-9.
[2]. Drees M, Dengler WA, Roth T, et al. Flavopiridol (L86-8275): selective antitumor activity in vitro and activity in vivo for prostate carcinoma cells. Clin Cancer Res, 1997, 3(2): 273-279.
[3]. Carlson BA, Dubay MM, Sausville EA, et al. Flavopiridol induces G1 arrest with inhibition of cyclin-dependent kinase (CDK) 2 and CDK4 in human breast carcinoma cells. Cancer Res, 1996, 56(13): 2973-2978.

Physical Appearance

A crystalline solid

Chemical Properties

StorageStore at -20°C
Cas No.146426-40-6
SynonymsL868275; HMR-1275; Alvocidib
Solubility≥40.2 mg/mL in DMSO, ≥85.4 mg/mL in EtOH with ultrasonic and warming, <2.27 mg/mL in H2O
Chemical Name2-(2-chlorophenyl)-5,7-dihydroxy-8-[(3S,4R)-3-hydroxy-1-methylpiperidin-4-yl]chromen-4-one
SDFDownload SDF
Canonical SMILESCN1CCC(C(C1)O)C2=C(C=C(C3=C2OC(=CC3=O)C4=CC=CC=C4Cl)O)O
Shipping ConditionEvaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.


Cell experiment [1]:

Cell lines

23 human tumor cells

Preparation method

This compound is soluble in DMSO. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 °C for several months.

Reacting condition

0.1 ng/mL ~ 10 μg/mL; 6 ~ 18 days


In 3 prostate cancer cell lines (PRXFI369, PC3MX and LNCaPX) and 1 melanoma cell line (MEXFI341), Flavopiridol potently inhibited colony formation, even at the concentration down to 0.1 ng/mL. At the concentrations between 10 and 100 ng/mL, Flavopiridol significantly inhibited colony formation of human bone marrow cells. For most of the human tumor cells, the inhibitory effect of Flavopiridol on colony formation was first observed at 10 ng/mL.

Animal experiment [1]:

Animal models

Nude mice bearing PRXFI369 xenografts

Dosage form

10 mg/kg/day; p.o.


In tumor-bearing nude mice, Flavopiridol caused 12.5% deaths at the maximum tolerated dose (MTD). In nude mice bearing PRXFI369 xenografts, Flavopiridol at MTD resulted in an optimal T/C value of 33% and a growth delay of 30 days. However, at day 28, tumor volume increased slightly to 115%. Flavopiridol at the dose of 15 mg/kg/day was toxic, whereas at the dose of 5 mg/kg/day was inactive.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1]. Drees M, Dengler WA, Roth T, Labonte H, Mayo J, Malspeis L, Grever M, Sausville EA, Fiebig HH. Flavopiridol (L86-8275): selective antitumor activity in vitro and activity in vivo for prostate carcinoma cells. Clin Cancer Res. 1997 Feb;3(2):273-9.

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