Flavopiridol (Alvocidib)

製品コードS1230 別名:NSC 649890 HCl,HMR-1275

Flavopiridol (Alvocidib)化学構造

分子量(MW):401.84

Flavopiridol (Alvocidib)はATPと一緒に、CDKs(CDK1、CDK2、CDK4とCDK6を含める)を競争性的に抑制して、このIC50値が約40nMになりますが、CDK1、2、4と6に作用する選択性はCDK7に作用する選択性より7.5倍が高くなって、最初に発見したことは EGFRとPKAを抑制することができるということです。臨床 1/2。

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カスタマーフィードバック(1)

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

製品安全説明書

CDK阻害剤の選択性比較

生物活性

製品説明 Flavopiridol (Alvocidib)はATPと一緒に、CDKs(CDK1、CDK2、CDK4とCDK6を含める)を競争性的に抑制して、このIC50値が約40nMになりますが、CDK1、2、4と6に作用する選択性はCDK7に作用する選択性より7.5倍が高くなって、最初に発見したことは EGFRとPKAを抑制することができるということです。臨床 1/2。
特性 First CDK inhibitor to be used in human clinical trials.
靶点
CDK1 [1] CDK2 [1] CDK4 [1] CDK6 [1] CDK7 [1]
40 nM 40 nM 40 nM 40 nM 300 nM
In vitro試験

Flavopiridol displays less activity against unrelated kinases such as MAP, PAK, PKC, and EGFR with IC50 of >14 μM. Flavopiridol significantly inhibits the colony growth of HCT116, A2780, PC3, and Mia PaCa-2 cells with IC50 of 13 nM, 15 nM, 10 nM and 36 nM, respecitively. [1] Flavopiridol also potently inhibits the activity of Glycogen synthase kinase-3 (GSK-3) with an IC50 of 280 nm. [2] Compared with other CDKs, Flavopiridol inhibits the activity of CDK7 less potently with IC50 of 875 nM. Flavopiridol (0.5 μM) inhibits both pSer807/811 Rb and pThr199 NPM, whereas mild changes are observed at pThr821 Rb. Flavopiridol also decreases the overall RNA polymerase II level, as well as the phosphorylation of RNA polymerase II on the CTD repeats at Ser2 Ser5. [3] As a broad spectrum CDK inhibitor, Flavopiridol can inhibit cell cycle progression in either G1 or G2. Flavopiridol (0.3 μM) induces G1 arrest in either MCF-7 or MDA-MB-468 cells by inhibition of the CDK4 or CDK2 kinase activity. [4] Flavopiridol exhibits potent cytotoxicity against a wide variety of tumor cell lines with IC50 values ranging form 16 nM for LNCAP to 130 nM for K562. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
ID8 cells M{fBTXBzd2yrZnXyZZRqd25iYYPzZZk> NUf2XIdpSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBKTDhiY3XscJMtKEmFNUC9O{BvVQ>? MYmxO|EzOzh{MR?=
Sf9 cells Ml\WSpVv[3Srb36gZZN{[Xl? MV3Jcohq[mm2aX;uJI9nKHKnY3;tZolv[W62IHP5Z4xqdiCDL1PET|Ih\XiycnXzd4VlKGmwIGPmPUBk\WyuczygTWM2OD1zMjDuUS=> MYKxO|kxPDN4Nh?=
LNCaP human prostate carcinoma cell M1m2O3Bzd2yrZnXyZZRqd25iYYPzZZk> MmfZTY5pcWKrdHnvckBw\iCOTlPhVEBpfW2jbjDwdo9{fGG2ZTDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;u MnS4NVIyQTB|MUO=
HCT116/VP35 human colon carcinoma cell NIOxS5FRem:uaX\ldoF1cW:wIHHzd4F6 M3nxeWlvcGmkaYTpc44hd2ZiSFPUNVE3N1[SM{WgbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF0yPyCwTR?= NUjPdpBXOTJzOUCzNVM>
HCT116 human colon carcinoma cell NWTOcZpkWHKxbHnm[ZJifGmxbjDhd5NigQ>? MmT2TY5pcWKrdHnvckBw\iCKQ2SxNVYhcHWvYX6gZ49td25iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD1zODDuUS=> NWXKfHk6OTJzOUCzNVM>
HCT116/VM46 human colon carcinoma cell MkXXVJJwdGmoZYLheIlwdiCjc4PhfS=> NXvWZ2ppUW6qaXLpeIlwdiCxZjDIR3QyOTZxVl20OkBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTJzIH7N NXjzXmM2OTJzOUCzNVM>
human A2780 cells NXvESHRGS3m2b4TvfIlkyqCjc4PhfS=> MlnaNlQhcA>? M3fTW2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFI1KGi{czDifUBOXFRiYYPzZZktKEeLNUC9NlMhdk1? NFi5S5UzOzNyMUe2Oy=>
MCF7 cells NIS4OpZRem:uaX\ldoF1cW:wIHHzd4F6 NFjrcHJCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JG1ETjdiY3XscJMtKEmFNUC9NlYhdk1? Mn\lNVcyOjN6MkG=
human MRC5 cells NWK5N5dSS3m2b4TvfIlkyqCjc4PhfS=> MlLKO|IhcA>? Ml;0R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUXJEPSClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUK4JI5O NF7lXZAzOzNyMUe2Oy=>
human A2780 cells NF72fmlEgXSxdH;4bYPDqGG|c3H5 NYfrUphJPzJiaB?= M3jBNGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9Nlkhdk1? MVWyN|MxOTd4Nx?=
human A2780 cells NGLWXmZEgXSxdH;4bYPDqGG|c3H5 MVi0PEBp MVzDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBNlc5OCClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUOxJI5O NWj4U5RUOjN|MEG3Olc>
A2780/DDP-R human ovarian carcinoma cell MkfpVJJwdGmoZYLheIlwdiCjc4PhfS=> M1;UO2lvcGmkaYTpc44hd2ZiQUK3PFAwTESSLWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTN6IH7N NHO0bHEyOjF7MEOxNy=>
human MRC5 cells NUnve2JSS3m2b4TvfIlkyqCjc4PhfS=> MnzwOFghcA>? NXTodFJSS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkA1QCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVM6KG6P NHS0[|gzOzNyMUe2Oy=>
ABAE human fibroblast cell NYPyZ2x7WHKxbHnm[ZJifGmxbjDhd5NigQ>? M2nSOWlvcGmkaYTpc44hd2ZiQVLBSUBpfW2jbjDmbYJzd2KuYYP0JINmdGxicILvcIln\XKjdHnvckwhUUN3ME20OUBvVQ>? MVSxNlE6ODNzMx?=
HL60 human leukemia cell NYXpZVVzWHKxbHnm[ZJifGmxbjDhd5NigQ>? M3u5UmlvcGmkaYTpc44hd2ZiSFy2NEBpfW2jbjDs[ZVs\W2rYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;NE[gcm0> M2rpPVEzOTlyM{Gz
human MRC5 cells NVnLco9yS3m2b4TvfIlkyqCjc4PhfS=> MV6yOEBp MVfDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNVmM2KGOnbHzzJIFnfGW{IEK0JIhzeyCkeTDNWHQh[XO|YYmsJGdKPTB;NEmgcm0> Ml7UNlM{ODF5Nke=
Hs 27 human fibroblast cell NWfST49yWHKxbHnm[ZJifGmxbjDhd5NigQ>? M1rTVWlvcGmkaYTpc44hd2ZiSIOgNlchcHWvYX6g[oljem:kbHHzeEBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9OVEhdk1? M3\XPVEzOTlyM{Gz
CCRF-CEM human leukemia cell MVXQdo9tcW[ncnH0bY9vKGG|c3H5 M1T4dWlvcGmkaYTpc44hd2ZiQ1PSSk1ETU1iaIXtZY4hdGW3a3XtbYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVUzKG6P MXOxNlE6ODNzMx?=
OVCAR-3 human ovarian carcinoma cell MYLQdo9tcW[ncnH0bY9vKGG|c3H5 MlfmTY5pcWKrdHnvckBw\iCRVlPBVk0{KGi3bXHuJI93[XKrYX6gZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME21OEBvVQ>? NELqWmsyOjF7MEOxNy=>
A2780/DDP-S human ovarian carcinoma cell MULQdo9tcW[ncnH0bY9vKGG|c3H5 NWLRfphqUW6qaXLpeIlwdiCxZjDBNlc5OC:GRGCtV{BpfW2jbjDveoFzcWGwIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;NU[gcm0> MWGxNlE6ODNzMx?=
human HMEC1 cells MX\DfZRwfG:6aXRCpIF{e2G7 NYr6ZXpHOjRiaB?= NUTYdnNxS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhOjRiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03OSCwTR?= NWP6NpdKOjN|MEG3Olc>
human HMEC1 cells Mnm0R5l1d3SxeHnjxsBie3OjeR?= MmThOFghcA>? MUXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPU[yJI5O NFjy[pEzOzNyMUe2Oy=>
A2780/TAX-S human ovarian carcinoma cell MUjQdo9tcW[ncnH0bY9vKGG|c3H5 M3vPcGlvcGmkaYTpc44hd2ZiQUK3PFAwXEG[LWOgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTZ3IH7N NVHRSZFWOTJzOUCzNVM>
LS174T human colon carcinoma cell M1\PNnBzd2yrZnXyZZRqd25iYYPzZZk> NGf5[XJKdmirYnn0bY9vKG:oIFzTNVc1XCCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPU[1JI5O MknsNVIyQTB|MUO=
MCF-7 human breast carcinoma cell Ml;1VJJwdGmoZYLheIlwdiCjc4PhfS=> Mn:5TY5pcWKrdHnvckBw\iCPQ1[tO{BpfW2jbjDidoVie3RiY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD14NjDuUS=> MkTXNVIyQTB|MUO=
human HMEC1 cells M{XxXWN6fG:2b4jpZ:Kh[XO|YYm= MkewO|IhcA>? NG\kZm1EgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJVUWFMTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVY3KG6P M4\wNFI{OzBzN{[3
PC3 human prostate carcinoma cell M1\iUXBzd2yrZnXyZZRqd25iYYPzZZk> M1zRcmlvcGmkaYTpc44hd2ZiUFOzJIh2dWGwIIDyc5N1[XSnIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;Nk[gcm0> MVSxNlE6ODNzMx?=
human A2780 cell line MlTTVJJwdGmoZYLheIlwdiCjc4PhfS=> MnP6O|IhcA>? MmDHRY51cXC{b3zp[oVz[XSrdnWg[YZn\WO2IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdCCuaX7lJJdieyCmZYTldo1qdmWmIHnuJIEhf2ixbHWgZ4VtdCB5MjDodkBkgXSxdH;4bYNqfHliYYPzZZktKEmFNUC9O|Ehdk1? M2ToUFE2ODJ5OE[z
human ovarian (A2780) cancer cell MW\DfZRwfG:6aXRCpIF{e2G7 NFvBTVREgXSxdH;4bYMh\W[oZXP0JI9vKGi3bXHuJI93[XKrYX6gLGEzPzhyKTDjZY5k\XJiY3XscEBtcW6nLDDJR|UxRTdzIH7N M{HiTFE2OTJ3OUex
MLF mouse lung fibroblast cell MWDQdo9tcW[ncnH0bY9vKGG|c3H5 M4jvWmlvcGmkaYTpc44hd2ZiTVzGJI1wfXOnIHz1coch\mmkcn;icIF{fCClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PzJibl2= NVrmN2ZSOTJzOUCzNVM>
human NCI60 cells M4K3RnBzd2yrZnXyZZRqd25iYYPzZZk> MkD6O|IhcA>? NH3KfWNCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF7DTVYxKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDzeYxnd3Kqb3ThcYlv\SCEIHHzd4F6NCCJSUWwQVc1Njdibl2= MlLSNlExQDB5MEO=
LX-1 human lung carcinoma NYPGUIxtWHKxbHnm[ZJifGmxbjDhd5NigQ>? NHjhZVJKdmirYnn0bY9vKG:oIFzYMVEhcHWvYX6gcJVv\yClYYLjbY5wdWFicILvcIln\XKjdHnvckwhUUN3ME23OUBvVQ>? NX3lUotPOTJzOUCzNVM>
A431 human squamous cell NUW0XINEWHKxbHnm[ZJifGmxbjDhd5NigQ>? NVfpO4VSUW6qaXLpeIlwdiCxZjDBOFMyKGi3bXHuJJNyfWGvb4XzJINmdGxiY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD15NTDuUS=> MY[xNlE6ODNzMx?=
SKBR-3 human breast carcinoma cell NFi3WmNRem:uaX\ldoF1cW:wIHHzd4F6 NEHoV3hKdmirYnn0bY9vKG:oIGPLRnIuOyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME23O{BvVQ>? MlzMNVIyQTB|MUO=
A2780/TAX-R human ovarian carcinoma cell NVftUpJuWHKxbHnm[ZJifGmxbjDhd5NigQ>? M2XJT2lvcGmkaYTpc44hd2ZiQUK3PFAwXEG[LWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTd6IH7N MoLNNVIyQTB|MUO=
M109 mouse lung carcinoma cell M2S3VnBzd2yrZnXyZZRqd25iYYPzZZk> NILtfpdKdmirYnn0bY9vKG:oIF2xNFkhdW:3c3WgcJVv\yClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRThyIH7N M3L0[|EzOTlyM{Gz
CACO-2 human colon carcinoma cell MYXQdo9tcW[ncnH0bY9vKGG|c3H5 MYPJcohq[mm2aX;uJI9nKEODQ1:tNkBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTh4IH7N NYP1VFR7OTJzOUCzNVM>
A549 human lung carcinoma cell NHy0cWZRem:uaX\ldoF1cW:wIHHzd4F6 MWXJcohq[mm2aX;uJI9nKEF3NEmgbJVu[W5ibIXu[{Bk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVk3KG6P NVvVbpczOTJzOUCzNVM>
MIP human colon carcinoma cell NXjncpNGTnWwY4Tpc44h[XO|YYm= NGXM[FlKdmirYnn0bY9vKG:oIF3JVEBpfW2jbjDjc4xwdiClYYLjbY5wdWFiY3XscEBtcW6nLDDJR|UxRTBwMUKg{txO M1XVTVEzOTlyM{Gz
K562 human leukemia cell M{nOTHBzd2yrZnXyZZRqd25iYYPzZZk> NUHoT3pwUW6qaXLpeIlwdiCxZjDLOVYzKGi3bXHuJIxmfWunbXnhJINmdGxicILvcIln\XKjdHnvckwhUUN3ME2wMlE{KM7:TR?= M3PCfVEzOTlyM{Gz
MCF-7 tumor cell MlrZVJJwdGmoZYLheIlwdiCjc4PhfS=> NUezUJd4UW6qaXLpeIlwdiCxZjDNR2YuPyC2dX3vdkBk\WyuIIDyc4xq\mW{YYTpc44> MUWxNFg1OzJzMR?=
human NCI60 cells NV3qfnBYWHKxbHnm[ZJifGmxbjDhd5NigQ>? MXi3NkBp MVfBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE6FSU[wJINmdGy|IHHzd4V{e2WmIHHzJIxmfGijbDDl[oZm[3RiYX\0[ZIhPzJiaILzJIJ6KHO3bH\vdohw\GGvaX7lJGIh[XO|YYmsJGxEPTB;MD65NFQh|ryP M4rNPFIyODhyN{Cz
PC3 cell M3HOT2Z2dmO2aX;uJIF{e2G7 NX7ScmYxUW6qaXLpeIlwdiCxZjDQR|Mh[2WubDDjcI9vd2enbnnjJIF{e2G7LDDJR|UxRTFyIN88US=> M3;RXFEyODZ|NkC5
HCT116 cell MUPGeY5kfGmxbjDhd5NigQ>? NFLIUZhKdmirYnn0bY9vKG:oIFjDWFEyPiClZXzsJINtd26xZ3XubYMh[XO|YYmsJGlEPTB;MUOg{txO M2fERVEyODZ|NkC5
A2780 cell MX3GeY5kfGmxbjDhd5NigQ>? NGP2VGVKdmirYnn0bY9vKG:oIFGyO|gxKGOnbHygZ4xwdm:pZX7pZ{Bie3Ojef-8kEBKSzVyPUG1JO69VQ>? MXixNVA3OzZyOR?=
Mia PaCa-2 cell NX\nVFc5TnWwY4Tpc44h[XO|YYm= NFO1VmZKdmirYnn0bY9vKG:oIF3pZUBR[UOjLUKgZ4VtdCClbH;uc4dmdmmlIHHzd4F6NCCLQ{WwQVM3KM7:TR?= NFzPZogyOTB4M{[wPS=>
human A2780 cells NUPObVdSTnWwY4Tpc44h[XO|YYm= M3T2fWlvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJG5RVSCyaH;zdIhwenmuYYTpc44h[XRidHjyNVk6KGmwIHj1cYFvKEF{N{iwJINmdGy| NGXqVHoyQDR4OUiwPS=>
human A2780 cells M3XJSWZ2dmO2aX;uJIF{e2G7 MWeyOEBp M{\RPGlvcGmkaYTpc44hd2ZiY3TrMY1m\GmjdHXkJHJjKHCqb4PwbI9zgWyjdHnvckBifCC2aIK4NlEhcW5iaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhOjRiaILz M3;VVVE5PDZ7OEC5

... Click to View More Cell Line Experimental Data

In vivo試験 Administration of Flavopiridol at 7.5 mg/kg for 7 days displays slight antitumor activity against P388 murine leukemia, resulting in %T/C value of 110, and active against the human A2780 ovarian carcinoma implanted sc in nude mice, producing 1.5 log cell kill (LCK). [5] Flavopiridol treatment at 1-2.5 mg/kg for 10 days significantly suppresses collagen-induced arthritis in mice in a dose-dependent manner, by inhibiting synovial hyperplasia and joint destruction, whereas serum concentrations of anti-collagen type II (CII) Abs and proliferative responses to CII are maintained. [6] In the p21-intact Hct116 xenografts in nude mice, administration of CPT-11 (100 mg/kg) followed by Flavopiridol (3 mg/kg) 7 and 16 hours later significantly inhibits tumor regression by 86% and 82%, respectively, displaying >2 fold inhibition compared with CPT-11 alone by 40 %. The combination produces ~30% complete response rate (CR) in contrast to CPT-11 alone where no CR is found. [7]

プロトコル(参考用のみ)

キナーゼアッセイ:

[1]

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CDK kinase assay:

For CDK1/cyclin B1 kinase assay, kinase reactions consist of 100 ng of baculovirus expressed GST-CDK1/cyclin B1 (human) complex, 1 μg histone HI, 0.2 μCi [γ-33P]ATP, 25 μM ATP in 50 μL kinase buffer (50 mM Tris, pH 8.0, 10 mM MgCl2, 1 mM EGTA, 0.5 mM DTT). For CDK2/cyclin E kinase assay, kinase reactions consist of 5 ng of baculovirus expressed GST-CDK2/cyclin E (human) complex, 0.5 μg GST-RB fusion protein (amino acids 776-928 of retinoblastoma protein), 0.2 μCi [γ-33P]ATP, 25 μM ATP in 50 μL kinase buffer (50 mM Hepes, pH 8.0, 10 mM MgCl2, 1 mM EGTA, 2 mM DTT). For CDK4/cyclin D1 kinase assay, kinase reactions consist of 150 ng of baculovirus expressed GST-CDK4/cyclin D1 (human), 280 ng of Stag-cyclin D1, 0.5 μg GST-RB fusion protein (amino acids 776-928 of retinoblastoma protein), 0.2 μCi [γ-33P]ATP, 25 μM ATP in 50 μL kinase buffer (50 mM Hepes, pH 8.0, 10 mM MgCl2, 1 mM EGTA, 2 mM DTT). Reactions are incubated for 45 minutes for CDK1 and CDK2, or 1 hour for CDK4 at 30 °C and stopped by the addition of cold trichloroacetic acid (TCA) to a final concentration 15%. TCA precipitates are collected onto GF/C unifilter plates using a Filtermate universal harvester and the filters are quantitated using a TopCount 96-well liquid scintillation counter. Flavopiridol is dissolved at 10 mM in dimethylformamide (DMF) and evaluated at six concentrations, each in triplicate. The final concentration of DMF in the assay = 2%. IC50 values are derived by nonlinear regression analysis and have a coefficient of variance = 16%. To assay Flavopiridol activity on CDK6, a filter-binding assay is established. The following are combined in the reaction mixture: 2 μL of CDK6 (0.7 mg/μL), 5 μL of histone H1 (6 mg/mL), 14 μL of kinase buffer (60 mM β-glycerophosphate, 30 mM p-nitrophenyl phosphate, 25 mM MOPS (pH 7.0), 5 mM EGTA, 15 mM MgCl2, 1 mM DTT, 0.1 mM Na-vanadate), 3 μL of increasing concentrations of Flavopiridol diluted in 50% DMSO, and 6 μL of 33P-ATP (1 mCi/mL) in nonradioactive ATP at 90 μM concentration (final concentration: 15 μM). The assay is initiated by the addition of 33P-ATP. The reaction is incubated for 20 minutes at 30°C. A 25 μL aliquot of the supernatant is then spotted onto Whatman P81 phosphocellulose paper. Filters are washed 5 times with 1% phosphoric acid solution. Wet filters are counted in the presence of 1 mL of scintillation fluid. Cdk9 activity is measured using 50 nM of recombinant Cdk9/cyclin T in 50 mM HEPES pH 7.5, 10 mM MgCl2, 1 mM DTT, 3 μM Na3VO4, 150 μM RNA polymerase CDT peptide and 80 μM ATP. Cdk7 assay is performed in the same buffer using 37 nM of purified kinase in the presence of 200 μM ATP and 10 μM myelin binding protein as a substrate. The potency of Flavopiridol toward CDK9 and CDK7 is determined using either a strong anion exchanger (Dowex 1-X8 resin, formate form)-based assay or a scintillation proximity assay. IC50 values are calculated from the dose-response curves.
細胞アッセイ:

[5]

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  • 細胞株: MCF-7, LNCAP, PC3, HCT116, CACO-2, A549, HL60, K562 cells and et al.
  • 濃度: Dissolved in DMSO, final concentrations ~10 μM
  • 反応時間: 72 hours
  • 実験の流れ:

    Cells are exposed to various concentrations of Flavopiridol for 72 hours at which time the tetrazolium dye, MTS in combination with phenazine methosulfate, is added. After 3 hours, the absorbency is measured at 492 nm, which is proportional to the number of viable cells. The results are expressed as IC50 values. For cell Cycle analysis, cells are fixed in paraformaldehyde and ethanol, washed, resuspended in staining solution of TdT enzyme and FITC-dUTP, washed, stained with PI following RNase treatment, and then analyzed by flow cytometry.


    (参考用のみ)
動物実験:

[5]

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  • 動物モデル: Female Balb/c×DBA/2J F1 mice inoculated ip with P388 ascites leukemic cells, and Balb/c nu/nu nude mice subcutaneous implanted with A2780, Br-cycE, or A431 cells
  • 製剤: Dissolved in a mixture of Cremophor/ethanol (50:50), and diluted in water
  • 投薬量: ~7.5 mg/kg/day
  • 投与方法: Injection i.p.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 15 mg/mL (37.32 mM)
Ethanol 8 mg/mL (19.9 mM)
Water <1 mg/mL
体内 5% DMSO+30% PEG 300+ddH2O 2.5mg/mL

* <1 mg/mlは製品が微弱に溶解する或いは溶解しないことを示します。
* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。

化学情報

分子量 401.84
化学式

C21H20ClNO5

CAS No. 146426-40-6
保管
in solvent
別名 NSC 649890 HCl,HMR-1275

便利ツール

モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • 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):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

マス 濃度 ボリューム 分子量

臨床試験

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
NCT02520011 Recruiting Acute Myeloid Leukemia Tolero Pharmaceuticals, Inc. December 2015 Phase 2
NCT01349972 Completed Acute Myeloid Leukemia With Multilineage Dysplasia Following Myelodysplastic Syndrome|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 Del(5q)|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)|Secondary Acute Myeloid Leukemia|Untreated Adult Acute Myeloid Leukemia National Cancer Institute (NCI) April 2011 Phase 2
NCT01076556 Terminated Chronic Lymphocytic Leukemia|Prolymphocytic Leukemia|Recurrent Small Lymphocytic Lymphoma|Refractory Chronic Lymphocytic Leukemia|Stage I Chronic Lymphocytic Leukemia|Stage I Small Lymphocytic Lymphoma|Stage II Chronic Lymphocytic Leukemia|Stage II Small Lymphocytic Lymphoma|Stage III Chronic Lymphocytic Leukemia|Stage III Small Lymphocytic Lymphoma|Stage IV Chronic Lymphocytic Leukemia|Stage IV Small Lymphocytic Lymphoma National Cancer Institute (NCI) April 2010 Phase 1
NCT00991952 Completed Adenocarcinoma of the Gastroesophageal Junction|Diffuse Adenocarcinoma of the Stomach|Intestinal Adenocarcinoma of the Stomach|Mixed Adenocarcinoma of the Stomach|Recurrent Gastric Cancer|Stage IIIA Gastric Cancer|Stage IIIB Gastric Cancer|Stage IIIC Gastric Cancer|Stage IV Gastric Cancer National Cancer Institute (NCI) September 2009 Phase 2
NCT00957905 Completed Recurrent Extragonadal Seminoma|Recurrent Malignant Extragonadal Germ Cell Tumor|Recurrent Malignant Extragonadal Non-Seminomatous Germ Cell Tumor|Recurrent Malignant Testicular Germ Cell Tumor|Recurrent Ovarian Germ Cell Tumor|Stage III Testicular Cancer|Stage IV Extragonadal Non-Seminomatous Germ Cell Tumor|Stage IV Extragonadal Seminoma|Stage IV Ovarian Germ Cell Tumor National Cancer Institute (NCI) June 2009 Phase 2

技術サポート

ストックの作り方、阻害剤の保管する方法、細胞実験や動物実験に注意すべきな点を全部含めており、製品を取扱う時よくあった質問に対して取扱説明書でお答えいたします。

Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

  • * 必須

CDK信号経路図

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID