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	MVrQdo9tcW[ncnH0bY9vKGG\|c3H5		NWfW[pV1SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBKTDhiY3XscJMtKEmFNUC9O{BvVQ>?	M3vZ[FE4OTJ\|OEKx
Sf9 cells	MmXpSpVv[3Srb36gZZN{[Xl?		M1vFeGlvcGmkaYTpc44hd2ZicnXjc41jcW6jboSgZ5lkdGmwIFGvR2RMOiCneIDy[ZN{\WRiaX6gV4Y6KGOnbHzzMEBKSzVyPUGyJI5O	NHuyW\|YyPzlyNEO2Oi=>
LNCaP human prostate carcinoma cell	MkPkVJJwdGmoZYLheIlwdiCjc4PhfS=>		NFO2RYxKdmirYnn0bY9vKG:oIFzOR4FRKGi3bXHuJJBzd3O2YYTlJINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44>	NIGxVIQyOjF7MEOxNy=>
HCT116/VP35 human colon carcinoma cell	MYPQdo9tcW[ncnH0bY9vKGG\|c3H5		NYj0SY9VUW6qaXLpeIlwdiCxZjDIR3QyOTZxVmCzOUBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR\|UxRTF5IH7N	NWPhVpZzOTJzOUCzNVM>
HCT116 human colon carcinoma cell	NETYXJhRem:uaX\ldoF1cW:wIHHzd4F6		Mn7YTY5pcWKrdHnvckBw\iCKQ2SxNVYhcHWvYX6gZ49td25iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD1zODDuUS=>	NGPBU5QyOjF7MEOxNy=>
HCT116/VM46 human colon carcinoma cell	NEjaOGJRem:uaX\ldoF1cW:wIHHzd4F6		NW[yWJhvUW6qaXLpeIlwdiCxZjDIR3QyOTZxVl20OkBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR\|UxRTJzIH7N	M1zGPFEzOTlyM{Gz
human A2780 cells	NI\nSVBEgXSxdH;4bYPDqGG\|c3H5	NEjQe3IzPCCq	NWrI[WxKS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhOjRiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0zOyCwTR?=	MUGyN\|MxOTd4Nx?=
MCF7 cells	M3e2bnBzd2yrZnXyZZRqd25iYYPzZZk>		NUnqN2g2SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBOS0Z5IHPlcIx{NCCLQ{WwQVI3KG6P	MV6xO\|EzOzh{MR?=
human MRC5 cells	MlHXR5l1d3SxeHnjxsBie3OjeR?=	MY[3NkBp	NFjWXZNEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOWkN3IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9Nlghdk1?	MoHvNlM{ODF5Nke=
human A2780 cells	MnzVR5l1d3SxeHnjxsBie3OjeR?=	NH;yVJE4OiCq	NVPseHJoS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0zQSCwTR?=	NGD0Z3MzOzNyMUe2Oy=>
human A2780 cells	NETn[FlEgXSxdH;4bYPDqGG\|c3H5	NWnB[WZEPDhiaB?=	MorGR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVI4QDBiY3XscJMh[W[2ZYKgOFghcHK\|IHL5JG1VXCCjc4PhfUwhT0l3ME2zNUBvVQ>?	NGeySIMzOzNyMUe2Oy=>
A2780/DDP-R human ovarian carcinoma cell	MmDTVJJwdGmoZYLheIlwdiCjc4PhfS=>		MVnJcohq[mm2aX;uJI9nKEF{N{iwM2RFWC2UIHj1cYFvKG:4YYLpZY4h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF0{QCCwTR?=	NUfZVVE3OTJzOUCzNVM>
human MRC5 cells	M{XaXGN6fG:2b4jpZ:Kh[XO\|YYm=	NHe5[Wc1QCCq	MUXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNVmM2KGOnbHzzJIFnfGW{IES4JIhzeyCkeTDNWHQh[XO\|YYmsJGdKPTB;M{mgcm0>	NYfHPGNnOjN\|MEG3Olc>
ABAE human fibroblast cell	M4LD[3Bzd2yrZnXyZZRqd25iYYPzZZk>		MYPJcohq[mm2aX;uJI9nKEGEQVWgbJVu[W5iZnnido9jdGG\|dDDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;NEWgcm0>	Mnj1NVIyQTB\|MUO=
HL60 human leukemia cell	MWrQdo9tcW[ncnH0bY9vKGG\|c3H5		NVzN[\|R4UW6qaXLpeIlwdiCxZjDIUFYxKGi3bXHuJIxmfWunbXnhJINmdGxicILvcIln\XKjdHnvckwhUUN3ME20OkBvVQ>?	M2Hy[\|EzOTlyM{Gz
human MRC5 cells	M1[xdmN6fG:2b4jpZ:Kh[XO\|YYm=	NEHOblAzPCCq	Ml\ZR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUXJEPSClZXzsd{Bi\nSncjCyOEBpenNiYomgUXRVKGG\|c3H5MEBIUTVyPUS5JI5O	MlPONlM{ODF5Nke=
Hs 27 human fibroblast cell	MojtVJJwdGmoZYLheIlwdiCjc4PhfS=>		M3j3Z2lvcGmkaYTpc44hd2ZiSIOgNlchcHWvYX6g[oljem:kbHHzeEBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9OVEhdk1?	NFrO[ZUyOjF7MEOxNy=>
CCRF-CEM human leukemia cell	NVLUXlB6WHKxbHnm[ZJifGmxbjDhd5NigQ>?		M3rISGlvcGmkaYTpc44hd2ZiQ1PSSk1ETU1iaIXtZY4hdGW3a3XtbYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVUzKG6P	NG\l[lcyOjF7MEOxNy=>
OVCAR-3 human ovarian carcinoma cell	NGe0SGdRem:uaX\ldoF1cW:wIHHzd4F6		MmDQTY5pcWKrdHnvckBw\iCRVlPBVk0{KGi3bXHuJI93[XKrYX6gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME21OEBvVQ>?	NFzkW3EyOjF7MEOxNy=>
A2780/DDP-S human ovarian carcinoma cell	Mof0VJJwdGmoZYLheIlwdiCjc4PhfS=>		NFr0e3pKdmirYnn0bY9vKG:oIFGyO\|gxN0SGUD3TJIh2dWGwIH;2ZZJq[W5iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD13NjDuUS=>	NHW2PWgyOjF7MEOxNy=>
human HMEC1 cells	MYLDfZRwfG:6aXRCpIF{e2G7	NFiwT\|MzPCCq	NGTpcnVEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJVUWFMTDj[YxteyCjZoTldkAzPCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVYyKG6P	M3fld\|I{OzBzN{[3
human HMEC1 cells	NVy5Voh7S3m2b4TvfIlkyqCjc4PhfS=>	NHHZeI81QCCq	NXTkVGtCS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03OiCwTR?=	NF;2XmMzOzNyMUe2Oy=>
A2780/TAX-S human ovarian carcinoma cell	M{njXnBzd2yrZnXyZZRqd25iYYPzZZk>		Mn:1TY5pcWKrdHnvckBw\iCDMke4NE9VSVhvUzDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PjVibl2=	MVGxNlE6ODNzMx?=
LS174T human colon carcinoma cell	MlTGVJJwdGmoZYLheIlwdiCjc4PhfS=>		MmXiTY5pcWKrdHnvckBw\iCOU{G3OHQhcHWvYX6gZ49td25iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD14NTDuUS=>	NXvTSFhJOTJzOUCzNVM>
MCF-7 human breast carcinoma cell	NEXUR4lRem:uaX\ldoF1cW:wIHHzd4F6		NXHYSm4{UW6qaXLpeIlwdiCxZjDNR2YuPyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OkBvVQ>?	MX[xNlE6ODNzMx?=
human HMEC1 cells	NXniSYdqS3m2b4TvfIlkyqCjc4PhfS=>	Moe2O\|IhcA>?	MoiyR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTG1GSzFiY3XscJMh[W[2ZYKgO\|IhcHK\|IHL5JG1VXCCjc4PhfUwhT0l3ME22OkBvVQ>?	NECzRokzOzNyMUe2Oy=>
PC3 human prostate carcinoma cell	NFWzV3RRem:uaX\ldoF1cW:wIHHzd4F6		NUDJXZVKUW6qaXLpeIlwdiCxZjDQR\|MhcHWvYX6gdJJwe3SjdHWgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OkBvVQ>?	NYnmRYNuOTJzOUCzNVM>
human A2780 cell line	NEm2bHFRem:uaX\ldoF1cW:wIHHzd4F6	NUGzSI15PzJiaB?=	Mn\tRY51cXC{b3zp[oVz[XSrdnWg[YZn\WO2IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdCCuaX7lJJdieyCmZYTldo1qdmWmIHnuJIEhf2ixbHWgZ4VtdCB5MjDodkBkgXSxdH;4bYNqfHliYYPzZZktKEmFNUC9O\|Ehdk1?	NF60ZYoyPTB{N{i2Ny=>
human ovarian (A2780) cancer cell	NWnmPFQ3S3m2b4TvfIlkyqCjc4PhfS=>		MVHDfZRwfG:6aXOg[YZn\WO2IH;uJIh2dWGwIH;2ZZJq[W5iKFGyO\|gxMSClYX7j[ZIh[2WubDDsbY5mNCCLQ{WwQVcyKG6P	NYP0NGl5OTVzMkW5O\|E>
MLF mouse lung fibroblast cell	NGHQSm1Rem:uaX\ldoF1cW:wIHHzd4F6		MVvJcohq[mm2aX;uJI9nKE2ORjDtc5V{\SCudX7nJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVczKG6P	MWOxNlE6ODNzMx?=
human NCI60 cells	NIq1PIpRem:uaX\ldoF1cW:wIHHzd4F6	MX:3NkBp	NYD5SZg4SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2k3OCClZXzsd{Bi\nSncjC3NkBpenNiYomgd5Vt\m:{aH;kZY1qdmViQjDhd5NigSxiR1m1NF04PC55IH7N	M32we\|IyODhyN{Cz
LX-1 human lung carcinoma	M3u4U3Bzd2yrZnXyZZRqd25iYYPzZZk>		MWrJcohq[mm2aX;uJI9nKEy[LUGgbJVu[W5ibIXu[{Bk[XKlaX7vcYEheHKxbHnm[ZJifGmxbjygTWM2OD15NTDuUS=>	M3\y[VEzOTlyM{Gz
A431 human squamous cell	MV\Qdo9tcW[ncnH0bY9vKGG\|c3H5		MVLJcohq[mm2aX;uJI9nKEF2M{GgbJVu[W5ic4H1ZY1wfXNiY3XscEBk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVc2KG6P	MliwNVIyQTB\|MUO=
SKBR-3 human breast carcinoma cell	M4DYNnBzd2yrZnXyZZRqd25iYYPzZZk>		NHzXV3dKdmirYnn0bY9vKG:oIGPLRnIuOyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME23O{BvVQ>?	MU[xNlE6ODNzMx?=
A2780/TAX-R human ovarian carcinoma cell	NF7wc3RRem:uaX\ldoF1cW:wIHHzd4F6		MnrETY5pcWKrdHnvckBw\iCDMke4NE9VSVhvUjDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:Pzhibl2=	MVixNlE6ODNzMx?=
M109 mouse lung carcinoma cell	M1;pWXBzd2yrZnXyZZRqd25iYYPzZZk>		NIHkfIpKdmirYnn0bY9vKG:oIF2xNFkhdW:3c3WgcJVv\yClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR\|UxRThyIH7N	MoXtNVIyQTB\|MUO=
CACO-2 human colon carcinoma cell	M{H1bXBzd2yrZnXyZZRqd25iYYPzZZk>		MXLJcohq[mm2aX;uJI9nKEODQ1:tNkBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR\|UxRTh4IH7N	NETXV3cyOjF7MEOxNy=>
A549 human lung carcinoma cell	MUDQdo9tcW[ncnH0bY9vKGG\|c3H5		M1nRV2lvcGmkaYTpc44hd2ZiQUW0PUBpfW2jbjDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QTZibl2=	NEnQOXYyOjF7MEOxNy=>
MIP human colon carcinoma cell	NV7vOHh1TnWwY4Tpc44h[XO\|YYm=		NHPkZWhKdmirYnn0bY9vKG:oIF3JVEBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBtcW6nLDDJR\|UxRTBwMUKg{txO	M2m5PVEzOTlyM{Gz
K562 human leukemia cell	MkDBVJJwdGmoZYLheIlwdiCjc4PhfS=>		M4\Bd2lvcGmkaYTpc44hd2ZiS{W2NkBpfW2jbjDs[ZVs\W2rYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;MD6xN{DPxE1?	M{H0UVEzOTlyM{Gz
MCF-7 tumor cell	MYrQdo9tcW[ncnH0bY9vKGG\|c3H5		NYOxbY5DUW6qaXLpeIlwdiCxZjDNR2YuPyC2dX3vdkBk\WyuIIDyc4xq\mW{YYTpc44>	MYCxNFg1OzJzMR?=
human NCI60 cells	NYjWTGJjWHKxbHnm[ZJifGmxbjDhd5NigQ>?	MYW3NkBp	NVKwSmNJSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2k3OCClZXzsd{Bie3Onc4Pl[EBieyCuZYToZYwh\W[oZXP0JIFnfGW{IEeyJIhzeyCkeTDzeYxnd3Kqb3ThcYlv\SCEIHHzd4F6NCCOQ{WwQVAvQTB2IN88US=>	NUDSPVE1OjFyOEC3NFM>
PC3 cell	M3T3WGZ2dmO2aX;uJIF{e2G7		M4C0UWlvcGmkaYTpc44hd2ZiUFOzJINmdGxiY3zvco9o\W6rYzDhd5NigSxiSVO1NF0yOCEQvF2=	MX2xNVA3OzZyOR?=
HCT116 cell	MX;GeY5kfGmxbjDhd5NigQ>?		NYTzbodzUW6qaXLpeIlwdiCxZjDIR3QyOTZiY3XscEBkdG:wb3flcolkKGG\|c3H5MEBKSzVyPUGzJO69VQ>?	M2GyeVEyODZ\|NkC5
A2780 cell	M{nK[WZ2dmO2aX;uJIF{e2G7		NIjLT5hKdmirYnn0bY9vKG:oIFGyO\|gxKGOnbHygZ4xwdm:pZX7pZ{Bie3Ojef-8kEBKSzVyPUG1JO69VQ>?	Mnm3NVExPjN4MEm=
Mia PaCa-2 cell	MVjGeY5kfGmxbjDhd5NigQ>?		MXXJcohq[mm2aX;uJI9nKE2rYTDQZWNiNTJiY3XscEBkdG:wb3flcolkKGG\|c3H5MEBKSzVyPUO2JO69VQ>?	NIfTZngyOTB4M{[wPS=>
human A2780 cells	NUHkOGlQTnWwY4Tpc44h[XO\|YYm=		M{j6VmlvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJG5RVSCyaH;zdIhwenmuYYTpc44h[XRidHjyNVk6KGmwIHj1cYFvKEF{N{iwJINmdGy\|	M3\KNFE5PDZ7OEC5
human A2780 cells	MVzGeY5kfGmxbjDhd5NigQ>?	MoX0NlQhcA>?	MWLJcohq[mm2aX;uJI9nKGOmaz3t[YRq[XSnZDDSZkBxcG:\|cHjvdplt[XSrb36gZZQhfGi{OEKxJIlvKGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFI1KGi{cx?=	NHLHSIYyQDR4OUiwPS=>

... 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