Flavopiridol HCl

For research use only.

Catalog No.S2679 Synonyms: NSC 649890 HCl,alvocidib,L86-8275,HMR-1275,DSP-2033

18 publications

Flavopiridol HCl Chemical Structure

Molecular Weight(MW): 438.3

Flavopiridol HCl competes with ATP to inhibit CDKs including CDK1, CDK2, CDK4 and CDK6 with IC50 of ~ 40 nM in cell-free assays. It is 7.5-fold more selective for CDK1/2/4/6 than CDK7. Flavopiridol is initially found to inhibit EGFR and PKA. Flavopiridol HCl induces autophagy and ER stress. Flavopiridol HCl blocks HIV-1 replication. Phase 1/2.

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Selleck's Flavopiridol HCl has been cited by 18 publications

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  • Comparative efficacy of anticancer therapies (Flavopiridol, vincristine, daunorubicin, et al.) in NMC vs non-NMC cell lines. Mean IC50 (± s.e.m.) of the indicated agents in three NMC (PER-403, PER-624, and PER-704) and two non-NMC cell lines (PER-535 and SAOS2), ***P<0.001, unpaired t-test, corrected for multiple testing.

    Br J Cancer 2014 110(5), 1189-98. Flavopiridol HCl purchased from Selleck.

  • RPMI-8226 cells were treated with the indicated CDK inhibitors for 8 hours. Western blots are shown. The following drug concentrations were used: SLM6 at 250 nM, flavopiridol at 250 nM, roscovitine at 5 uM, purvalanol A at 10 uM, and alsterpaullone at 5 uM.

    Mol Cancer Ther 2012 11(11), 2321-2330. Flavopiridol HCl purchased from Selleck.

  • (C) In vivo treatment of Tg:Pomc-Pttg;Pomc-eGFP embryos with small-molecule CDK inhibitors (50μM) 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 HCl purchased from Selleck.

Purity & Quality Control

Choose Selective CDK Inhibitors

Biological Activity

Description Flavopiridol HCl competes with ATP to inhibit CDKs including CDK1, CDK2, CDK4 and CDK6 with IC50 of ~ 40 nM in cell-free assays. It is 7.5-fold more selective for CDK1/2/4/6 than CDK7. Flavopiridol is initially found to inhibit EGFR and PKA. Flavopiridol HCl induces autophagy and ER stress. Flavopiridol HCl blocks HIV-1 replication. Phase 1/2.
Targets
CDK1 [1]
(Cell-free assay)
CDK2 [1]
(Cell-free assay)
CDK4 [1]
(Cell-free assay)
CDK6 [1]
(Cell-free assay)
CDK7 [1]
(Cell-free assay)
40 nM 40 nM 40 nM 40 nM 300 nM
In vitro

Flavopiridol is initially found to inhibit the epidermal growth factor receptor and protein kinase A (IC50 = 21 and 122 μM). Flavopiridol is later shown to inhibit cell proliferation, at more physiologically relevant concentrations (IC50 = 66 nM) when Flavopiridol is tested in the National Cancer Institute Development Therapeutics Program panel of 60 human tumor cell lines. [1] Flavopiridol induces G1 arrest with inhibition of CDK2 and CDK4 in human breast carcinoma cells in a time and concentration dependent manner. [2] Short time treatment of Flavopiridol (~12 hours) induce apoptosis in hematopoietic cell lines including SUDHL4, SUDHL6 (B-cell lines), Jurkat and MOLT4 (T-cell lines ), and HL60 (myeloid). [3] In the clonogenic assay, Flavopiridol functions as a highly potent cytotoxic compound with a mean IC70 with 8 ng/mL in 23 human tumor models. [4] A recent study shows Flavopiridol treatment induces a substantial AKT-Ser473 phosphorylation in human glioblastoma T98G cell line. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
ID8 cells MWTQdo9tcW[ncnH0bY9vKGG|c3H5 NUfZXZFSSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBKTDhiY3XscJMtKEmFNUC9O{BvVQ>? M4PJUlE4OTJ|OEKx
Sf9 cells MXHGeY5kfGmxbjDhd5NigQ>? NUPOOZZ4UW6qaXLpeIlwdiCxZjDy[YNwdWKrbnHueEBkgWOuaX6gRU9ETEt{IHX4dJJme3OnZDDpckBU\jliY3XscJMtKEmFNUC9NVIhdk1? MlTSNVc6ODR|Nk[=
LNCaP human prostate carcinoma cell M4TNNHBzd2yrZnXyZZRqd25iYYPzZZk> MXjJcohq[mm2aX;uJI9nKEyQQ3HQJIh2dWGwIIDyc5N1[XSnIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36= MWSxNlE6ODNzMx?=
HCT116/VP35 human colon carcinoma cell M3vOdXBzd2yrZnXyZZRqd25iYYPzZZk> Mnq4TY5pcWKrdHnvckBw\iCKQ2SxNVYwXlB|NTDoeY1idiClb3zvckBk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVE4KG6P MUOxNlE6ODNzMx?=
HCT116 human colon carcinoma cell MojWVJJwdGmoZYLheIlwdiCjc4PhfS=> NYTkVVlTUW6qaXLpeIlwdiCxZjDIR3QyOTZiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME2xPEBvVQ>? MVSxNlE6ODNzMx?=
HCT116/VM46 human colon carcinoma cell MWfQdo9tcW[ncnH0bY9vKGG|c3H5 MXXJcohq[mm2aX;uJI9nKEiFVEGxOk9XVTR4IHj1cYFvKGOxbH;uJINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9NlEhdk1? MVSxNlE6ODNzMx?=
human A2780 cells NIPHbI1EgXSxdH;4bYPDqGG|c3H5 NEnGUm0zPCCq NGXId|ZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBCOjd6MDDj[YxteyCjZoTldkAzPCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVI{KG6P NEnxb20zOzNyMUe2Oy=>
MCF7 cells NYrtPFJHWHKxbHnm[ZJifGmxbjDhd5NigQ>? MYjBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IF3DSlch[2WubIOsJGlEPTB;Mk[gcm0> NFm4WpEyPzF{M{iyNS=>
human MRC5 cells NFjCflJEgXSxdH;4bYPDqGG|c3H5 MoTnO|IhcA>? NHftR2lEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOWkN3IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9Nlghdk1? MoG1NlM{ODF5Nke=
human A2780 cells NHnRV5REgXSxdH;4bYPDqGG|c3H5 M1S4VFczKGh? MXvDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBNlc5OCClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUK5JI5O NG[wcpAzOzNyMUe2Oy=>
human A2780 cells NVnzbWRZS3m2b4TvfIlkyqCjc4PhfS=> NVTD[HVOPDhiaB?= MV7DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBNlc5OCClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUOxJI5O MV[yN|MxOTd4Nx?=
A2780/DDP-R human ovarian carcinoma cell MnfBVJJwdGmoZYLheIlwdiCjc4PhfS=> M4fWSmlvcGmkaYTpc44hd2ZiQUK3PFAwTESSLWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTN6IH7N M3zTSlEzOTlyM{Gz
human MRC5 cells Ml:2R5l1d3SxeHnjxsBie3OjeR?= MVG0PEBp NYW0NJBxS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVM6KG6P MUCyN|MxOTd4Nx?=
ABAE human fibroblast cell NELMeXlRem:uaX\ldoF1cW:wIHHzd4F6 M{e0UWlvcGmkaYTpc44hd2ZiQVLBSUBpfW2jbjDmbYJzd2KuYYP0JINmdGxicILvcIln\XKjdHnvckwhUUN3ME20OUBvVQ>? MWSxNlE6ODNzMx?=
HL60 human leukemia cell MmruVJJwdGmoZYLheIlwdiCjc4PhfS=> NFqwPYNKdmirYnn0bY9vKG:oIFjMOlAhcHWvYX6gcIV2c2WvaXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUS2JI5O NF\QRmwyOjF7MEOxNy=>
human MRC5 cells MVjDfZRwfG:6aXRCpIF{e2G7 M4XO[FI1KGh? NVjmdVFYS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkAzPCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVQ6KG6P NYnnPGlnOjN|MEG3Olc>
Hs 27 human fibroblast cell M1nEWnBzd2yrZnXyZZRqd25iYYPzZZk> NH7k[lBKdmirYnn0bY9vKG:oIFjzJFI4KGi3bXHuJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVUyKG6P MX:xNlE6ODNzMx?=
CCRF-CEM human leukemia cell MVjQdo9tcW[ncnH0bY9vKGG|c3H5 NWrJSFN2UW6qaXLpeIlwdiCxZjDDR3JHNUOHTTDoeY1idiCuZYXr[Y1q[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PTJibl2= NUDmRYJJOTJzOUCzNVM>
OVCAR-3 human ovarian carcinoma cell NY\uUGtVWHKxbHnm[ZJifGmxbjDhd5NigQ>? NWfQTnF2UW6qaXLpeIlwdiCxZjDPWmNCWi1|IHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF02PCCwTR?= MUKxNlE6ODNzMx?=
A2780/DDP-S human ovarian carcinoma cell MXTQdo9tcW[ncnH0bY9vKGG|c3H5 M{jGeGlvcGmkaYTpc44hd2ZiQUK3PFAwTESSLWOgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTV4IH7N M{n4T|EzOTlyM{Gz
human HMEC1 cells MorUR5l1d3SxeHnjxsBie3OjeR?= M1XZfFI1KGh? NFWwT4FEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJVUWFMTDj[YxteyCjZoTldkAzPCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVYyKG6P MUmyN|MxOTd4Nx?=
human HMEC1 cells MXXDfZRwfG:6aXRCpIF{e2G7 M4C4[FQ5KGh? MVPDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPU[yJI5O NYTaOZZuOjN|MEG3Olc>
A2780/TAX-S human ovarian carcinoma cell NIfvNFdRem:uaX\ldoF1cW:wIHHzd4F6 NVTKcIVIUW6qaXLpeIlwdiCxZjDBNlc5OC:WQWitV{BpfW2jbjDveoFzcWGwIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;NkWgcm0> MmnTNVIyQTB|MUO=
LS174T human colon carcinoma cell MXnQdo9tcW[ncnH0bY9vKGG|c3H5 MomxTY5pcWKrdHnvckBw\iCOU{G3OHQhcHWvYX6gZ49td25iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD14NTDuUS=> NVjLNHd5OTJzOUCzNVM>
MCF-7 human breast carcinoma cell NVuySJRHWHKxbHnm[ZJifGmxbjDhd5NigQ>? MWPJcohq[mm2aX;uJI9nKE2FRj23JIh2dWGwIHLy[YF{fCClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTZ4IH7N MnXrNVIyQTB|MUO=
human HMEC1 cells MWnDfZRwfG:6aXRCpIF{e2G7 MVS3NkBp MoPiR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTG1GSzFiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME22OkBvVQ>? NHnaZXkzOzNyMUe2Oy=>
PC3 human prostate carcinoma cell M3XLbXBzd2yrZnXyZZRqd25iYYPzZZk> M{P1UGlvcGmkaYTpc44hd2ZiUFOzJIh2dWGwIIDyc5N1[XSnIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;Nk[gcm0> NE\LV4syOjF7MEOxNy=>
human A2780 cell line NVTrUYl{WHKxbHnm[ZJifGmxbjDhd5NigQ>? NEfSbJA4OiCq NV:1OHFoSW62aYDyc4xq\mW{YYTpeoUh\W[oZXP0JIFo[Wmwc4SgbJVu[W5iQUK3PFAh[2WubDDsbY5mKHejczDk[ZRmem2rbnXkJIlvKGFid3jvcIUh[2WubDC3NkBpeiCleYTveI95cWOrdImgZZN{[XluIFnDOVA:PzFibl2= MXKxOVAzPzh4Mx?=
human ovarian (A2780) cancer cell Ml7MR5l1d3SxeHnjxsBie3OjeR?= NGr3WoNEgXSxdH;4bYMh\W[oZXP0JI9vKGi3bXHuJI93[XKrYX6gLGEzPzhyKTDjZY5k\XJiY3XscEBtcW6nLDDJR|UxRTdzIH7N NULlcopvOTVzMkW5O|E>
MLF mouse lung fibroblast cell MmrqVJJwdGmoZYLheIlwdiCjc4PhfS=> MUjJcohq[mm2aX;uJI9nKE2ORjDtc5V{\SCudX7nJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVczKG6P M4no[VEzOTlyM{Gz
human NCI60 cells MoPzVJJwdGmoZYLheIlwdiCjc4PhfS=> NUfrS2l6PzJiaB?= MmHNRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1m2NEBk\WyuczDh[pRmeiB5MjDodpMh[nlic4Xs[o9zcG:mYX3pcoUhSiCjc4PhfUwhT0l3ME23OE44KG6P NFPocoIzOTB6MEewNy=>
LX-1 human lung carcinoma M4LaPXBzd2yrZnXyZZRqd25iYYPzZZk> M4XVT2lvcGmkaYTpc44hd2ZiTGitNUBpfW2jbjDseY5oKGOjcnPpco9u[SCycn;sbYZmemG2aX;uMEBKSzVyPUe1JI5O MlfJNVIyQTB|MUO=
A431 human squamous cell MlPyVJJwdGmoZYLheIlwdiCjc4PhfS=> M3nJ[GlvcGmkaYTpc44hd2ZiQUSzNUBpfW2jbjDzdZVidW:3czDj[YxtKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PzVibl2= MWOxNlE6ODNzMx?=
SKBR-3 human breast carcinoma cell M4i4UXBzd2yrZnXyZZRqd25iYYPzZZk> NI\qUVlKdmirYnn0bY9vKG:oIGPLRnIuOyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME23O{BvVQ>? NUDUV2RFOTJzOUCzNVM>
A2780/TAX-R human ovarian carcinoma cell NU\ieo97WHKxbHnm[ZJifGmxbjDhd5NigQ>? MmC3TY5pcWKrdHnvckBw\iCDMke4NE9VSVhvUjDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:Pzhibl2= M2frdlEzOTlyM{Gz
M109 mouse lung carcinoma cell NF\sd|NRem:uaX\ldoF1cW:wIHHzd4F6 NXvibFdQUW6qaXLpeIlwdiCxZjDNNVA6KG2xdYPlJIx2dmdiY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD16MDDuUS=> MVqxNlE6ODNzMx?=
CACO-2 human colon carcinoma cell NVezbXU3WHKxbHnm[ZJifGmxbjDhd5NigQ>? M3fPcGlvcGmkaYTpc44hd2ZiQ1HDU{0zKGi3bXHuJINwdG:wIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;OE[gcm0> M2PrclEzOTlyM{Gz
A549 human lung carcinoma cell MlraVJJwdGmoZYLheIlwdiCjc4PhfS=> M{XYeGlvcGmkaYTpc44hd2ZiQUW0PUBpfW2jbjDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QTZibl2= M1qxdVEzOTlyM{Gz
MIP human colon carcinoma cell NVfhVY9qTnWwY4Tpc44h[XO|YYm= MlL1TY5pcWKrdHnvckBw\iCPSWCgbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygcIlv\SxiSVO1NF0xNjF{IN88US=> NIPIcVcyOjF7MEOxNy=>
K562 human leukemia cell NHvjNFRRem:uaX\ldoF1cW:wIHHzd4F6 M3PtfGlvcGmkaYTpc44hd2ZiS{W2NkBpfW2jbjDs[ZVs\W2rYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;MD6xN{DPxE1? MkThNVIyQTB|MUO=
MCF-7 tumor cell MVTQdo9tcW[ncnH0bY9vKGG|c3H5 NEDmXGxKdmirYnn0bY9vKG:oIF3DSk04KHS3bX;yJINmdGxicILvcIln\XKjdHnvci=> MYSxNFg1OzJzMR?=
human NCI60 cells MX7Qdo9tcW[ncnH0bY9vKGG|c3H5 NWTmT|VpPzJiaB?= MW\BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE6FSU[wJINmdGy|IHHzd4V{e2WmIHHzJIxmfGijbDDl[oZm[3RiYX\0[ZIhPzJiaILzJIJ6KHO3bH\vdohw\GGvaX7lJGIh[XO|YYmsJGxEPTB;MD65NFQh|ryP NYfZcnNNOjFyOEC3NFM>
PC3 cell MmGySpVv[3Srb36gZZN{[Xl? NF3GbI9KdmirYnn0bY9vKG:oIGDDN{Bk\WyuIHPsc45w\2WwaXOgZZN{[XluIFnDOVA:OTBizszN NYfoelJ4OTFyNkO2NFk>
HCT116 cell Mo[2SpVv[3Srb36gZZN{[Xl? Mlu2TY5pcWKrdHnvckBw\iCKQ2SxNVYh[2WubDDjcI9vd2enbnnjJIF{e2G7LDDJR|UxRTF|IN88US=> MWOxNVA3OzZyOR?=
A2780 cell MX\GeY5kfGmxbjDhd5NigQ>? NWnuS3g3UW6qaXLpeIlwdiCxZjDBNlc5OCClZXzsJINtd26xZ3XubYMh[XO|YYpvwKwhUUN3ME2xOUDPxE1? NYntN4RoOTFyNkO2NFk>
Mia PaCa-2 cell NYPzOWh6TnWwY4Tpc44h[XO|YYm= M3nlZWlvcGmkaYTpc44hd2ZiTXnhJHBiS2FvMjDj[YxtKGOub37v[4VvcWNiYYPzZZktKEmFNUC9N|Yh|ryP MmGxNVExPjN4MEm=
human A2780 cells M3L4SGZ2dmO2aX;uJIF{e2G7 M2\rS2lvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJG5RVSCyaH;zdIhwenmuYYTpc44h[XRidHjyNVk6KGmwIHj1cYFvKEF{N{iwJINmdGy| NXLCVHhROTh2Nkm4NFk>
human A2780 cells M2e3OmZ2dmO2aX;uJIF{e2G7 MmDsNlQhcA>? M4rpS2lvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJHJjKHCqb4PwbI9zgWyjdHnvckBifCC2aIK4NlEhcW5iaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhOjRiaILz MXWxPFQ3QThyOR?=

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
Cleaved caspase-8 / Cleaved caspase-9 / Cleaved caspase-3; 

PubMed: 31193061     


(C) Caspase activation was determined by western blotting. Flavopiridol treatment (300 nM) induced the expressions of cleaved caspase-8, -9 and -3 in a time-dependent manner. 

p-RNAPII / p-eIF4E / Mnk1; 

PubMed: 24572052     


After 24 h drug exposure, CDKI-73 or flavopiridol also abolished p-eIF4E(S209) at 0.25 μM, indicating cellular inhibition of Mnk kinase activity. The same treatment with CDKI-73 or flavopiridol caused a loss in Mnk1 protein expression. CGP57380-treated cells abrogated p-RNAPIIS2 as well as p-eIF4E(S209) with a minimal effect on Mnk1 protein level.

p-ERK / ERK / p-p38 / p-4EBP1 / 4EBP1 / p-S6; 

PubMed: 24572052     


0.25 μM CDKI-73 or flavopiridol caused little changes in the phosphorylation of Erk and p38 MAPK; however, inhibited the 4E-BP1 phosphorylation [p-4E-BP1(Thr70)] by 24 h. CGP57380 had a minimal effect on these proteins.

CDK2 / CDK4 / Cyclin A / p21 / p27 / Rb; 

PubMed: 24572052     


Effect of flavopiridol on cell cycle-related protein expression in uterine leiomyoma cells. Twenty-four hours after treatment, cell extracts were prepared and subjected to immunoblotting analysis. β-Actin was used as an internal loading control.

31193061 24572052
Growth inhibition assay
Cell viability; 

PubMed: 31193061     


The antiproliferative effect of flavopiridol on CCA cell lines was determined using an MTT assay. KKU-055, KKU-100, KKU-213 and KKU-214 cells were treated with 50, 100, 200 or 300 nM of flavopiridol at 24, 48 or 72 h. The percentage of cell number in vehicle control was taken as 100%. Data are mean ± SD of three independent experiments. *P < 0.05 in all CCA cell lines, significantly different for each time point compared with vehicle control.

31193061
In vivo At the maximal tolerated dose of 10 mg/kg/day administered p.o. on days 1-4 and 7-11, Flavopiridol effects tumor regression in PRXF1337 and tumor stasis lasting for 4 weeks in PRXF1369. [4] After treatment with 7.5 mg/kg Flavopiridol bolus intravenous (IV) or intraperitoneal on each of 5 consecutive days, 11 out of 12 advanced stage subcutaneous (s.c.) human HL-60 xenografts undergo complete regressions, and animals remain disease-free several months after one course of Flavopiridol treatment. SUDHL-4 s.c. lymphomas treated with flavopiridol at 7.5 mg/kg bolus IV for 5 days undergo either major (two out of eight mice) or complete (four out of eight mice) regression, with two animals remaining disease-free for more than 60 days. The overall growth delay is 73.2%. Daily IV or IP administration of flavopiridol results in peak plasma levels of about 7 µM, followed by a progressive decline to approximately 100 nM in 8 hours.[6]

Protocol

Kinase Assay:[1]
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Recombinant CDKs Kinase Reactions:

CDKs activities are determined in microtiter plates as follows. Forty μg Gst-Rb are mixed with different amounts of Flavopiridol and unlabeled ATP. Reactions are then started by the addition of an ammonium sulfate cut of the S100 fraction obtained from insect cells expressing recombinant human CDKs. The final reaction conditions are 10 mM MgCl2, 50 mM Tris-HCl (pH 7.5), and 1 mM DTT. The final concentration of ATP is adjusted accordingly. Radiolabeled ATP is used as a phosphoryl donor. The reaction is carried out for 2.5 minutes at 30 °C after addition of enzyme and then terminated with the addition of EDTA. The Gst-Rb is then captured with glutathione-Sepharose and the incorporated radioactivity is determined by liquid scintillation counting.
Cell Research:[2]
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  • Cell lines: SUDHL4, SUDHL6, Jurkat, MOLT4, and HL60
  • Concentrations: 0, 100 500, 5000 nM
  • Incubation Time: 14 hours
  • Method: Cells grown at a density of 1 × 106 cells/mL are exposed to Flavopiridol for different concentrations and time periods. DNA is extracted. Briefly, cells are washed once with cold phosphate-buffered saline (PBS) and lysed with 3 mL lysis buffer (5 mM Tris-HCL [pH 7.5]; 20 mM EDTA; 0.5% Triton X-100) for 15 minutes at 4 °C. The chromatin of the cell lysates is isolated by centrifugation (20 minutes at 26,000g, 4 °C). The supernatants containing small DNA fragments are extracted sequentially with phenol, phenol:chloroform (1:1), and chloroform. Nucleic acids are precipitated in 0.5 M NaCl, 90% ethanol at -20 °C overnight. RNA is then digested by bovine RNAaseA (60 μg/mL). After sequential reextraction and reprecipitation, DNA is dissolved in 10 mM Tris-HCL (pH 7.5), 1 mM EDTA, 0.5% sodium dodecyl sulfate (SDS) before electrophoresis on 1.6% agarose gel.
    (Only for Reference)
Animal Research:[4] [6]
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  • Animal Models: Human prostate cancer xenografts, PRXFI337 and PRXFI369, grown s.c. in nude mice [4] Human promyelocytic leukemia HL-60, human B-cell follicular lymphoma SUDHL-4, and acquired immunodeficiency syndrome (AIDS)-r
  • Dosages: 10 mg/kg/d [4]; 7.5 mg/kg/d [6]
  • Administration: p.o.[4]; i.p. or i.v. [6]
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 88 mg/mL (200.77 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.
5mg/mL

* 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 438.3
Formula

C21H20ClNO5.HCl

CAS No. 131740-09-5
Storage powder
in solvent
Synonyms NSC 649890 HCl,alvocidib,L86-8275,HMR-1275,DSP-2033
Smiles CN1CCC(C(C1)O)C2=C(C=C(C3=C2OC(=CC3=O)C4=CC=CC=C4Cl)O)O.Cl

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
Dosage mg/kg Average weight of animals g Dosing volume per animal ul Number of animals
Step 2: Enter the in vivo formulation ()
% DMSO % % Tween 80 % ddH2O
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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 (mg) = Concentration (mM) × Volume (mL) × 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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    C2
    V2

* 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

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  • Computed Result

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    C4=C3/X C4: LOG(C4):
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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

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT00112723 Terminated Drug: alvocidib Adult Lymphocyte Depletion Hodgkin Lymphoma|Adult Lymphocyte Predominant Hodgkin Lymphoma|Adult Mixed Cellularity Hodgkin Lymphoma|Adult Nodular Sclerosis Hodgkin Lymphoma|Anaplastic Large Cell Lymphoma|Angioimmunoblastic T-cell Lymphoma|Extranodal Marginal Zone B-cell Lymphoma of Mucosa-associated Lymphoid Tissue|Nodal Marginal Zone B-cell Lymphoma|Recurrent Adult Diffuse Large Cell Lymphoma|Recurrent Adult Diffuse Mixed Cell Lymphoma|Recurrent Adult Diffuse Small Cleaved Cell Lymphoma|Recurrent Adult Grade III Lymphomatoid Granulomatosis|Recurrent Adult Hodgkin Lymphoma|Recurrent Adult T-cell Leukemia/Lymphoma|Recurrent Cutaneous T-cell Non-Hodgkin Lymphoma|Recurrent Grade 1 Follicular Lymphoma|Recurrent Grade 2 Follicular Lymphoma|Recurrent Grade 3 Follicular Lymphoma|Recurrent Mantle Cell Lymphoma|Recurrent Marginal Zone Lymphoma|Recurrent Mycosis Fungoides/Sezary Syndrome|Recurrent Small Lymphocytic Lymphoma|Refractory Multiple Myeloma|Splenic Marginal Zone Lymphoma|Stage I Multiple Myeloma|Stage II Multiple Myeloma|Stage III Multiple Myeloma|Waldenström Macroglobulinemia National Cancer Institute (NCI) December 2005 Phase 1|Phase 2
NCT00098371 Terminated Drug: alvocidib B-cell Chronic Lymphocytic Leukemia|Prolymphocytic Leukemia|Refractory Chronic Lymphocytic Leukemia National Cancer Institute (NCI) April 2005 Phase 2
NCT00101231 Terminated Drug: alvocidib Adult Acute Basophilic Leukemia|Adult Acute Eosinophilic Leukemia|Adult Acute Megakaryoblastic Leukemia (M7)|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 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)|Blastic Phase Chronic Myelogenous Leukemia|Recurrent Adult Acute Lymphoblastic Leukemia|Recurrent Adult Acute Myeloid Leukemia|Relapsing Chronic Myelogenous Leukemia National Cancer Institute (NCI) October 2004 Phase 1
NCT00058240 Completed Drug: alvocidib B-cell Chronic Lymphocytic Leukemia|Recurrent Small Lymphocytic Lymphoma|Refractory Chronic Lymphocytic Leukemia|Waldenström Macroglobulinemia National Cancer Institute (NCI) April 2003 Phase 1|Phase 2

Tech Support

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Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID