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.

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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. 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 MWPQdo9tcW[ncnH0bY9vKGG|c3H5 NH\RS2VCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGlFQCClZXzsd{whUUN3ME23JI5O M{TveVE4OTJ|OEKx
Sf9 cells MVjGeY5kfGmxbjDhd5NigQ>? Mn3YTY5pcWKrdHnvckBw\iC{ZXPvcYJqdmGwdDDjfYNtcW5iQT;DSGszKGW6cILld5Nm\CCrbjDT[lkh[2WubIOsJGlEPTB;MUKgcm0> Mn;HNVc6ODR|Nk[=
LNCaP human prostate carcinoma cell M1vsOnBzd2yrZnXyZZRqd25iYYPzZZk> MkSxTY5pcWKrdHnvckBw\iCOTlPhVEBpfW2jbjDwdo9{fGG2ZTDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;u M3n2cVEzOTlyM{Gz
HCT116/VP35 human colon carcinoma cell NF3MeFRRem:uaX\ldoF1cW:wIHHzd4F6 MoLkTY5pcWKrdHnvckBw\iCKQ2SxNVYwXlB|NTDoeY1idiClb3zvckBk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVE4KG6P NULmb2dJOTJzOUCzNVM>
HCT116 human colon carcinoma cell MnfrVJJwdGmoZYLheIlwdiCjc4PhfS=> NEHNZ|lKdmirYnn0bY9vKG:oIFjDWFEyPiCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUG4JI5O NIr1O|UyOjF7MEOxNy=>
HCT116/VM46 human colon carcinoma cell MYLQdo9tcW[ncnH0bY9vKGG|c3H5 NHnudodKdmirYnn0bY9vKG:oIFjDWFEyPi:YTUS2JIh2dWGwIHPvcI9vKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:OjFibl2= MUWxNlE6ODNzMx?=
human A2780 cells MWnDfZRwfG:6aXRCpIF{e2G7 NFrrSFQzPCCq MlnnR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVI4QDBiY3XscJMh[W[2ZYKgNlQhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2yN{BvVQ>? MXOyN|MxOTd4Nx?=
MCF7 cells MkjpVJJwdGmoZYLheIlwdiCjc4PhfS=> NXfjWZhJSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBOS0Z5IHPlcIx{NCCLQ{WwQVI3KG6P MVmxO|EzOzh{MR?=
human MRC5 cells NXPFOZV2S3m2b4TvfIlkyqCjc4PhfS=> M2L5RlczKGh? MYDDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNVmM2KGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGdKPTB;Mkigcm0> MXeyN|MxOTd4Nx?=
human A2780 cells NXTNVFVLS3m2b4TvfIlkyqCjc4PhfS=> NXHVOW8xPzJiaB?= M{LmV2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9Nlkhdk1? NUPyVmlmOjN|MEG3Olc>
human A2780 cells MXXDfZRwfG:6aXRCpIF{e2G7 MYi0PEBp NUj2VopzS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0{OSCwTR?= Ml3ONlM{ODF5Nke=
A2780/DDP-R human ovarian carcinoma cell NVfNTnNiWHKxbHnm[ZJifGmxbjDhd5NigQ>? M4LhUWlvcGmkaYTpc44hd2ZiQUK3PFAwTESSLWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTN6IH7N MX2xNlE6ODNzMx?=
human MRC5 cells M3TEPWN6fG:2b4jpZ:Kh[XO|YYm= MnqyOFghcA>? MYnDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNVmM2KGOnbHzzJIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGdKPTB;M{mgcm0> MUmyN|MxOTd4Nx?=
ABAE human fibroblast cell M2\x[3Bzd2yrZnXyZZRqd25iYYPzZZk> M1LxWWlvcGmkaYTpc44hd2ZiQVLBSUBpfW2jbjDmbYJzd2KuYYP0JINmdGxicILvcIln\XKjdHnvckwhUUN3ME20OUBvVQ>? NEP4d2syOjF7MEOxNy=>
HL60 human leukemia cell Mlj1VJJwdGmoZYLheIlwdiCjc4PhfS=> MWnJcohq[mm2aX;uJI9nKEiONkCgbJVu[W5ibHX1b4VucWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTR4IH7N Mn;tNVIyQTB|MUO=
human MRC5 cells MXrDfZRwfG:6aXRCpIF{e2G7 NVOzZoE{OjRiaB?= MWfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNVmM2KGOnbHzzJIFnfGW{IEK0JIhzeyCkeTDNWHQh[XO|YYmsJGdKPTB;NEmgcm0> NF;RVlgzOzNyMUe2Oy=>
Hs 27 human fibroblast cell Ml:zVJJwdGmoZYLheIlwdiCjc4PhfS=> NHfRdJFKdmirYnn0bY9vKG:oIFjzJFI4KGi3bXHuJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVUyKG6P MV6xNlE6ODNzMx?=
CCRF-CEM human leukemia cell NIfmcJhRem:uaX\ldoF1cW:wIHHzd4F6 M1r5SWlvcGmkaYTpc44hd2ZiQ1PSSk1ETU1iaIXtZY4hdGW3a3XtbYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVUzKG6P MnzoNVIyQTB|MUO=
OVCAR-3 human ovarian carcinoma cell M4WyTnBzd2yrZnXyZZRqd25iYYPzZZk> NYe3WGt1UW6qaXLpeIlwdiCxZjDPWmNCWi1|IHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF02PCCwTR?= NXiz[opEOTJzOUCzNVM>
A2780/DDP-S human ovarian carcinoma cell M1u0TXBzd2yrZnXyZZRqd25iYYPzZZk> MWPJcohq[mm2aX;uJI9nKEF{N{iwM2RFWC2VIHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF02PiCwTR?= M2P0TFEzOTlyM{Gz
human HMEC1 cells MknVR5l1d3SxeHnjxsBie3OjeR?= NYDSd21kOjRiaB?= M2LoNWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhOTUNzIHPlcIx{KGGodHXyJFI1KGi{czDifUBOXFRiYYPzZZktKEeLNUC9OlEhdk1? MlPiNlM{ODF5Nke=
human HMEC1 cells NVS2bJdYS3m2b4TvfIlkyqCjc4PhfS=> M{O5[lQ5KGh? NG\hWINEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJVUWFMTDj[YxteyCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVYzKG6P M3nxUVI{OzBzN{[3
A2780/TAX-S human ovarian carcinoma cell MmS1VJJwdGmoZYLheIlwdiCjc4PhfS=> MX;Jcohq[mm2aX;uJI9nKEF{N{iwM3RCYC2VIHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF03PSCwTR?= MmT1NVIyQTB|MUO=
LS174T human colon carcinoma cell NF;lXZVRem:uaX\ldoF1cW:wIHHzd4F6 NIPqOmpKdmirYnn0bY9vKG:oIFzTNVc1XCCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPU[1JI5O Mki2NVIyQTB|MUO=
MCF-7 human breast carcinoma cell MlToVJJwdGmoZYLheIlwdiCjc4PhfS=> NH61e5BKdmirYnn0bY9vKG:oIF3DSk04KGi3bXHuJIJz\WG|dDDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPU[2JI5O NXTG[HF6OTJzOUCzNVM>
human HMEC1 cells MV;DfZRwfG:6aXRCpIF{e2G7 NIDQe4U4OiCq MVjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPU[2JI5O M{nt[lI{OzBzN{[3
PC3 human prostate carcinoma cell NFG5Vm1Rem:uaX\ldoF1cW:wIHHzd4F6 MXTJcohq[mm2aX;uJI9nKFCFMzDoeY1idiCycn;zeIF1\SClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTZ4IH7N MlLINVIyQTB|MUO=
human A2780 cell line NYXVSXp6WHKxbHnm[ZJifGmxbjDhd5NigQ>? MnPUO|IhcA>? NF7mVFFCdnSrcILvcIln\XKjdHn2[UBm\m[nY4SgZYdicW6|dDDoeY1idiCDMke4NEBk\WyuIHzpcoUhf2G|IHTleIVzdWmwZXSgbY4h[SC5aH;s[UBk\WyuIEeyJIhzKGO7dH;0c5hq[2m2eTDhd5NigSxiSVO1NF04OSCwTR?= M3r5dVE2ODJ5OE[z
human ovarian (A2780) cancer cell M3\3bmN6fG:2b4jpZ:Kh[XO|YYm= NU\idFdqS3m2b4TvfIlkKGWoZnXjeEBwdiCqdX3hckBwfmG{aXHuJEhCOjd6MDmgZ4Fv[2W{IHPlcIwhdGmwZTygTWM2OD15MTDuUS=> NHHPXoYyPTF{NUm3NS=>
MLF mouse lung fibroblast cell NHjRXHdRem:uaX\ldoF1cW:wIHHzd4F6 NF7GfJZKdmirYnn0bY9vKG:oIF3MSkBud3W|ZTDseY5oKG[rYoLvZoxie3RiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTd{IH7N MWCxNlE6ODNzMx?=
human NCI60 cells M33WRnBzd2yrZnXyZZRqd25iYYPzZZk> NX:zXFBmPzJiaB?= M2LUb2FvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iTlPJOlAh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IIP1cIZwemixZHHtbY5mKEJiYYPzZZktKEeLNUC9O|QvPyCwTR?= M37LOFIyODhyN{Cz
LX-1 human lung carcinoma NVToNI1HWHKxbHnm[ZJifGmxbjDhd5NigQ>? MmTSTY5pcWKrdHnvckBw\iCOWD2xJIh2dWGwIHz1coch[2G{Y3nuc41iKHC{b3zp[oVz[XSrb36sJGlEPTB;N{Wgcm0> NV\vV251OTJzOUCzNVM>
A431 human squamous cell NYHveJpMWHKxbHnm[ZJifGmxbjDhd5NigQ>? NXTZZoFRUW6qaXLpeIlwdiCxZjDBOFMyKGi3bXHuJJNyfWGvb4XzJINmdGxiY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD15NTDuUS=> M1T5WlEzOTlyM{Gz
SKBR-3 human breast carcinoma cell M2LofHBzd2yrZnXyZZRqd25iYYPzZZk> NEfGWY9KdmirYnn0bY9vKG:oIGPLRnIuOyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME23O{BvVQ>? Mn\lNVIyQTB|MUO=
A2780/TAX-R human ovarian carcinoma cell MVnQdo9tcW[ncnH0bY9vKGG|c3H5 M3iyfWlvcGmkaYTpc44hd2ZiQUK3PFAwXEG[LWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTd6IH7N MmLENVIyQTB|MUO=
M109 mouse lung carcinoma cell MkS0VJJwdGmoZYLheIlwdiCjc4PhfS=> M2O2UGlvcGmkaYTpc44hd2ZiTUGwPUBud3W|ZTDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QDBibl2= MmHwNVIyQTB|MUO=
CACO-2 human colon carcinoma cell MoTYVJJwdGmoZYLheIlwdiCjc4PhfS=> NF3POVNKdmirYnn0bY9vKG:oIFPBR28uOiCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUi2JI5O M{HIS|EzOTlyM{Gz
A549 human lung carcinoma cell NHy1SoxRem:uaX\ldoF1cW:wIHHzd4F6 M4LjbGlvcGmkaYTpc44hd2ZiQUW0PUBpfW2jbjDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QTZibl2= M4DLbFEzOTlyM{Gz
MIP human colon carcinoma cell NIHseFJHfW6ldHnvckBie3OjeR?= M2H1Z2lvcGmkaYTpc44hd2ZiTVnQJIh2dWGwIHPvcI9vKGOjcnPpco9u[SClZXzsJIxqdmVuIFnDOVA:OC5zMjFOwG0> NGPNOGIyOjF7MEOxNy=>
K562 human leukemia cell MVPQdo9tcW[ncnH0bY9vKGG|c3H5 M3\4XGlvcGmkaYTpc44hd2ZiS{W2NkBpfW2jbjDs[ZVs\W2rYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;MD6xN{DPxE1? MUexNlE6ODNzMx?=
MCF-7 tumor cell MlrlVJJwdGmoZYLheIlwdiCjc4PhfS=> MlTTTY5pcWKrdHnvckBw\iCPQ1[tO{B1fW2xcjDj[YxtKHC{b3zp[oVz[XSrb36= M1nC[lExQDR|MkGx
human NCI60 cells NHzGWppRem:uaX\ldoF1cW:wIHHzd4F6 MkDiO|IhcA>? NWTEWYVkSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2k3OCClZXzsd{Bie3Onc4Pl[EBieyCuZYToZYwh\W[oZXP0JIFnfGW{IEeyJIhzeyCkeTDzeYxnd3Kqb3ThcYlv\SCEIHHzd4F6NCCOQ{WwQVAvQTB2IN88US=> M3mzS|IyODhyN{Cz
PC3 cell NH6ycFJHfW6ldHnvckBie3OjeR?= MlLYTY5pcWKrdHnvckBw\iCSQ{OgZ4VtdCClbH;uc4dmdmmlIHHzd4F6NCCLQ{WwQVExKM7:TR?= MWixNVA3OzZyOR?=
HCT116 cell MofwSpVv[3Srb36gZZN{[Xl? NUXjPGdNUW6qaXLpeIlwdiCxZjDIR3QyOTZiY3XscEBkdG:wb3flcolkKGG|c3H5MEBKSzVyPUGzJO69VQ>? M3P0XlEyODZ|NkC5
A2780 cell NGXxfZRHfW6ldHnvckBie3OjeR?= M3zvOmlvcGmkaYTpc44hd2ZiQUK3PFAh[2WubDDjcI9vd2enbnnjJIF{e2G778{MJGlEPTB;MUWg{txO NGDoU|MyOTB4M{[wPS=>
Mia PaCa-2 cell NIGxSYRHfW6ldHnvckBie3OjeR?= M1;iPGlvcGmkaYTpc44hd2ZiTXnhJHBiS2FvMjDj[YxtKGOub37v[4VvcWNiYYPzZZktKEmFNUC9N|Yh|ryP NV7u[3N3OTFyNkO2NFk>
human A2780 cells NH\C[JFHfW6ldHnvckBie3OjeR?= NWnU[WpuUW6qaXLpeIlwdiCxZjDj[IsudWWmaXH0[YQhVlCPIIDoc5NxcG:{eXzheIlwdiCjdDD0bJIyQTliaX6gbJVu[W5iQUK3PFAh[2WubIO= NVfxfph5OTh2Nkm4NFk>
human A2780 cells NGjBUIxHfW6ldHnvckBie3OjeR?= MYOyOEBp NFrITIJKdmirYnn0bY9vKG:oIHPkb{1u\WSrYYTl[EBT[iCyaH;zdIhwenmuYYTpc44h[XRidHjyPFIyKGmwIHj1cYFvKEF{N{iwJINmdGy|IHHmeIVzKDJ2IHjydy=> MV6xPFQ3QThyOR?=

... 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
  • 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)

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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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* 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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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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Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

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

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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 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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID