Flavopiridol (Alvocidib)

Catalog No.S1230 Synonyms: NSC 649890 HCl,HMR-1275

Flavopiridol (Alvocidib) Chemical Structure

Molecular Weight(MW): 401.84

Flavopiridol (Alvocidib) competes with ATP to inhibit CDKs including CDK1, CDK2, CDK4, CDK6, and CDK9 with IC50 values in the 20-100 nM range. It is more selective for CDK1, 2, 4, 6, 9 versus CDK7. Flavopiridol is initially found to inhibit EGFR and PKA. Phase 1/2.

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Cited by 16 Publications

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  • (C) In vivo treatment of Tg:Pomc-Pttg;Pomc-eGFP embryos with small-molecule CDK inhibitors (50 μM) or 0.2% DMSO as control from 18 to 40 hpf. One hundred to one hundred fifty embryos were treated with each compound. Representative images of live embryos are shown with gross morphology (Right) and pituitary Pomc-GFP-positive cells at higher magnification (Left) at 40 hpf. Embryos exposed to flavopiridol developed early developmental defect before pituitary POMC cell ontogeny occurs. (D) Relative expression of pituitary Pomc-eGFP fluorescence analyzed using Volocity 5.2 software (Improvision; mean ±SE of relative expression, n = 7). (E) R-roscovitine specifically suppresses expansion of pituitary POMC cells overexpressing zPttg from 18 to 48 hpf. Double transgenic Tg:Pomc-Pttg;Prl-RFP embryos were generated by breeding Tg:Pomc-Pttg fish with a previously generated PRL-RFP transgenic line, in which RFP was targeted to pituitary lactotrophs by a zebrafish Prolactin promoter (34). Representative fluorescent microscopy of pituitary POMC-eGFP (a and b) and PRL-RFP (c and d) expression in live Tg:Pomc-Pttg; Pomc-eGFP and Tg:Pomc-Pttg;Prl-RFP embryos treated with 0.2% DMSO (a and c) or 50 μM R-roscovitine (b and d). (F) Relative expression of pituitary POMC-eGFP or PRL-RFP fluorescence were analyzed (mean ±SE of relative expression; n = 10). Results represent one of three similar experiments;*P < 0.02 and **P < 0.000005. (Scale bar, 50 μm.)

    PNAS 2011 108, 8417. Flavopiridol (Alvocidib) purchased from Selleck.

  • (A) After mitotic arrest and treatment with the proteasome inhibitor MG132, HeLa cells were treated with the indicated kinase inhibitors The cells were harvested, and the lysates were separated by SDS-PAGE and immunoblotted for phosphorylated RV[S/T]F (p-RV[S/T]F, top). The blot was quantified using ImageJ software and normalized to the mitotic sample (bottom). MLN8054, Aurora A and Aurora B inhibitor; ZM447439 and hesperadin, Aurora B inhibitors; BI2536, PLK1 inhibitor; flavopiridol, CDK1 inhibitor. n = 3. **P < 0.01, paired Student’s t test.

    Science, 2018, 11(530), doi: 10.1126/scisignal.aai8669. Flavopiridol (Alvocidib) purchased from Selleck.

  • G, human THP-1 cells were treated with various small-molecule inhibitors or chemotherapy at increasing concentrations for 24 hours and then analyzed for viability by flow cytometry for PI exclusion. Cells concurrently treated with palbociclib or dinaciclib were analyzed for cytostatis according to nuclear DNA content.

    Cancer Res, 2016, 76(5):1158-69. Flavopiridol (Alvocidib) purchased from Selleck.

  • UM cell lines OMM1, MM66, OMM2.3, MEL202 and MEL270 were treated with 20 nM quisinostat and 100 nM flavopiridol for 24 hours after which cells were harvested. Protein lysates were analyzed for the expression levels of c-Myc, RNA pol2-CTD Ser2 phosphorylation and acetylated histone 3 by Western blot. Expression of vinculin was analyzed to control for equal loading.

    Oncotarget, 2018, 9(5): 6174-6187. Flavopiridol (Alvocidib) purchased from Selleck.

  • Pharmacological inhibition of either CDK1/2 or E2F1 prevented the induction of the expression of MAD2 by SKP2 overexpression. Notes: (A) Human lung cancer A549 cells were transfected with 2 μg of vector pcDNA3.1 or pcDNA-SKP2 for 48 h, then treated with CDK1/2 inhibitor flavopiridol or E2F1 inhibitor HLM006474 for additional 24 h. Total RNAs were extracted for the detection of the mRNA levels MAD2 by RT-QPCR with GAPDH as internal control. Quantitative analysis are expressed as mean ± SEM. n=3, *P<0.05 vs control. (B) Human lung cancer A549 cells were transfected with 2 μg of vector pcDNA3.1 or pcDNA-SKP2 for 48 h, then treated with CDK1/2 inhibitor flavopiridol or E2F1 inhibitor HLM006474 for additional 24 h. Total proteins were extracted for the detection of the protein levels Skp2 and Mad2 and the phosphorylation of Rb at Ser780 (pRb-S780) by Western blotting. GAPDH served as the loading control. (C) Human lung cancer A549 cells were transfected with 50 nM control or SKP2-specific siRNA with lipofectamine 2000 for 48 h, then treated with CDK1/2 inhibitor flavopiridol or E2F1 inhibitor HLM006474 for additional 24 h. Total proteins were extracted for the detection of the protein levels Skp2 and Mad2 by Western blotting. GAPDH served as the loading control. Abbreviations: MAD2, mitotic arrest deficient 2; SKP2, S-phase kinase-associated protein 2; mRNA, messenger RNA; SEM, standard error of the mean; Rb, retinoblastoma; siRNA, small interfering RNA.

    Onco Targets Ther, 2017, 10:439-446. Flavopiridol (Alvocidib) purchased from Selleck.

Purity & Quality Control

Choose Selective CDK Inhibitors

Biological Activity

Description Flavopiridol (Alvocidib) competes with ATP to inhibit CDKs including CDK1, CDK2, CDK4, CDK6, and CDK9 with IC50 values in the 20-100 nM range. It is more selective for CDK1, 2, 4, 6, 9 versus CDK7. Flavopiridol is initially found to inhibit EGFR and PKA. Phase 1/2.
Features First CDK inhibitor to be used in human clinical trials.
CDK9 [8]
(Cell-free assay)
CDK1 [8]
(Cell-free assay)
CDK4 [9]
(Cell-free assay)
CDK2 [8]
(Cell-free assay)
CDK6 [9]
(Cell-free assay)
20 nM 30 nM 20-40 nM 40 nM 60 nM
In vitro

Flavopiridol displays less activity against unrelated kinases such as MAP, PAK, PKC, and EGFR with IC50 of >14 μM. Flavopiridol significantly inhibits the colony growth of HCT116, A2780, PC3, and Mia PaCa-2 cells with IC50 of 13 nM, 15 nM, 10 nM and 36 nM, respecitively. [1] Flavopiridol also potently inhibits the activity of Glycogen synthase kinase-3 (GSK-3) with an IC50 of 280 nm. [2] Compared with other CDKs, Flavopiridol inhibits the activity of CDK7 less potently with IC50 of 875 nM. Flavopiridol (0.5 μM) inhibits both pSer807/811 Rb and pThr199 NPM, whereas mild changes are observed at pThr821 Rb. Flavopiridol also decreases the overall RNA polymerase II level, as well as the phosphorylation of RNA polymerase II on the CTD repeats at Ser2 Ser5. [3] As a broad spectrum CDK inhibitor, Flavopiridol can inhibit cell cycle progression in either G1 or G2. Flavopiridol (0.3 μM) induces G1 arrest in either MCF-7 or MDA-MB-468 cells by inhibition of the CDK4 or CDK2 kinase activity. [4] Flavopiridol exhibits potent cytotoxicity against a wide variety of tumor cell lines with IC50 values ranging form 16 nM for LNCAP to 130 nM for K562. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
ID8 cells MYHQdo9tcW[ncnH0bY9vKGG|c3H5 Mme4RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDJSFgh[2WubIOsJGlEPTB;NzDuUS=> MWKxO|EzOzh{MR?=
Sf9 cells MWDGeY5kfGmxbjDhd5NigQ>? M3rHfGlvcGmkaYTpc44hd2ZicnXjc41jcW6jboSgZ5lkdGmwIFGvR2RMOiCneIDy[ZN{\WRiaX6gV4Y6KGOnbHzzMEBKSzVyPUGyJI5O NF\6cFgyPzlyNEO2Oi=>
LNCaP human prostate carcinoma cell MoO4VJJwdGmoZYLheIlwdiCjc4PhfS=> M4P0bmlvcGmkaYTpc44hd2ZiTF7DZXAhcHWvYX6gdJJwe3SjdHWgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvci=> NIDxbIQyOjF7MEOxNy=>
HCT116/VP35 human colon carcinoma cell NGLiZ5RRem:uaX\ldoF1cW:wIHHzd4F6 MkfzTY5pcWKrdHnvckBw\iCKQ2SxNVYwXlB|NTDoeY1idiClb3zvckBk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVE4KG6P M4SzZVEzOTlyM{Gz
HCT116 human colon carcinoma cell NUDtWVRrWHKxbHnm[ZJifGmxbjDhd5NigQ>? NXKxV4puUW6qaXLpeIlwdiCxZjDIR3QyOTZiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME2xPEBvVQ>? MYWxNlE6ODNzMx?=
HCT116/VM46 human colon carcinoma cell M334bnBzd2yrZnXyZZRqd25iYYPzZZk> NYrNXlRrUW6qaXLpeIlwdiCxZjDIR3QyOTZxVl20OkBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTJzIH7N MWSxNlE6ODNzMx?=
human A2780 cells Mon1R5l1d3SxeHnjxsBie3OjeR?= MWWyOEBp MlnRR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVI4QDBiY3XscJMh[W[2ZYKgNlQhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2yN{BvVQ>? NVLxXmhzOjN|MEG3Olc>
MCF7 cells M1Ls[3Bzd2yrZnXyZZRqd25iYYPzZZk> NX\rRYY2SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBOS0Z5IHPlcIx{NCCLQ{WwQVI3KG6P NXT5O4VrOTdzMkO4NlE>
human MRC5 cells MlnNR5l1d3SxeHnjxsBie3OjeR?= NEDGcYk4OiCq M4jVfmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1TSzViY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2yPEBvVQ>? MkjiNlM{ODF5Nke=
human A2780 cells NGDEXZJEgXSxdH;4bYPDqGG|c3H5 NE\wOmM4OiCq M4rsemN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9Nlkhdk1? NVf6SIJ{OjN|MEG3Olc>
human A2780 cells NHO2RXVEgXSxdH;4bYPDqGG|c3H5 NIXYZWM1QCCq MmjvR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVI4QDBiY3XscJMh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2zNUBvVQ>? NFfzd2czOzNyMUe2Oy=>
A2780/DDP-R human ovarian carcinoma cell NH62PVJRem:uaX\ldoF1cW:wIHHzd4F6 NVXCd5hXUW6qaXLpeIlwdiCxZjDBNlc5OC:GRGCtVkBpfW2jbjDveoFzcWGwIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;M{igcm0> MUmxNlE6ODNzMx?=
human MRC5 cells MlW4R5l1d3SxeHnjxsBie3OjeR?= M{S2flQ5KGh? NHTWflJEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOWkN3IHPlcIx{KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEeLNUC9N|khdk1? NWHE[ZBWOjN|MEG3Olc>
ABAE human fibroblast cell MnvoVJJwdGmoZYLheIlwdiCjc4PhfS=> M3vUeGlvcGmkaYTpc44hd2ZiQVLBSUBpfW2jbjDmbYJzd2KuYYP0JINmdGxicILvcIln\XKjdHnvckwhUUN3ME20OUBvVQ>? NV73cZVVOTJzOUCzNVM>
HL60 human leukemia cell MWnQdo9tcW[ncnH0bY9vKGG|c3H5 NYLYNGpyUW6qaXLpeIlwdiCxZjDIUFYxKGi3bXHuJIxmfWunbXnhJINmdGxicILvcIln\XKjdHnvckwhUUN3ME20OkBvVQ>? M3\pT|EzOTlyM{Gz
human MRC5 cells MlrJR5l1d3SxeHnjxsBie3OjeR?= M{X2bVI1KGh? NYnrTIJlS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkAzPCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVQ6KG6P NUTXNJZnOjN|MEG3Olc>
Hs 27 human fibroblast cell MlzjVJJwdGmoZYLheIlwdiCjc4PhfS=> NF3aS3dKdmirYnn0bY9vKG:oIFjzJFI4KGi3bXHuJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVUyKG6P NIH2UlIyOjF7MEOxNy=>
CCRF-CEM human leukemia cell NIr6ZldRem:uaX\ldoF1cW:wIHHzd4F6 NFnmcY9KdmirYnn0bY9vKG:oIFPDVmYuS0WPIHj1cYFvKGyndXvlcYliKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF02OiCwTR?= M2XiV|EzOTlyM{Gz
OVCAR-3 human ovarian carcinoma cell MlXFVJJwdGmoZYLheIlwdiCjc4PhfS=> MV;Jcohq[mm2aX;uJI9nKE:YQ1HSMVMhcHWvYX6gc5ZiemmjbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUW0JI5O M{HhdlEzOTlyM{Gz
A2780/DDP-S human ovarian carcinoma cell Mk\yVJJwdGmoZYLheIlwdiCjc4PhfS=> NFnIbHhKdmirYnn0bY9vKG:oIFGyO|gxN0SGUD3TJIh2dWGwIH;2ZZJq[W5iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD13NjDuUS=> NIPQco0yOjF7MEOxNy=>
human HMEC1 cells NEfsPZJEgXSxdH;4bYPDqGG|c3H5 M4ft[FI1KGh? MWXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjCyOEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPU[xJI5O M2\P[VI{OzBzN{[3
human HMEC1 cells M{\XSmN6fG:2b4jpZ:Kh[XO|YYm= M{XEOFQ5KGh? NXz0bFR4S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03OiCwTR?= M2j2eFI{OzBzN{[3
A2780/TAX-S human ovarian carcinoma cell NFHZcGxRem:uaX\ldoF1cW:wIHHzd4F6 MWnJcohq[mm2aX;uJI9nKEF{N{iwM3RCYC2VIHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF03PSCwTR?= MnnFNVIyQTB|MUO=
LS174T human colon carcinoma cell NUPKWHZSWHKxbHnm[ZJifGmxbjDhd5NigQ>? MVTJcohq[mm2aX;uJI9nKEyVMUe0WEBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTZ3IH7N M3fwbFEzOTlyM{Gz
MCF-7 human breast carcinoma cell M{jaSHBzd2yrZnXyZZRqd25iYYPzZZk> NX7kVm5QUW6qaXLpeIlwdiCxZjDNR2YuPyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OkBvVQ>? NG\k[mwyOjF7MEOxNy=>
human HMEC1 cells NE\jd4lEgXSxdH;4bYPDqGG|c3H5 MmW3O|IhcA>? NYfqfm9rS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03PiCwTR?= NYC3OYlHOjN|MEG3Olc>
PC3 human prostate carcinoma cell MX7Qdo9tcW[ncnH0bY9vKGG|c3H5 MkO0TY5pcWKrdHnvckBw\iCSQ{OgbJVu[W5icILvd5RifGViY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD14NjDuUS=> MWexNlE6ODNzMx?=
human A2780 cell line MkfXVJJwdGmoZYLheIlwdiCjc4PhfS=> NUHqOoNyPzJiaB?= MoPYRY51cXC{b3zp[oVz[XSrdnWg[YZn\WO2IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdCCuaX7lJJdieyCmZYTldo1qdmWmIHnuJIEhf2ixbHWgZ4VtdCB5MjDodkBkgXSxdH;4bYNqfHliYYPzZZktKEmFNUC9O|Ehdk1? NET3S4EyPTB{N{i2Ny=>
human ovarian (A2780) cancer cell NF3nVHpEgXSxdH;4bYPDqGG|c3H5 NETwZYdEgXSxdH;4bYMh\W[oZXP0JI9vKGi3bXHuJI93[XKrYX6gLGEzPzhyKTDjZY5k\XJiY3XscEBtcW6nLDDJR|UxRTdzIH7N Mn3WNVUyOjV7N{G=
MLF mouse lung fibroblast cell M2TjfXBzd2yrZnXyZZRqd25iYYPzZZk> MYDJcohq[mm2aX;uJI9nKE2ORjDtc5V{\SCudX7nJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVczKG6P M3zIb|EzOTlyM{Gz
human NCI60 cells NVXlR|VyWHKxbHnm[ZJifGmxbjDhd5NigQ>? NEHJdYY4OiCq MoTzRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1m2NEBk\WyuczDh[pRmeiB5MjDodpMh[nlic4Xs[o9zcG:mYX3pcoUhSiCjc4PhfUwhT0l3ME23OE44KG6P NYLEWYNQOjFyOEC3NFM>
LX-1 human lung carcinoma NVKzVpA1WHKxbHnm[ZJifGmxbjDhd5NigQ>? Mk[4TY5pcWKrdHnvckBw\iCOWD2xJIh2dWGwIHz1coch[2G{Y3nuc41iKHC{b3zp[oVz[XSrb36sJGlEPTB;N{Wgcm0> MU[xNlE6ODNzMx?=
A431 human squamous cell M{nPPHBzd2yrZnXyZZRqd25iYYPzZZk> MlOwTY5pcWKrdHnvckBw\iCDNEOxJIh2dWGwIIPxeYFud3W|IHPlcIwh[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF04PSCwTR?= Mn\TNVIyQTB|MUO=
SKBR-3 human breast carcinoma cell NV3Cb40zWHKxbHnm[ZJifGmxbjDhd5NigQ>? NHHhXYFKdmirYnn0bY9vKG:oIGPLRnIuOyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME23O{BvVQ>? NHXqZpoyOjF7MEOxNy=>
A2780/TAX-R human ovarian carcinoma cell Ml\RVJJwdGmoZYLheIlwdiCjc4PhfS=> MoHQTY5pcWKrdHnvckBw\iCDMke4NE9VSVhvUjDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:Pzhibl2= MYCxNlE6ODNzMx?=
M109 mouse lung carcinoma cell M3XSdnBzd2yrZnXyZZRqd25iYYPzZZk> M{TEV2lvcGmkaYTpc44hd2ZiTUGwPUBud3W|ZTDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QDBibl2= M1HTTlEzOTlyM{Gz
CACO-2 human colon carcinoma cell NF36OoJRem:uaX\ldoF1cW:wIHHzd4F6 NUnTRWNJUW6qaXLpeIlwdiCxZjDDRWNQNTJiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME24OkBvVQ>? MnrhNVIyQTB|MUO=
A549 human lung carcinoma cell MnPIVJJwdGmoZYLheIlwdiCjc4PhfS=> MojqTY5pcWKrdHnvckBw\iCDNUS5JIh2dWGwIHz1coch[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF06PiCwTR?= MUSxNlE6ODNzMx?=
MIP human colon carcinoma cell MV;GeY5kfGmxbjDhd5NigQ>? MmHUTY5pcWKrdHnvckBw\iCPSWCgbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygcIlv\SxiSVO1NF0xNjF{IN88US=> MVyxNlE6ODNzMx?=
K562 human leukemia cell M{jQcHBzd2yrZnXyZZRqd25iYYPzZZk> MkjJTY5pcWKrdHnvckBw\iCNNU[yJIh2dWGwIHzleYtmdWmjIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD1yLkGzJO69VQ>? NIn1SncyOjF7MEOxNy=>
MCF-7 tumor cell MYLQdo9tcW[ncnH0bY9vKGG|c3H5 M{K2cWlvcGmkaYTpc44hd2ZiTVPGMVchfHWvb4KgZ4VtdCCycn;sbYZmemG2aX;u Mo\NNVA5PDN{MUG=
human NCI60 cells NXj0S3BIWHKxbHnm[ZJifGmxbjDhd5NigQ>? M3HQV|czKGh? Ml:1RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1m2NEBk\WyuczDhd5Nme3OnZDDhd{Bt\XSqYXyg[YZn\WO2IHHmeIVzKDd{IHjyd{BjgSC|dXzmc5Jpd2SjbXnu[UBDKGG|c3H5MEBNSzVyPUCuPVA1KM7:TR?= MnzXNlExQDB5MEO=
PC3 cell NWPteYVqTnWwY4Tpc44h[XO|YYm= M1HQZWlvcGmkaYTpc44hd2ZiUFOzJINmdGxiY3zvco9o\W6rYzDhd5NigSxiSVO1NF0yOCEQvF2= M{LZZVEyODZ|NkC5
HCT116 cell M3y3NmZ2dmO2aX;uJIF{e2G7 NH\0Z5pKdmirYnn0bY9vKG:oIFjDWFEyPiClZXzsJINtd26xZ3XubYMh[XO|YYmsJGlEPTB;MUOg{txO NET4b3cyOTB4M{[wPS=>
A2780 cell M{nUbGZ2dmO2aX;uJIF{e2G7 MVrJcohq[mm2aX;uJI9nKEF{N{iwJINmdGxiY3zvco9o\W6rYzDhd5Nige,:jDDJR|UxRTF3IN88US=> MnXRNVExPjN4MEm=
Mia PaCa-2 cell NEDpNpFHfW6ldHnvckBie3OjeR?= M1rOfmlvcGmkaYTpc44hd2ZiTXnhJHBiS2FvMjDj[YxtKGOub37v[4VvcWNiYYPzZZktKEmFNUC9N|Yh|ryP Ml;qNVExPjN4MEm=
human A2780 cells NFXQbpdHfW6ldHnvckBie3OjeR?= M{TXTmlvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJG5RVSCyaH;zdIhwenmuYYTpc44h[XRidHjyNVk6KGmwIHj1cYFvKEF{N{iwJINmdGy| M2PKNFE5PDZ7OEC5
human A2780 cells M{D3OmZ2dmO2aX;uJIF{e2G7 NFXuZokzPCCq NXrXWplzUW6qaXLpeIlwdiCxZjDj[IsudWWmaXH0[YQhWmJicHjvd5Bpd3K7bHH0bY9vKGG2IITodlgzOSCrbjDoeY1idiCDMke4NEBk\WyuczDh[pRmeiB{NDDodpM> Mlq3NVg1Pjl6MEm=

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In vivo Administration of Flavopiridol at 7.5 mg/kg for 7 days displays slight antitumor activity against P388 murine leukemia, resulting in %T/C value of 110, and active against the human A2780 ovarian carcinoma implanted sc in nude mice, producing 1.5 log cell kill (LCK). [5] Flavopiridol treatment at 1-2.5 mg/kg for 10 days significantly suppresses collagen-induced arthritis in mice in a dose-dependent manner, by inhibiting synovial hyperplasia and joint destruction, whereas serum concentrations of anti-collagen type II (CII) Abs and proliferative responses to CII are maintained. [6] In the p21-intact Hct116 xenografts in nude mice, administration of CPT-11 (100 mg/kg) followed by Flavopiridol (3 mg/kg) 7 and 16 hours later significantly inhibits tumor regression by 86% and 82%, respectively, displaying >2 fold inhibition compared with CPT-11 alone by 40 %. The combination produces ~30% complete response rate (CR) in contrast to CPT-11 alone where no CR is found. [7]


Kinase Assay:


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CDK kinase assay:

For CDK1/cyclin B1 kinase assay, kinase reactions consist of 100 ng of baculovirus expressed GST-CDK1/cyclin B1 (human) complex, 1 μg histone HI, 0.2 μCi [γ-33P]ATP, 25 μM ATP in 50 μL kinase buffer (50 mM Tris, pH 8.0, 10 mM MgCl2, 1 mM EGTA, 0.5 mM DTT). For CDK2/cyclin E kinase assay, kinase reactions consist of 5 ng of baculovirus expressed GST-CDK2/cyclin E (human) complex, 0.5 μg GST-RB fusion protein (amino acids 776-928 of retinoblastoma protein), 0.2 μCi [γ-33P]ATP, 25 μM ATP in 50 μL kinase buffer (50 mM Hepes, pH 8.0, 10 mM MgCl2, 1 mM EGTA, 2 mM DTT). For CDK4/cyclin D1 kinase assay, kinase reactions consist of 150 ng of baculovirus expressed GST-CDK4/cyclin D1 (human), 280 ng of Stag-cyclin D1, 0.5 μg GST-RB fusion protein (amino acids 776-928 of retinoblastoma protein), 0.2 μCi [γ-33P]ATP, 25 μM ATP in 50 μL kinase buffer (50 mM Hepes, pH 8.0, 10 mM MgCl2, 1 mM EGTA, 2 mM DTT). Reactions are incubated for 45 minutes for CDK1 and CDK2, or 1 hour for CDK4 at 30 °C and stopped by the addition of cold trichloroacetic acid (TCA) to a final concentration 15%. TCA precipitates are collected onto GF/C unifilter plates using a Filtermate universal harvester and the filters are quantitated using a TopCount 96-well liquid scintillation counter. Flavopiridol is dissolved at 10 mM in dimethylformamide (DMF) and evaluated at six concentrations, each in triplicate. The final concentration of DMF in the assay = 2%. IC50 values are derived by nonlinear regression analysis and have a coefficient of variance = 16%. To assay Flavopiridol activity on CDK6, a filter-binding assay is established. The following are combined in the reaction mixture: 2 μL of CDK6 (0.7 mg/μL), 5 μL of histone H1 (6 mg/mL), 14 μL of kinase buffer (60 mM β-glycerophosphate, 30 mM p-nitrophenyl phosphate, 25 mM MOPS (pH 7.0), 5 mM EGTA, 15 mM MgCl2, 1 mM DTT, 0.1 mM Na-vanadate), 3 μL of increasing concentrations of Flavopiridol diluted in 50% DMSO, and 6 μL of 33P-ATP (1 mCi/mL) in nonradioactive ATP at 90 μM concentration (final concentration: 15 μM). The assay is initiated by the addition of 33P-ATP. The reaction is incubated for 20 minutes at 30°C. A 25 μL aliquot of the supernatant is then spotted onto Whatman P81 phosphocellulose paper. Filters are washed 5 times with 1% phosphoric acid solution. Wet filters are counted in the presence of 1 mL of scintillation fluid. Cdk9 activity is measured using 50 nM of recombinant Cdk9/cyclin T in 50 mM HEPES pH 7.5, 10 mM MgCl2, 1 mM DTT, 3 μM Na3VO4, 150 μM RNA polymerase CDT peptide and 80 μM ATP. Cdk7 assay is performed in the same buffer using 37 nM of purified kinase in the presence of 200 μM ATP and 10 μM myelin binding protein as a substrate. The potency of Flavopiridol toward CDK9 and CDK7 is determined using either a strong anion exchanger (Dowex 1-X8 resin, formate form)-based assay or a scintillation proximity assay. IC50 values are calculated from the dose-response curves.
Cell Research:


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  • Cell lines: MCF-7, LNCAP, PC3, HCT116, CACO-2, A549, HL60, K562 cells and et al.
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 72 hours
  • Method:

    Cells are exposed to various concentrations of Flavopiridol for 72 hours at which time the tetrazolium dye, MTS in combination with phenazine methosulfate, is added. After 3 hours, the absorbency is measured at 492 nm, which is proportional to the number of viable cells. The results are expressed as IC50 values. For cell Cycle analysis, cells are fixed in paraformaldehyde and ethanol, washed, resuspended in staining solution of TdT enzyme and FITC-dUTP, washed, stained with PI following RNase treatment, and then analyzed by flow cytometry.

    (Only for Reference)
Animal Research:


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  • Animal Models: Female Balb/c×DBA/2J F1 mice inoculated ip with P388 ascites leukemic cells, and Balb/c nu/nu nude mice subcutaneous implanted with A2780, Br-cycE, or A431 cells
  • Formulation: Dissolved in a mixture of Cremophor/ethanol (50:50), and diluted in water
  • Dosages: ~7.5 mg/kg/day
  • Administration: Injection i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 15 mg/mL (37.32 mM)
Ethanol 8 mg/mL (19.9 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 401.84


CAS No. 146426-40-6
Storage powder
in solvent
Synonyms NSC 649890 HCl,HMR-1275

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

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The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
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    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
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    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

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Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03593915 Recruiting Myelodysplastic Syndromes (MDS) Tolero Pharmaceuticals Inc. August 29 2018 Phase 1|Phase 2
NCT03593915 Recruiting Myelodysplastic Syndromes (MDS) Tolero Pharmaceuticals Inc. August 29 2018 Phase 1|Phase 2
NCT03563560 Recruiting Acute Myeloid Leukemia Sumitomo Dainippon Pharma Co. Ltd. May 15 2018 Phase 1
NCT03441555 Recruiting Acute Myeloid Leukemia (AML) AbbVie|Tolero Pharmaceuticals Inc. May 30 2018 Phase 1
NCT03563560 Recruiting Acute Myeloid Leukemia Sumitomo Dainippon Pharma Co. Ltd. May 15 2018 Phase 1
NCT03441555 Recruiting Acute Myeloid Leukemia (AML) AbbVie|Tolero Pharmaceuticals Inc. May 30 2018 Phase 1

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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CDK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID