Flavopiridol HCl

Catalog No.S2679 Synonyms: NSC 649890 HCl

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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(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.

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.
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.

Purity & Quality Control

Choose Selective CDK Inhibitors

Biological Activity

Description

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	Incubation Time	Activity Description	PMID
ID8 cells	NYey[4NjWHKxbHnm[ZJifGmxbjDhd5NigQ>?		NVHGc2VFSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBKTDhiY3XscJMtKEmFNUC9O{BvVQ>?	MoflNVcyOjN6MkG=
Sf9 cells	MYLGeY5kfGmxbjDhd5NigQ>?		NHjFSWpKdmirYnn0bY9vKG:oIILlZ49u[mmwYX70JIN6[2yrbjDBM2NFUzJiZYjwdoV{e2WmIHnuJHNnQSClZXzsd{whUUN3ME2xNkBvVQ>?	MkKzNVc6ODR\|Nk[=
LNCaP human prostate carcinoma cell	MkPsVJJwdGmoZYLheIlwdiCjc4PhfS=>		NYroOmpVUW6qaXLpeIlwdiCxZjDMUmNiWCCqdX3hckBxem:\|dHH0[UBk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9v	MV2xNlE6ODNzMx?=
HCT116/VP35 human colon carcinoma cell	Mlu4VJJwdGmoZYLheIlwdiCjc4PhfS=>		M{XudmlvcGmkaYTpc44hd2ZiSFPUNVE3N1[SM{WgbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF0yPyCwTR?=	M33HTVEzOTlyM{Gz
HCT116 human colon carcinoma cell	MYXQdo9tcW[ncnH0bY9vKGG\|c3H5		NGDO[mFKdmirYnn0bY9vKG:oIFjDWFEyPiCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUG4JI5O	NFLtVWQyOjF7MEOxNy=>
HCT116/VM46 human colon carcinoma cell	M4fabHBzd2yrZnXyZZRqd25iYYPzZZk>		NH7VVnFKdmirYnn0bY9vKG:oIFjDWFEyPi:YTUS2JIh2dWGwIHPvcI9vKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:OjFibl2=	Mkj6NVIyQTB\|MUO=
human A2780 cells	MnTNR5l1d3SxeHnjxsBie3OjeR?=	Mn3UNlQhcA>?	MWPDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBNlc5OCClZXzsd{Bi\nSncjCyOEBpenNiYomgUXRVKGG\|c3H5MEBIUTVyPUKzJI5O	MX[yN\|MxOTd4Nx?=
MCF7 cells	Mmf1VJJwdGmoZYLheIlwdiCjc4PhfS=>		MV\BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IF3DSlch[2WubIOsJGlEPTB;Mk[gcm0>	NV7XT5poOTdzMkO4NlE>
human MRC5 cells	MmDiR5l1d3SxeHnjxsBie3OjeR?=	NUjtfohSPzJiaB?=	MoGzR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUXJEPSClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG\|c3H5MEBIUTVyPUK4JI5O	MWKyN\|MxOTd4Nx?=
human A2780 cells	NWHIfVNxS3m2b4TvfIlkyqCjc4PhfS=>	NHXiOVI4OiCq	NYX5S41sS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0zQSCwTR?=	M12yVlI{OzBzN{[3
human A2780 cells	MV;DfZRwfG:6aXRCpIF{e2G7	NGrmSVk1QCCq	NYnV[XVoS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0{OSCwTR?=	MV2yN\|MxOTd4Nx?=
A2780/DDP-R human ovarian carcinoma cell	MYjQdo9tcW[ncnH0bY9vKGG\|c3H5		M2fYWGlvcGmkaYTpc44hd2ZiQUK3PFAwTESSLWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR\|UxRTN6IH7N	MWmxNlE6ODNzMx?=
human MRC5 cells	MWTDfZRwfG:6aXRCpIF{e2G7	MVS0PEBp	MoCxR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUXJEPSClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG\|c3H5MEBIUTVyPUO5JI5O	NF;ZO3kzOzNyMUe2Oy=>
ABAE human fibroblast cell	M17KNXBzd2yrZnXyZZRqd25iYYPzZZk>		MVHJcohq[mm2aX;uJI9nKEGEQVWgbJVu[W5iZnnido9jdGG\|dDDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;NEWgcm0>	NYr4b2tFOTJzOUCzNVM>
HL60 human leukemia cell	M2Do[HBzd2yrZnXyZZRqd25iYYPzZZk>		NHH5XIVKdmirYnn0bY9vKG:oIFjMOlAhcHWvYX6gcIV2c2WvaXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUS2JI5O	Mk[2NVIyQTB\|MUO=
human MRC5 cells	NFPZfFNEgXSxdH;4bYPDqGG\|c3H5	MoHFNlQhcA>?	M3TWRmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1TSzViY3XscJMh[W[2ZYKgNlQhcHK\|IHL5JG1VXCCjc4PhfUwhT0l3ME20PUBvVQ>?	M4XTbVI{OzBzN{[3
Hs 27 human fibroblast cell	MXXQdo9tcW[ncnH0bY9vKGG\|c3H5		NVjneGFrUW6qaXLpeIlwdiCxZjDId{AzPyCqdX3hckBncWK{b3LsZZN1KGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF02OSCwTR?=	NY[5[WRDOTJzOUCzNVM>
CCRF-CEM human leukemia cell	M4LBSXBzd2yrZnXyZZRqd25iYYPzZZk>		MUjJcohq[mm2aX;uJI9nKEOFUl[tR2VOKGi3bXHuJIxmfWunbXnhJINmdGxicILvcIln\XKjdHnvckwhUUN3ME21NkBvVQ>?	MYqxNlE6ODNzMx?=
OVCAR-3 human ovarian carcinoma cell	M13vbXBzd2yrZnXyZZRqd25iYYPzZZk>		M1f3V2lvcGmkaYTpc44hd2ZiT2\DRXIuOyCqdX3hckBwfmG{aXHuJINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9OVQhdk1?	M2jZUlEzOTlyM{Gz
A2780/DDP-S human ovarian carcinoma cell	M4XNcnBzd2yrZnXyZZRqd25iYYPzZZk>		MonCTY5pcWKrdHnvckBw\iCDMke4NE9FTFBvUzDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PTZibl2=	NELvS\|AyOjF7MEOxNy=>
human HMEC1 cells	MVrDfZRwfG:6aXRCpIF{e2G7	NG\tR3kzPCCq	M1X5PGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhOTUNzIHPlcIx{KGGodHXyJFI1KGi{czDifUBOXFRiYYPzZZktKEeLNUC9OlEhdk1?	MmSxNlM{ODF5Nke=
human HMEC1 cells	MUjDfZRwfG:6aXRCpIF{e2G7	MYG0PEBp	MUHDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG\|c3H5MEBIUTVyPU[yJI5O	M{Xu[VI{OzBzN{[3
A2780/TAX-S human ovarian carcinoma cell	M1vqdXBzd2yrZnXyZZRqd25iYYPzZZk>		NIjGSIpKdmirYnn0bY9vKG:oIFGyO\|gxN1SDWD3TJIh2dWGwIH;2ZZJq[W5iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD14NTDuUS=>	M1izPFEzOTlyM{Gz
LS174T human colon carcinoma cell	MV3Qdo9tcW[ncnH0bY9vKGG\|c3H5		MlXHTY5pcWKrdHnvckBw\iCOU{G3OHQhcHWvYX6gZ49td25iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD14NTDuUS=>	M1OwPFEzOTlyM{Gz
MCF-7 human breast carcinoma cell	NVW0S3FCWHKxbHnm[ZJifGmxbjDhd5NigQ>?		M4TjPGlvcGmkaYTpc44hd2ZiTVPGMVchcHWvYX6gZpJm[XO2IHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;Nk[gcm0>	M33iVlEzOTlyM{Gz
human HMEC1 cells	M2rXRWN6fG:2b4jpZ:Kh[XO\|YYm=	NVXI[GxMPzJiaB?=	MmTZR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTG1GSzFiY3XscJMh[W[2ZYKgO\|IhcHK\|IHL5JG1VXCCjc4PhfUwhT0l3ME22OkBvVQ>?	NX;qZ4VuOjN\|MEG3Olc>
PC3 human prostate carcinoma cell	MV7Qdo9tcW[ncnH0bY9vKGG\|c3H5		NH\MS2tKdmirYnn0bY9vKG:oIGDDN{BpfW2jbjDwdo9{fGG2ZTDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPU[2JI5O	MkXFNVIyQTB\|MUO=
human A2780 cell line	M1fyRnBzd2yrZnXyZZRqd25iYYPzZZk>	M{nNclczKGh?	NIrpfYdCdnSrcILvcIln\XKjdHn2[UBm\m[nY4SgZYdicW6\|dDDoeY1idiCDMke4NEBk\WyuIHzpcoUhf2G\|IHTleIVzdWmwZXSgbY4h[SC5aH;s[UBk\WyuIEeyJIhzKGO7dH;0c5hq[2m2eTDhd5NigSxiSVO1NF04OSCwTR?=	MYGxOVAzPzh4Mx?=
human ovarian (A2780) cancer cell	M1;yR2N6fG:2b4jpZ:Kh[XO\|YYm=		NGXLOpJEgXSxdH;4bYMh\W[oZXP0JI9vKGi3bXHuJI93[XKrYX6gLGEzPzhyKTDjZY5k\XJiY3XscEBtcW6nLDDJR\|UxRTdzIH7N	M3r1PVE2OTJ3OUex
MLF mouse lung fibroblast cell	MnPBVJJwdGmoZYLheIlwdiCjc4PhfS=>		MULJcohq[mm2aX;uJI9nKE2ORjDtc5V{\SCudX7nJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVczKG6P	Ml;jNVIyQTB\|MUO=
human NCI60 cells	NHPJfZBRem:uaX\ldoF1cW:wIHHzd4F6	NHr0Sos4OiCq	NX[wbIpiSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2k3OCClZXzsd{Bi\nSncjC3NkBpenNiYomgd5Vt\m:{aH;kZY1qdmViQjDhd5NigSxiR1m1NF04PC55IH7N	NH6xeGkzOTB6MEewNy=>
LX-1 human lung carcinoma	MkXtVJJwdGmoZYLheIlwdiCjc4PhfS=>		Mn3wTY5pcWKrdHnvckBw\iCOWD2xJIh2dWGwIHz1coch[2G{Y3nuc41iKHC{b3zp[oVz[XSrb36sJGlEPTB;N{Wgcm0>	NHrCXFIyOjF7MEOxNy=>
A431 human squamous cell	MVTQdo9tcW[ncnH0bY9vKGG\|c3H5		NUHlUoFNUW6qaXLpeIlwdiCxZjDBOFMyKGi3bXHuJJNyfWGvb4XzJINmdGxiY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD15NTDuUS=>	MkLYNVIyQTB\|MUO=
SKBR-3 human breast carcinoma cell	NXrxfWxLWHKxbHnm[ZJifGmxbjDhd5NigQ>?		NETKTIlKdmirYnn0bY9vKG:oIGPLRnIuOyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME23O{BvVQ>?	Mn:yNVIyQTB\|MUO=
A2780/TAX-R human ovarian carcinoma cell	NEPOR29Rem:uaX\ldoF1cW:wIHHzd4F6		M{KxbGlvcGmkaYTpc44hd2ZiQUK3PFAwXEG[LWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR\|UxRTd6IH7N	Ml6xNVIyQTB\|MUO=
M109 mouse lung carcinoma cell	MXvQdo9tcW[ncnH0bY9vKGG\|c3H5		M2r3RmlvcGmkaYTpc44hd2ZiTUGwPUBud3W\|ZTDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QDBibl2=	M3fV[\|EzOTlyM{Gz
CACO-2 human colon carcinoma cell	NGfE[JRRem:uaX\ldoF1cW:wIHHzd4F6		NVTQXpR4UW6qaXLpeIlwdiCxZjDDRWNQNTJiaIXtZY4h[2:ub36gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME24OkBvVQ>?	NV;UNVB1OTJzOUCzNVM>
A549 human lung carcinoma cell	MYrQdo9tcW[ncnH0bY9vKGG\|c3H5		MVvJcohq[mm2aX;uJI9nKEF3NEmgbJVu[W5ibIXu[{Bk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVk3KG6P	M2rHUVEzOTlyM{Gz
MIP human colon carcinoma cell	MkfXSpVv[3Srb36gZZN{[Xl?		MojRTY5pcWKrdHnvckBw\iCPSWCgbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygcIlv\SxiSVO1NF0xNjF{IN88US=>	MofNNVIyQTB\|MUO=
K562 human leukemia cell	NHvYNoZRem:uaX\ldoF1cW:wIHHzd4F6		NWPtemlVUW6qaXLpeIlwdiCxZjDLOVYzKGi3bXHuJIxmfWunbXnhJINmdGxicILvcIln\XKjdHnvckwhUUN3ME2wMlE{KM7:TR?=	MlSxNVIyQTB\|MUO=
MCF-7 tumor cell	M2\GbnBzd2yrZnXyZZRqd25iYYPzZZk>		MUTJcohq[mm2aX;uJI9nKE2FRj23JJR2dW:{IHPlcIwheHKxbHnm[ZJifGmxbh?=	NHrlcpkyODh2M{KxNS=>
human NCI60 cells	MV3Qdo9tcW[ncnH0bY9vKGG\|c3H5	NYX6S4g1PzJiaB?=	NYPJO4hCSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2k3OCClZXzsd{Bie3Onc4Pl[EBieyCuZYToZYwh\W[oZXP0JIFnfGW{IEeyJIhzeyCkeTDzeYxnd3Kqb3ThcYlv\SCEIHHzd4F6NCCOQ{WwQVAvQTB2IN88US=>	NUL3WZRNOjFyOEC3NFM>
PC3 cell	M{TR[2Z2dmO2aX;uJIF{e2G7		M4XTWmlvcGmkaYTpc44hd2ZiUFOzJINmdGxiY3zvco9o\W6rYzDhd5NigSxiSVO1NF0yOCEQvF2=	M1POUVEyODZ\|NkC5
HCT116 cell	NYS0VWpjTnWwY4Tpc44h[XO\|YYm=		NYS5cpZTUW6qaXLpeIlwdiCxZjDIR3QyOTZiY3XscEBkdG:wb3flcolkKGG\|c3H5MEBKSzVyPUGzJO69VQ>?	M1;OTlEyODZ\|NkC5
A2780 cell	MmLpSpVv[3Srb36gZZN{[Xl?		NInDcIVKdmirYnn0bY9vKG:oIFGyO\|gxKGOnbHygZ4xwdm:pZX7pZ{Bie3Ojef-8kEBKSzVyPUG1JO69VQ>?	NWfQWYU5OTFyNkO2NFk>
Mia PaCa-2 cell	Mnj4SpVv[3Srb36gZZN{[Xl?		NWm0UGFWUW6qaXLpeIlwdiCxZjDNbYEhWGGFYT2yJINmdGxiY3zvco9o\W6rYzDhd5NigSxiSVO1NF0{PiEQvF2=	MX2xNVA3OzZyOR?=
human A2780 cells	NHO2fY1HfW6ldHnvckBie3OjeR?=		MUnJcohq[mm2aX;uJI9nKGOmaz3t[YRq[XSnZDDOVG0heGixc4Doc5J6dGG2aX;uJIF1KHSqckG5PUBqdiCqdX3hckBCOjd6MDDj[Yxtew>?	MX2xPFQ3QThyOR?=
human A2780 cells	M4DLSmZ2dmO2aX;uJIF{e2G7	MmfzNlQhcA>?	M3TWeWlvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJHJjKHCqb4PwbI9zgWyjdHnvckBifCC2aIK4NlEhcW5iaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhOjRiaILz	NHrLfWsyQDR4OUiwPS=>

... Click to View More Cell Line Experimental Data

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]	+ Expand 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]	+ Expand 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]	+ Expand 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)

References

+ Expand

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: 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 Download Flavopiridol HCl SDF

Molecular Weight	438.3
Formula	C₂₁H₂₀ClNO₅.HCl
CAS No.	131740-09-5
Storage	3 years -20°C powder
Synonyms	NSC 649890 HCl

Bio Calculators

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)

*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

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 )

* 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
Concertration (start):
Dilution-folds:

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

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

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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

Clinical Trial Information (data from http://clinicaltrials.gov, updated on 2017-12-12)

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
NCT00445341	Completed	Lymphoma	National Cancer Institute (NCI)\|National Institutes of Health Clinical Center (CC)	January 2007	Phase 1\|Phase 2
NCT00083122	Completed	Recurrent Ovarian Epithelial Cancer\|Recurrent Primary Peritoneal Cavity Cancer\|Stage IIIA Ovarian Epithelial Cancer\|Stage IIIA Primary Peritoneal Cavity Cancer\|Stage IIIB Ovarian Epithelial Cancer\|Stage IIIB Primary Peritoneal Cavity Cancer\|Stage IIIC Ovarian Epithelial Cancer\|Stage IIIC Primary Peritoneal Cavity Cancer\|Stage IV Ovarian Epithelial Cancer\|Stage IV Primary Peritoneal Cavity Cancer	National Cancer Institute (NCI)	April 2004	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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CDK Signaling Pathway Map

CDK Inhibitors with Unique Features

Selective CDK Inhibitors

BS-181 HCl CDK7-selective, IC50=21 nM.

SNS-032 (BMS-387032) CDK2-selective, IC50=48 nM.
Most Potent CDK Inhibitor

LY2835219 CDK4, IC50=2 nM; CDK6, IC50=10 nM.
CDK Inhibitor in Clinical Trial

Palbociclib (PD0332991) Isethionate Phase III for Metastatic Breast Cancer.
Newest CDK Inhibitor

NU6027 Potent ATR/CDK inhibitor, inhibits CDK1/2, ATR and DNA-PK with K_i of 2.5 μM/1.3 μM, 0.4 μM and 2.2 μM, enter cells more readily than the 6-aminopurine-based inhibitors.

Related CDK Products

SU9516 ^New

SU 9516 is a 3-substituted indolinone CDK inhibitor with IC50 of 22 nM, 40 nM, and 200 nM for CDK2, CDK1, and CDK4, respectively.
Ro-3306 ^New

RO-3306 is an ATP-competitive, and selective CDK1 inhibitor with K_i of 20 nM, >15-fold selectivity against a diverse panel of human kinases.
Purvalanol A ^New

Purvalanol A is a potent, and cell-permeable CDK inhibitor with IC50 of 4 nM, 70 nM, 35 nM, and 850 nM for cdc2-cyclin B, cdk2-cyclin A, cdk2-cyclin E, and cdk4-cyclin D1, respectively.
Palbociclib (PD-0332991) HCl

Palbociclib (PD-0332991) HCl is a highly selective inhibitor of CDK4/6 with IC50 of 11 nM/16 nM in cell-free assays, respectively. It shows no activity against CDK1/2/5, EGFR, FGFR, PDGFR, InsR, etc. Phase 3.

Features:Non-cytotoxic, and halts cancer cell growth & could be used in glioblastoma that has relapsed after temozolomide treatment (a chemotherapeutic used to treat many cancers).
Palbociclib (PD0332991) Isethionate

Palbociclib (PD0332991) Isethionate is a highly selective inhibitor of CDK4/6 with IC50 of 11 nM/16 nM in cell-free assays. It shows no activity against CDK1/2/5, EGFR, FGFR, PDGFR, InsR, etc. Phase 3.

Features:The 1st specific inhibitor for CDK4/6 to show promise in multiple cancers.
Dinaciclib (SCH727965)

Dinaciclib (SCH727965) is a novel and potent CDK inhibitor for CDK2, CDK5, CDK1 and CDK9 with IC50 of 1 nM, 1 nM, 3 nM and 4 nM in cell-free assays, respectively. It also blocks thymidine (dThd) DNA incorporation. Phase 3.
Roscovitine (Seliciclib,CYC202)

Roscovitine (Seliciclib, CYC202) is a potent and selective CDK inhibitor for Cdc2, CDK2 and CDK5 with IC50 of 0.65 μM, 0.7 μM and 0.16 μM in cell-free assays. It shows little effect on CDK4/6. Phase 2.
abemaciclib (LY2835219)

abemaciclib (LY2835219) is a potent and selective inhibitor of CDK4 and CDK6 with IC50 of 2 nM and 10 nM in cell-free assays, respectively. Phase 3.
Ribociclib (LEE011)

Ribociclib (LEE011) is an orally available, and highly specific CDK4/6 inhibitor. Phase 3.
SNS-032 (BMS-387032)

SNS-032 (BMS-387032) has firstly been described as a selective inhibitor of CDK2 with IC50 of 48 nM in cell-free assays and is 10- and 20-fold selective over CDK1/CDK4. It is also found to be sensitive to CDK7/9 with IC50 of 62 nM/4 nM, with little effect on CDK6. Phase 1.

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Flavopiridol HCl