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 and CDK6 with IC50 of ~ 40 nM. It is 7.5-fold more selective for CDK1, 2, 4, 6 versus CDK7. Flavopiridol is initially found to inhibit EGFR and PKA. Phase 1/2.

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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.

    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.

  • 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 and CDK6 with IC50 of ~ 40 nM. It is 7.5-fold more selective for CDK1, 2, 4, 6 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.
CDK1 [1] CDK2 [1] CDK4 [1] CDK6 [1] CDK7 [1]
40 nM 40 nM 40 nM 40 nM 300 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 NUPPS5dKWHKxbHnm[ZJifGmxbjDhd5NigQ>? Mnf2RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDJSFgh[2WubIOsJGlEPTB;NzDuUS=> MUKxO|EzOzh{MR?=
Sf9 cells M164S2Z2dmO2aX;uJIF{e2G7 NIHaSW5KdmirYnn0bY9vKG:oIILlZ49u[mmwYX70JIN6[2yrbjDBM2NFUzJiZYjwdoV{e2WmIHnuJHNnQSClZXzsd{whUUN3ME2xNkBvVQ>? M1m5NlE4QTB2M{[2
LNCaP human prostate carcinoma cell NGDySGVRem:uaX\ldoF1cW:wIHHzd4F6 NFm2bFdKdmirYnn0bY9vKG:oIFzOR4FRKGi3bXHuJJBzd3O2YYTlJINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44> M2i0N|EzOTlyM{Gz
HCT116/VP35 human colon carcinoma cell NX3yUm9UWHKxbHnm[ZJifGmxbjDhd5NigQ>? MX7Jcohq[mm2aX;uJI9nKEiFVEGxOk9XWDN3IHj1cYFvKGOxbH;uJINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9NVchdk1? NInvPZkyOjF7MEOxNy=>
HCT116 human colon carcinoma cell NHHycmJRem:uaX\ldoF1cW:wIHHzd4F6 NIDWVYpKdmirYnn0bY9vKG:oIFjDWFEyPiCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUG4JI5O NFraNVgyOjF7MEOxNy=>
HCT116/VM46 human colon carcinoma cell MV\Qdo9tcW[ncnH0bY9vKGG|c3H5 M4nM[mlvcGmkaYTpc44hd2ZiSFPUNVE3N1[PNE[gbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF0zOSCwTR?= Mk\pNVIyQTB|MUO=
human A2780 cells NH;4T|dEgXSxdH;4bYPDqGG|c3H5 NEXNeIIzPCCq M4H5Z2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFI1KGi{czDifUBOXFRiYYPzZZktKEeLNUC9NlMhdk1? MYCyN|MxOTd4Nx?=
MCF7 cells NXvu[Hp1WHKxbHnm[ZJifGmxbjDhd5NigQ>? Ml3LRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDNR2Y4KGOnbHzzMEBKSzVyPUK2JI5O MUmxO|EzOzh{MR?=
human MRC5 cells NXzDVFk{S3m2b4TvfIlkyqCjc4PhfS=> NV\CU5hKPzJiaB?= NWTlZW5yS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVI5KG6P NIDWZmUzOzNyMUe2Oy=>
human A2780 cells MVPDfZRwfG:6aXRCpIF{e2G7 M3[1elczKGh? M1jybmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9Nlkhdk1? MX2yN|MxOTd4Nx?=
human A2780 cells MUfDfZRwfG:6aXRCpIF{e2G7 NF\sc5k1QCCq MXfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBNlc5OCClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUOxJI5O MXqyN|MxOTd4Nx?=
A2780/DDP-R human ovarian carcinoma cell MXnQdo9tcW[ncnH0bY9vKGG|c3H5 MlfqTY5pcWKrdHnvckBw\iCDMke4NE9FTFBvUjDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:Ozhibl2= M2T1VVEzOTlyM{Gz
human MRC5 cells NF\DPXJEgXSxdH;4bYPDqGG|c3H5 NXrkR3NuPDhiaB?= NYqxU2UyS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVM6KG6P M3LLT|I{OzBzN{[3
ABAE human fibroblast cell NFfFbXpRem:uaX\ldoF1cW:wIHHzd4F6 MlzZTY5pcWKrdHnvckBw\iCDQlHFJIh2dWGwIH\pZpJw[myjc4SgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUS1JI5O NVu4OldOOTJzOUCzNVM>
HL60 human leukemia cell NHrpb49Rem:uaX\ldoF1cW:wIHHzd4F6 Mnv5TY5pcWKrdHnvckBw\iCKTE[wJIh2dWGwIHzleYtmdWmjIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD12NjDuUS=> NYGyW|NPOTJzOUCzNVM>
human MRC5 cells MVrDfZRwfG:6aXRCpIF{e2G7 MXmyOEBp NET2PZpEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOWkN3IHPlcIx{KGGodHXyJFI1KGi{czDifUBOXFRiYYPzZZktKEeLNUC9OFkhdk1? MmO4NlM{ODF5Nke=
Hs 27 human fibroblast cell MWLQdo9tcW[ncnH0bY9vKGG|c3H5 NIjYXHpKdmirYnn0bY9vKG:oIFjzJFI4KGi3bXHuJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVUyKG6P NHHEfXMyOjF7MEOxNy=>
CCRF-CEM human leukemia cell NWXkPFhlWHKxbHnm[ZJifGmxbjDhd5NigQ>? NV7YW|FyUW6qaXLpeIlwdiCxZjDDR3JHNUOHTTDoeY1idiCuZYXr[Y1q[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PTJibl2= NUm0WpVpOTJzOUCzNVM>
OVCAR-3 human ovarian carcinoma cell MnvPVJJwdGmoZYLheIlwdiCjc4PhfS=> NWHtTGtmUW6qaXLpeIlwdiCxZjDPWmNCWi1|IHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF02PCCwTR?= Mn\2NVIyQTB|MUO=
A2780/DDP-S human ovarian carcinoma cell MVnQdo9tcW[ncnH0bY9vKGG|c3H5 NF;qfGVKdmirYnn0bY9vKG:oIFGyO|gxN0SGUD3TJIh2dWGwIH;2ZZJq[W5iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD13NjDuUS=> M13LbFEzOTlyM{Gz
human HMEC1 cells NIHWU4FEgXSxdH;4bYPDqGG|c3H5 NYHZ[VdiOjRiaB?= MmXCR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTG1GSzFiY3XscJMh[W[2ZYKgNlQhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME22NUBvVQ>? MXyyN|MxOTd4Nx?=
human HMEC1 cells M2GySGN6fG:2b4jpZ:Kh[XO|YYm= M2jvPFQ5KGh? NUPIS3d4S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03OiCwTR?= NIWxcowzOzNyMUe2Oy=>
A2780/TAX-S human ovarian carcinoma cell M1;C[3Bzd2yrZnXyZZRqd25iYYPzZZk> M1\RZ2lvcGmkaYTpc44hd2ZiQUK3PFAwXEG[LWOgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTZ3IH7N MV2xNlE6ODNzMx?=
LS174T human colon carcinoma cell Mn20VJJwdGmoZYLheIlwdiCjc4PhfS=> NXTKbWtWUW6qaXLpeIlwdiCxZjDMV|E4PFRiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OUBvVQ>? M3KwSlEzOTlyM{Gz
MCF-7 human breast carcinoma cell MUXQdo9tcW[ncnH0bY9vKGG|c3H5 MlKxTY5pcWKrdHnvckBw\iCPQ1[tO{BpfW2jbjDidoVie3RiY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD14NjDuUS=> MojSNVIyQTB|MUO=
human HMEC1 cells M4\mXWN6fG:2b4jpZ:Kh[XO|YYm= MV63NkBp MUHDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPU[2JI5O MYCyN|MxOTd4Nx?=
PC3 human prostate carcinoma cell M4\tV3Bzd2yrZnXyZZRqd25iYYPzZZk> NFXyWG9KdmirYnn0bY9vKG:oIGDDN{BpfW2jbjDwdo9{fGG2ZTDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPU[2JI5O NGDCN4MyOjF7MEOxNy=>
human A2780 cell line NVz1fJBJWHKxbHnm[ZJifGmxbjDhd5NigQ>? NF\X[mg4OiCq NV3xV44xSW62aYDyc4xq\mW{YYTpeoUh\W[oZXP0JIFo[Wmwc4SgbJVu[W5iQUK3PFAh[2WubDDsbY5mKHejczDk[ZRmem2rbnXkJIlvKGFid3jvcIUh[2WubDC3NkBpeiCleYTveI95cWOrdImgZZN{[XluIFnDOVA:PzFibl2= Ml7INVUxOjd6NkO=
human ovarian (A2780) cancer cell M2L6bGN6fG:2b4jpZ:Kh[XO|YYm= M{jCXGN6fG:2b4jpZ{Bm\m[nY4Sgc44hcHWvYX6gc5ZiemmjbjCoRVI4QDBrIHPhcoNmeiClZXzsJIxqdmVuIFnDOVA:PzFibl2= NFPGU3QyPTF{NUm3NS=>
MLF mouse lung fibroblast cell NXjO[I5SWHKxbHnm[ZJifGmxbjDhd5NigQ>? MkDPTY5pcWKrdHnvckBw\iCPTF[gcY92e2VibIXu[{BncWK{b3LsZZN1KGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF04OiCwTR?= NWfLb2NFOTJzOUCzNVM>
human NCI60 cells M13hOXBzd2yrZnXyZZRqd25iYYPzZZk> MV63NkBp Mmf3RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1m2NEBk\WyuczDh[pRmeiB5MjDodpMh[nlic4Xs[o9zcG:mYX3pcoUhSiCjc4PhfUwhT0l3ME23OE44KG6P NEnGdXczOTB6MEewNy=>
LX-1 human lung carcinoma MULQdo9tcW[ncnH0bY9vKGG|c3H5 MlXLTY5pcWKrdHnvckBw\iCOWD2xJIh2dWGwIHz1coch[2G{Y3nuc41iKHC{b3zp[oVz[XSrb36sJGlEPTB;N{Wgcm0> MYmxNlE6ODNzMx?=
A431 human squamous cell NHuxeZVRem:uaX\ldoF1cW:wIHHzd4F6 MUjJcohq[mm2aX;uJI9nKEF2M{GgbJVu[W5ic4H1ZY1wfXNiY3XscEBk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVc2KG6P NYH6TItCOTJzOUCzNVM>
SKBR-3 human breast carcinoma cell M1XkdnBzd2yrZnXyZZRqd25iYYPzZZk> NY\XUVFsUW6qaXLpeIlwdiCxZjDTT2JTNTNiaIXtZY4h[nKnYYP0JINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9O|chdk1? M3HpW|EzOTlyM{Gz
A2780/TAX-R human ovarian carcinoma cell M3fUVXBzd2yrZnXyZZRqd25iYYPzZZk> MXrJcohq[mm2aX;uJI9nKEF{N{iwM3RCYC2UIHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF04QCCwTR?= Mki4NVIyQTB|MUO=
M109 mouse lung carcinoma cell NXy4PYRwWHKxbHnm[ZJifGmxbjDhd5NigQ>? MUPJcohq[mm2aX;uJI9nKE1zMEmgcY92e2VibIXu[{Bk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVgxKG6P MYSxNlE6ODNzMx?=
CACO-2 human colon carcinoma cell NYfwdnNEWHKxbHnm[ZJifGmxbjDhd5NigQ>? NVjrWGV7UW6qaXLpeIlwdiCxZjDDRWNQNTJiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME24OkBvVQ>? M2r3[lEzOTlyM{Gz
A549 human lung carcinoma cell M2rkRXBzd2yrZnXyZZRqd25iYYPzZZk> Mkm0TY5pcWKrdHnvckBw\iCDNUS5JIh2dWGwIHz1coch[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF06PiCwTR?= MXWxNlE6ODNzMx?=
MIP human colon carcinoma cell M4PmTWZ2dmO2aX;uJIF{e2G7 M3zoVWlvcGmkaYTpc44hd2ZiTVnQJIh2dWGwIHPvcI9vKGOjcnPpco9u[SClZXzsJIxqdmVuIFnDOVA:OC5zMjFOwG0> Ml7TNVIyQTB|MUO=
K562 human leukemia cell M3;qTXBzd2yrZnXyZZRqd25iYYPzZZk> MlfaTY5pcWKrdHnvckBw\iCNNU[yJIh2dWGwIHzleYtmdWmjIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD1yLkGzJO69VQ>? MY[xNlE6ODNzMx?=
MCF-7 tumor cell MmrnVJJwdGmoZYLheIlwdiCjc4PhfS=> MYPJcohq[mm2aX;uJI9nKE2FRj23JJR2dW:{IHPlcIwheHKxbHnm[ZJifGmxbh?= NVO5dppvOTB6NEOyNVE>
human NCI60 cells MXzQdo9tcW[ncnH0bY9vKGG|c3H5 MkSyO|IhcA>? NFr4bm1CdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7DTVYxKGOnbHzzJIF{e2W|c3XkJIF{KGyndHjhcEBm\m[nY4SgZYZ1\XJiN{KgbJJ{KGK7IIP1cIZwemixZHHtbY5mKEJiYYPzZZktKEyFNUC9NE46ODRizszN M4H6b|IyODhyN{Cz
PC3 cell NEexSpRHfW6ldHnvckBie3OjeR?= MWjJcohq[mm2aX;uJI9nKFCFMzDj[YxtKGOub37v[4VvcWNiYYPzZZktKEmFNUC9NVAh|ryP NISxTFQyOTB4M{[wPS=>
HCT116 cell MYrGeY5kfGmxbjDhd5NigQ>? NHjSeZNKdmirYnn0bY9vKG:oIFjDWFEyPiClZXzsJINtd26xZ3XubYMh[XO|YYmsJGlEPTB;MUOg{txO NVHXXW9lOTFyNkO2NFk>
A2780 cell NVnhXGxKTnWwY4Tpc44h[XO|YYm= NXe0SJJ6UW6qaXLpeIlwdiCxZjDBNlc5OCClZXzsJINtd26xZ3XubYMh[XO|YYpvwKwhUUN3ME2xOUDPxE1? NVz2Xo5sOTFyNkO2NFk>
Mia PaCa-2 cell NFH2[o5HfW6ldHnvckBie3OjeR?= NGfGWoNKdmirYnn0bY9vKG:oIF3pZUBR[UOjLUKgZ4VtdCClbH;uc4dmdmmlIHHzd4F6NCCLQ{WwQVM3KM7:TR?= NI\HUIQyOTB4M{[wPS=>
human A2780 cells NUDydlFCTnWwY4Tpc44h[XO|YYm= MnTDTY5pcWKrdHnvckBw\iClZHutcYVlcWG2ZXSgUnBOKHCqb4PwbI9zgWyjdHnvckBifCC2aIKxPVkhcW5iaIXtZY4hSTJ5OECgZ4VtdHN? M3r3SVE5PDZ7OEC5
human A2780 cells MUTGeY5kfGmxbjDhd5NigQ>? NXPzUHFlOjRiaB?= NUPIb2R5UW6qaXLpeIlwdiCxZjDj[IsudWWmaXH0[YQhWmJicHjvd5Bpd3K7bHH0bY9vKGG2IITodlgzOSCrbjDoeY1idiCDMke4NEBk\WyuczDh[pRmeiB{NDDodpM> NUH3eGVzOTh2Nkm4NFk>

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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 individually and in order:
5% DMSO+30% PEG 300+ddH2O

* 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
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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    Molecular Weight

*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 )

  • C1

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

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    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:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
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
NCT00094978 Terminated Carcinoma, Small Cell|Carcinoma, Non-Small-Cell Lung|Esophageal Neoplasms|Mesothelioma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) October 25, 2004 Phase 1
NCT02520011 Recruiting Acute Myeloid Leukemia Tolero Pharmaceuticals, Inc. December 2015 Phase 2
NCT01349972 Completed Acute Myeloid Leukemia With Multilineage Dysplasia Following Myelodysplastic Syndrome|Adult Acute Minimally Differentiated Myeloid Leukemia (M0)|Adult Acute Monoblastic Leukemia (M5a)|Adult Acute Monocytic Leukemia (M5b)|Adult Acute Myeloblastic Leukemia With Maturation (M2)|Adult Acute Myeloblastic Leukemia Without Maturation (M1)|Adult Acute Myeloid Leukemia With 11q23 (MLL) Abnormalities|Adult Acute Myeloid Leukemia With Del(5q)|Adult Acute Myeloid Leukemia With Inv(16)(p13;q22)|Adult Acute Myeloid Leukemia With t(16;16)(p13;q22)|Adult Acute Myeloid Leukemia With t(8;21)(q22;q22)|Adult Acute Myelomonocytic Leukemia (M4)|Adult Erythroleukemia (M6a)|Adult Pure Erythroid Leukemia (M6b)|Secondary Acute Myeloid Leukemia|Untreated Adult Acute Myeloid Leukemia National Cancer Institute (NCI) April 2011 Phase 2
NCT01076556 Terminated Chronic Lymphocytic Leukemia|Prolymphocytic Leukemia|Recurrent Small Lymphocytic Lymphoma|Refractory Chronic Lymphocytic Leukemia|Stage I Chronic Lymphocytic Leukemia|Stage I Small Lymphocytic Lymphoma|Stage II Chronic Lymphocytic Leukemia|Stage II Small Lymphocytic Lymphoma|Stage III Chronic Lymphocytic Leukemia|Stage III Small Lymphocytic Lymphoma|Stage IV Chronic Lymphocytic Leukemia|Stage IV Small Lymphocytic Lymphoma National Cancer Institute (NCI) April 2010 Phase 1
NCT00991952 Completed Adenocarcinoma of the Gastroesophageal Junction|Diffuse Adenocarcinoma of the Stomach|Intestinal Adenocarcinoma of the Stomach|Mixed Adenocarcinoma of the Stomach|Recurrent Gastric Cancer|Stage IIIA Gastric Cancer|Stage IIIB Gastric Cancer|Stage IIIC Gastric Cancer|Stage IV Gastric Cancer National Cancer Institute (NCI) September 2009 Phase 2
NCT00957905 Completed Recurrent Extragonadal Seminoma|Recurrent Malignant Extragonadal Germ Cell Tumor|Recurrent Malignant Extragonadal Non-Seminomatous Germ Cell Tumor|Recurrent Malignant Testicular Germ Cell Tumor|Recurrent Ovarian Germ Cell Tumor|Stage III Testicular Cancer|Stage IV Extragonadal Non-Seminomatous Germ Cell Tumor|Stage IV Extragonadal Seminoma|Stage IV Ovarian Germ Cell Tumor National Cancer Institute (NCI) June 2009 Phase 2

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.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID