Flavopiridol HCl

For research use only. Not for use in humans.

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. Phase 1/2.

Size Price Stock Quantity  
10mM (1mL in DMSO) USD 100 In stock
USD 110 In stock
USD 220 In stock
USD 380 In stock
Bulk Discount

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

Selleck's Flavopiridol HCl has been cited by 18 publications

3 Customer Reviews

  • 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. 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 MXHQdo9tcW[ncnH0bY9vKGG|c3H5 M2TnbmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgTWQ5KGOnbHzzMEBKSzVyPUegcm0> NY\nNYVrOTdzMkO4NlE>
Sf9 cells MonvSpVv[3Srb36gZZN{[Xl? NEOy[HlKdmirYnn0bY9vKG:oIILlZ49u[mmwYX70JIN6[2yrbjDBM2NFUzJiZYjwdoV{e2WmIHnuJHNnQSClZXzsd{whUUN3ME2xNkBvVQ>? NYPHSldDOTd7MESzOlY>
LNCaP human prostate carcinoma cell NI\oWmhRem:uaX\ldoF1cW:wIHHzd4F6 MkHrTY5pcWKrdHnvckBw\iCOTlPhVEBpfW2jbjDwdo9{fGG2ZTDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;u M1j6S|EzOTlyM{Gz
HCT116/VP35 human colon carcinoma cell NIfiZnNRem:uaX\ldoF1cW:wIHHzd4F6 M2DYcGlvcGmkaYTpc44hd2ZiSFPUNVE3N1[SM{WgbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF0yPyCwTR?= MoXiNVIyQTB|MUO=
HCT116 human colon carcinoma cell MmC5VJJwdGmoZYLheIlwdiCjc4PhfS=> NXrTbmpWUW6qaXLpeIlwdiCxZjDIR3QyOTZiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME2xPEBvVQ>? MUixNlE6ODNzMx?=
HCT116/VM46 human colon carcinoma cell MVLQdo9tcW[ncnH0bY9vKGG|c3H5 MV\Jcohq[mm2aX;uJI9nKEiFVEGxOk9XVTR4IHj1cYFvKGOxbH;uJINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9NlEhdk1? MYSxNlE6ODNzMx?=
human A2780 cells MV7DfZRwfG:6aXRCpIF{e2G7 MoPCNlQhcA>? NXzNSHU5S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhOjRiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0zOyCwTR?= MUOyN|MxOTd4Nx?=
MCF7 cells M1\5SXBzd2yrZnXyZZRqd25iYYPzZZk> MoH4RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDNR2Y4KGOnbHzzMEBKSzVyPUK2JI5O NHzTcVIyPzF{M{iyNS=>
human MRC5 cells M1XtNmN6fG:2b4jpZ:Kh[XO|YYm= M3\GdVczKGh? Mn\VR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUXJEPSClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUK4JI5O MYeyN|MxOTd4Nx?=
human A2780 cells NIDHWWZEgXSxdH;4bYPDqGG|c3H5 NXfibXZLPzJiaB?= NWXTflRQS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0zQSCwTR?= M1zlPVI{OzBzN{[3
human A2780 cells M4LxT2N6fG:2b4jpZ:Kh[XO|YYm= Mn\aOFghcA>? NWHPeXRnS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0{OSCwTR?= MnnjNlM{ODF5Nke=
A2780/DDP-R human ovarian carcinoma cell MUfQdo9tcW[ncnH0bY9vKGG|c3H5 NX3GXlVUUW6qaXLpeIlwdiCxZjDBNlc5OC:GRGCtVkBpfW2jbjDveoFzcWGwIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;M{igcm0> MXexNlE6ODNzMx?=
human MRC5 cells NWDQdnF[S3m2b4TvfIlkyqCjc4PhfS=> NUT1TolpPDhiaB?= NHKxUYtEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOWkN3IHPlcIx{KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEeLNUC9N|khdk1? M4XabFI{OzBzN{[3
ABAE human fibroblast cell NVnOR5JqWHKxbHnm[ZJifGmxbjDhd5NigQ>? MWfJcohq[mm2aX;uJI9nKEGEQVWgbJVu[W5iZnnido9jdGG|dDDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;NEWgcm0> MUOxNlE6ODNzMx?=
HL60 human leukemia cell MWLQdo9tcW[ncnH0bY9vKGG|c3H5 Mn\vTY5pcWKrdHnvckBw\iCKTE[wJIh2dWGwIHzleYtmdWmjIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD12NjDuUS=> M1PVR|EzOTlyM{Gz
human MRC5 cells MY\DfZRwfG:6aXRCpIF{e2G7 NYLkWXc1OjRiaB?= NIThd3REgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOWkN3IHPlcIx{KGGodHXyJFI1KGi{czDifUBOXFRiYYPzZZktKEeLNUC9OFkhdk1? NUj6U4IzOjN|MEG3Olc>
Hs 27 human fibroblast cell NVz4eW5WWHKxbHnm[ZJifGmxbjDhd5NigQ>? MnLXTY5pcWKrdHnvckBw\iCKczCyO{BpfW2jbjDmbYJzd2KuYYP0JINmdGxicILvcIln\XKjdHnvckwhUUN3ME21NUBvVQ>? MlHjNVIyQTB|MUO=
CCRF-CEM human leukemia cell NWO2THRpWHKxbHnm[ZJifGmxbjDhd5NigQ>? MUHJcohq[mm2aX;uJI9nKEOFUl[tR2VOKGi3bXHuJIxmfWunbXnhJINmdGxicILvcIln\XKjdHnvckwhUUN3ME21NkBvVQ>? NGD4WYsyOjF7MEOxNy=>
OVCAR-3 human ovarian carcinoma cell NXT6fHhLWHKxbHnm[ZJifGmxbjDhd5NigQ>? Ml\kTY5pcWKrdHnvckBw\iCRVlPBVk0{KGi3bXHuJI93[XKrYX6gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME21OEBvVQ>? M4LXSVEzOTlyM{Gz
A2780/DDP-S human ovarian carcinoma cell MYHQdo9tcW[ncnH0bY9vKGG|c3H5 NEfYR4NKdmirYnn0bY9vKG:oIFGyO|gxN0SGUD3TJIh2dWGwIH;2ZZJq[W5iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD13NjDuUS=> Mm\UNVIyQTB|MUO=
human HMEC1 cells MVnDfZRwfG:6aXRCpIF{e2G7 NUfHdpFUOjRiaB?= Mnv3R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTG1GSzFiY3XscJMh[W[2ZYKgNlQhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME22NUBvVQ>? M{fLOFI{OzBzN{[3
human HMEC1 cells NFnESHVEgXSxdH;4bYPDqGG|c3H5 NXLaOoM6PDhiaB?= NXzYUWl{S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03OiCwTR?= MlHFNlM{ODF5Nke=
A2780/TAX-S human ovarian carcinoma cell NUnnTWxxWHKxbHnm[ZJifGmxbjDhd5NigQ>? MXTJcohq[mm2aX;uJI9nKEF{N{iwM3RCYC2VIHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF03PSCwTR?= NXfxeXRlOTJzOUCzNVM>
LS174T human colon carcinoma cell MljuVJJwdGmoZYLheIlwdiCjc4PhfS=> NXH5[ZJKUW6qaXLpeIlwdiCxZjDMV|E4PFRiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OUBvVQ>? MnfkNVIyQTB|MUO=
MCF-7 human breast carcinoma cell NIm2OWZRem:uaX\ldoF1cW:wIHHzd4F6 MUXJcohq[mm2aX;uJI9nKE2FRj23JIh2dWGwIHLy[YF{fCClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTZ4IH7N NFvGO4syOjF7MEOxNy=>
human HMEC1 cells MV\DfZRwfG:6aXRCpIF{e2G7 NIjCTW04OiCq NW\1S45bS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03PiCwTR?= NXWyd2prOjN|MEG3Olc>
PC3 human prostate carcinoma cell NHjEcVRRem:uaX\ldoF1cW:wIHHzd4F6 NX\DOVZvUW6qaXLpeIlwdiCxZjDQR|MhcHWvYX6gdJJwe3SjdHWgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OkBvVQ>? NV7yU5F3OTJzOUCzNVM>
human A2780 cell line NVfvcHNYWHKxbHnm[ZJifGmxbjDhd5NigQ>? NVe4PG53PzJiaB?= NYT5NWpOSW62aYDyc4xq\mW{YYTpeoUh\W[oZXP0JIFo[Wmwc4SgbJVu[W5iQUK3PFAh[2WubDDsbY5mKHejczDk[ZRmem2rbnXkJIlvKGFid3jvcIUh[2WubDC3NkBpeiCleYTveI95cWOrdImgZZN{[XluIFnDOVA:PzFibl2= MUSxOVAzPzh4Mx?=
human ovarian (A2780) cancer cell NUjD[GNCS3m2b4TvfIlkyqCjc4PhfS=> NEOzdm1EgXSxdH;4bYMh\W[oZXP0JI9vKGi3bXHuJI93[XKrYX6gLGEzPzhyKTDjZY5k\XJiY3XscEBtcW6nLDDJR|UxRTdzIH7N NYH4XYZ5OTVzMkW5O|E>
MLF mouse lung fibroblast cell MnLiVJJwdGmoZYLheIlwdiCjc4PhfS=> M4j3e2lvcGmkaYTpc44hd2ZiTVzGJI1wfXOnIHz1coch\mmkcn;icIF{fCClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PzJibl2= Mm\LNVIyQTB|MUO=
human NCI60 cells NX7PRYtQWHKxbHnm[ZJifGmxbjDhd5NigQ>? MmT1O|IhcA>? NF7LSoVCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7DTVYxKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDzeYxnd3Kqb3ThcYlv\SCEIHHzd4F6NCCJSUWwQVc1Njdibl2= MVuyNVA5ODdyMx?=
LX-1 human lung carcinoma MVXQdo9tcW[ncnH0bY9vKGG|c3H5 NXfBdFVsUW6qaXLpeIlwdiCxZjDMXE0yKGi3bXHuJIx2dmdiY3HyZ4lvd22jIIDyc4xq\mW{YYTpc44tKEmFNUC9O|Uhdk1? NXv4PXc5OTJzOUCzNVM>
A431 human squamous cell Mo\oVJJwdGmoZYLheIlwdiCjc4PhfS=> M1HWSWlvcGmkaYTpc44hd2ZiQUSzNUBpfW2jbjDzdZVidW:3czDj[YxtKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PzVibl2= NUP1UoxYOTJzOUCzNVM>
SKBR-3 human breast carcinoma cell MXHQdo9tcW[ncnH0bY9vKGG|c3H5 MnzKTY5pcWKrdHnvckBw\iCVS1LSMVMhcHWvYX6gZpJm[XO2IHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;N{egcm0> MkXSNVIyQTB|MUO=
A2780/TAX-R human ovarian carcinoma cell NVOycJpiWHKxbHnm[ZJifGmxbjDhd5NigQ>? MnnUTY5pcWKrdHnvckBw\iCDMke4NE9VSVhvUjDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:Pzhibl2= Ml\LNVIyQTB|MUO=
M109 mouse lung carcinoma cell NFLSVopRem:uaX\ldoF1cW:wIHHzd4F6 NWfFcHRsUW6qaXLpeIlwdiCxZjDNNVA6KG2xdYPlJIx2dmdiY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD16MDDuUS=> NIS5SJAyOjF7MEOxNy=>
CACO-2 human colon carcinoma cell NGj2[45Rem:uaX\ldoF1cW:wIHHzd4F6 NEXTXplKdmirYnn0bY9vKG:oIFPBR28uOiCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUi2JI5O NG\Ed3MyOjF7MEOxNy=>
A549 human lung carcinoma cell NG[5b2JRem:uaX\ldoF1cW:wIHHzd4F6 M4DpOGlvcGmkaYTpc44hd2ZiQUW0PUBpfW2jbjDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QTZibl2= NYTnOVlmOTJzOUCzNVM>
MIP human colon carcinoma cell NWHreIRrTnWwY4Tpc44h[XO|YYm= MVHJcohq[mm2aX;uJI9nKE2LUDDoeY1idiClb3zvckBk[XKlaX7vcYEh[2WubDDsbY5mNCCLQ{WwQVAvOTJizszN NIPiXZIyOjF7MEOxNy=>
K562 human leukemia cell NEfLcYhRem:uaX\ldoF1cW:wIHHzd4F6 MWnJcohq[mm2aX;uJI9nKEt3NkKgbJVu[W5ibHX1b4VucWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTBwMUOg{txO NYjQeodXOTJzOUCzNVM>
MCF-7 tumor cell NIfxRYxRem:uaX\ldoF1cW:wIHHzd4F6 NH3ncJVKdmirYnn0bY9vKG:oIF3DSk04KHS3bX;yJINmdGxicILvcIln\XKjdHnvci=> MmrqNVA5PDN{MUG=
human NCI60 cells MoPNVJJwdGmoZYLheIlwdiCjc4PhfS=> NHLnfI44OiCq MoX2RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCQQ1m2NEBk\WyuczDhd5Nme3OnZDDhd{Bt\XSqYXyg[YZn\WO2IHHmeIVzKDd{IHjyd{BjgSC|dXzmc5Jpd2SjbXnu[UBDKGG|c3H5MEBNSzVyPUCuPVA1KM7:TR?= M3\KPFIyODhyN{Cz
PC3 cell NXTMfGl4TnWwY4Tpc44h[XO|YYm= Mo\WTY5pcWKrdHnvckBw\iCSQ{OgZ4VtdCClbH;uc4dmdmmlIHHzd4F6NCCLQ{WwQVExKM7:TR?= M3TUXFEyODZ|NkC5
HCT116 cell MVzGeY5kfGmxbjDhd5NigQ>? MVvJcohq[mm2aX;uJI9nKEiFVEGxOkBk\WyuIHPsc45w\2WwaXOgZZN{[XluIFnDOVA:OTNizszN NV[zO3pTOTFyNkO2NFk>
A2780 cell MoX5SpVv[3Srb36gZZN{[Xl? NWe3OHdoUW6qaXLpeIlwdiCxZjDBNlc5OCClZXzsJINtd26xZ3XubYMh[XO|YYpvwKwhUUN3ME2xOUDPxE1? M4PndlEyODZ|NkC5
Mia PaCa-2 cell MX7GeY5kfGmxbjDhd5NigQ>? MYDJcohq[mm2aX;uJI9nKE2rYTDQZWNiNTJiY3XscEBkdG:wb3flcolkKGG|c3H5MEBKSzVyPUO2JO69VQ>? M1fXNlEyODZ|NkC5
human A2780 cells MX\GeY5kfGmxbjDhd5NigQ>? M1v5fmlvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJG5RVSCyaH;zdIhwenmuYYTpc44h[XRidHjyNVk6KGmwIHj1cYFvKEF{N{iwJINmdGy| M37XV|E5PDZ7OEC5
human A2780 cells M4XxOmZ2dmO2aX;uJIF{e2G7 M2TrfVI1KGh? NU\lVHFXUW6qaXLpeIlwdiCxZjDj[IsudWWmaXH0[YQhWmJicHjvd5Bpd3K7bHH0bY9vKGG2IITodlgzOSCrbjDoeY1idiCDMke4NEBk\WyuczDh[pRmeiB{NDDodpM> M3HmbFE5PDZ7OEC5

... 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]
- Collapse

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]
- Collapse
  • 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]
- Collapse
  • 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
  • Formulation: Water [4]; 1% DMSO [6]
  • 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 Cl.CN1CCC(C(O)C1)C2=C3OC(=CC(=O)C3=C(O)C=C2O)C4=C(Cl)C=CC=C4

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)

  • Mass
    Concentration
    Volume
    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
    V1
    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

  • 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 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

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

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

CDK Signaling Pathway Map

CDK Inhibitors with Unique Features

Related CDK Products

Tags: buy Flavopiridol HCl | Flavopiridol HCl supplier | purchase Flavopiridol HCl | Flavopiridol HCl cost | Flavopiridol HCl manufacturer | order Flavopiridol HCl | Flavopiridol HCl distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID