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。

サイズ 価格(税別) 在庫  
JPY 8300.00 あり
JPY 28220.00 あり
JPY 94620.00 あり

カスタマーフィードバック(3)

  • (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.

    G, human THP-1 cells were treated with various small-molecule inhibitors or chemotherapy at increasing concentrations for 24 hours and then analyzed for viability by flow cytometry for PI exclusion. Cells concurrently treated with palbociclib or dinaciclib were analyzed for cytostatis according to nuclear DNA content.

    Cancer Res, 2016, 76(5):1158-69. Flavopiridol (Alvocidib) purchased from Selleck.

  • Pharmacological inhibition of either CDK1/2 or E2F1 prevented the induction of the expression of MAD2 by SKP2 overexpression. Notes: (A) Human lung cancer A549 cells were transfected with 2 μg of vector pcDNA3.1 or pcDNA-SKP2 for 48 h, then treated with CDK1/2 inhibitor flavopiridol or E2F1 inhibitor HLM006474 for additional 24 h. Total RNAs were extracted for the detection of the mRNA levels MAD2 by RT-QPCR with GAPDH as internal control. Quantitative analysis are expressed as mean ± SEM. n=3, *P<0.05 vs control. (B) Human lung cancer A549 cells were transfected with 2 μg of vector pcDNA3.1 or pcDNA-SKP2 for 48 h, then treated with CDK1/2 inhibitor flavopiridol or E2F1 inhibitor HLM006474 for additional 24 h. Total proteins were extracted for the detection of the protein levels Skp2 and Mad2 and the phosphorylation of Rb at Ser780 (pRb-S780) by Western blotting. GAPDH served as the loading control. (C) Human lung cancer A549 cells were transfected with 50 nM control or SKP2-specific siRNA with lipofectamine 2000 for 48 h, then treated with CDK1/2 inhibitor flavopiridol or E2F1 inhibitor HLM006474 for additional 24 h. Total proteins were extracted for the detection of the protein levels Skp2 and Mad2 by Western blotting. GAPDH served as the loading control. Abbreviations: MAD2, mitotic arrest deficient 2; SKP2, S-phase kinase-associated protein 2; mRNA, messenger RNA; SEM, standard error of the mean; Rb, retinoblastoma; siRNA, small interfering RNA.

    Onco Targets Ther, 2017, 10:439-446. 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.
ターゲット
CDK1 [1] CDK2 [1] CDK4 [1] CDK6 [1] CDK7 [1]
40 nM 40 nM 40 nM 40 nM 300 nM
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
ID8 cells MVPQdo9tcW[ncnH0bY9vKGG|c3H5 NHvKbHdCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGlFQCClZXzsd{whUUN3ME23JI5O M1S5UlE4OTJ|OEKx
Sf9 cells M1jNTGZ2dmO2aX;uJIF{e2G7 M{\XVmlvcGmkaYTpc44hd2ZicnXjc41jcW6jboSgZ5lkdGmwIFGvR2RMOiCneIDy[ZN{\WRiaX6gV4Y6KGOnbHzzMEBKSzVyPUGyJI5O MYKxO|kxPDN4Nh?=
LNCaP human prostate carcinoma cell MVvQdo9tcW[ncnH0bY9vKGG|c3H5 NYHqPZNwUW6qaXLpeIlwdiCxZjDMUmNiWCCqdX3hckBxem:|dHH0[UBk[XKlaX7vcYEh[2WubDDwdo9tcW[ncnH0bY9v NYqyUI83OTJzOUCzNVM>
HCT116/VP35 human colon carcinoma cell M1;oNHBzd2yrZnXyZZRqd25iYYPzZZk> M37JU2lvcGmkaYTpc44hd2ZiSFPUNVE3N1[SM{WgbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF0yPyCwTR?= MXKxNlE6ODNzMx?=
HCT116 human colon carcinoma cell M1ntXnBzd2yrZnXyZZRqd25iYYPzZZk> NFHybHBKdmirYnn0bY9vKG:oIFjDWFEyPiCqdX3hckBkd2yxbjDjZZJkcW6xbXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUG4JI5O NEfUZlYyOjF7MEOxNy=>
HCT116/VM46 human colon carcinoma cell NVLVOJFtWHKxbHnm[ZJifGmxbjDhd5NigQ>? M1PtemlvcGmkaYTpc44hd2ZiSFPUNVE3N1[PNE[gbJVu[W5iY3;sc44h[2G{Y3nuc41iKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF0zOSCwTR?= MUSxNlE6ODNzMx?=
human A2780 cells NV3lbmV7S3m2b4TvfIlkyqCjc4PhfS=> M4LpelI1KGh? M1vMbWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFI1KGi{czDifUBOXFRiYYPzZZktKEeLNUC9NlMhdk1? Mn3sNlM{ODF5Nke=
MCF7 cells NYX3O|JvWHKxbHnm[ZJifGmxbjDhd5NigQ>? MnvxRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDNR2Y4KGOnbHzzMEBKSzVyPUK2JI5O NFzkdoUyPzF{M{iyNS=>
human MRC5 cells NHrnVYlEgXSxdH;4bYPDqGG|c3H5 NGDVdYM4OiCq M3jS[mN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1TSzViY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2yPEBvVQ>? MUiyN|MxOTd4Nx?=
human A2780 cells NGqx[IxEgXSxdH;4bYPDqGG|c3H5 M3frZ|czKGh? NXTMNHJDS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTJ5OECgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0zQSCwTR?= MnnBNlM{ODF5Nke=
human A2780 cells M4rUUWN6fG:2b4jpZ:Kh[XO|YYm= M13odFQ5KGh? M4TmbGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEeLNUC9N|Ehdk1? NFnR[4YzOzNyMUe2Oy=>
A2780/DDP-R human ovarian carcinoma cell MXzQdo9tcW[ncnH0bY9vKGG|c3H5 M{HnTWlvcGmkaYTpc44hd2ZiQUK3PFAwTESSLWKgbJVu[W5ib4\hdolidiClYYLjbY5wdWFiY3XscEBxem:uaX\ldoF1cW:wLDDJR|UxRTN6IH7N NGTPOHEyOjF7MEOxNy=>
human MRC5 cells MULDfZRwfG:6aXRCpIF{e2G7 NGXHfWo1QCCq M4nKNmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1TSzViY3XscJMh[W[2ZYKgOFghcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2zPUBvVQ>? NWi1Vo1qOjN|MEG3Olc>
ABAE human fibroblast cell M4rIS3Bzd2yrZnXyZZRqd25iYYPzZZk> NXvIU4FFUW6qaXLpeIlwdiCxZjDBRmFGKGi3bXHuJIZq[nKxYnzhd5Qh[2WubDDwdo9tcW[ncnH0bY9vNCCLQ{WwQVQ2KG6P M{TG[|EzOTlyM{Gz
HL60 human leukemia cell M1vtOHBzd2yrZnXyZZRqd25iYYPzZZk> NFPBVm1KdmirYnn0bY9vKG:oIFjMOlAhcHWvYX6gcIV2c2WvaXGgZ4VtdCCycn;sbYZmemG2aX;uMEBKSzVyPUS2JI5O M3rHT|EzOTlyM{Gz
human MRC5 cells M4TQcGN6fG:2b4jpZ:Kh[XO|YYm= NYmybXk{OjRiaB?= NUexcWpqS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkAzPCCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVQ6KG6P MXiyN|MxOTd4Nx?=
Hs 27 human fibroblast cell MXLQdo9tcW[ncnH0bY9vKGG|c3H5 MorRTY5pcWKrdHnvckBw\iCKczCyO{BpfW2jbjDmbYJzd2KuYYP0JINmdGxicILvcIln\XKjdHnvckwhUUN3ME21NUBvVQ>? NVXWTIp2OTJzOUCzNVM>
CCRF-CEM human leukemia cell MmXsVJJwdGmoZYLheIlwdiCjc4PhfS=> NGjOdIdKdmirYnn0bY9vKG:oIFPDVmYuS0WPIHj1cYFvKGyndXvlcYliKGOnbHygdJJwdGmoZYLheIlwdixiSVO1NF02OiCwTR?= M{XxV|EzOTlyM{Gz
OVCAR-3 human ovarian carcinoma cell MV;Qdo9tcW[ncnH0bY9vKGG|c3H5 M{fMVWlvcGmkaYTpc44hd2ZiT2\DRXIuOyCqdX3hckBwfmG{aXHuJINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9OVQhdk1? MkHHNVIyQTB|MUO=
A2780/DDP-S human ovarian carcinoma cell M3rvc3Bzd2yrZnXyZZRqd25iYYPzZZk> MkTITY5pcWKrdHnvckBw\iCDMke4NE9FTFBvUzDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PTZibl2= NGjxcGYyOjF7MEOxNy=>
human HMEC1 cells M{e1OGN6fG:2b4jpZ:Kh[XO|YYm= NHfncmgzPCCq NVrDeXpIS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUE2HQ{GgZ4VtdHNiYX\0[ZIhOjRiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF03OSCwTR?= Mm\JNlM{ODF5Nke=
human HMEC1 cells MXjDfZRwfG:6aXRCpIF{e2G7 MnjSOFghcA>? MWXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUWVEOSClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPU[yJI5O NVToT3B{OjN|MEG3Olc>
A2780/TAX-S human ovarian carcinoma cell M1jGW3Bzd2yrZnXyZZRqd25iYYPzZZk> MoXvTY5pcWKrdHnvckBw\iCDMke4NE9VSVhvUzDoeY1idiCxdnHybYFvKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PjVibl2= Mn7GNVIyQTB|MUO=
LS174T human colon carcinoma cell NXrrVWJ{WHKxbHnm[ZJifGmxbjDhd5NigQ>? M3m5e2lvcGmkaYTpc44hd2ZiTGOxO|RVKGi3bXHuJINwdG:wIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;NkWgcm0> NGHPO3EyOjF7MEOxNy=>
MCF-7 human breast carcinoma cell NEH2XpFRem:uaX\ldoF1cW:wIHHzd4F6 NYDvZWJmUW6qaXLpeIlwdiCxZjDNR2YuPyCqdX3hckBjemWjc4SgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OkBvVQ>? MUOxNlE6ODNzMx?=
human HMEC1 cells MkjHR5l1d3SxeHnjxsBie3OjeR?= MoS3O|IhcA>? NHPqdIZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJVUWFMTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVY3KG6P MVqyN|MxOTd4Nx?=
PC3 human prostate carcinoma cell M2XEUXBzd2yrZnXyZZRqd25iYYPzZZk> NWDBPYFTUW6qaXLpeIlwdiCxZjDQR|MhcHWvYX6gdJJwe3SjdHWgZ4Fz[2mwb33hJINmdGxicILvcIln\XKjdHnvckwhUUN3ME22OkBvVQ>? MXGxNlE6ODNzMx?=
human A2780 cell line NWrCeppjWHKxbHnm[ZJifGmxbjDhd5NigQ>? M{LBOFczKGh? NW\JOJNOSW62aYDyc4xq\mW{YYTpeoUh\W[oZXP0JIFo[Wmwc4SgbJVu[W5iQUK3PFAh[2WubDDsbY5mKHejczDk[ZRmem2rbnXkJIlvKGFid3jvcIUh[2WubDC3NkBpeiCleYTveI95cWOrdImgZZN{[XluIFnDOVA:PzFibl2= MXuxOVAzPzh4Mx?=
human ovarian (A2780) cancer cell NVf1eZNFS3m2b4TvfIlkyqCjc4PhfS=> NIexSmpEgXSxdH;4bYMh\W[oZXP0JI9vKGi3bXHuJI93[XKrYX6gLGEzPzhyKTDjZY5k\XJiY3XscEBtcW6nLDDJR|UxRTdzIH7N MnnsNVUyOjV7N{G=
MLF mouse lung fibroblast cell M3;4Z3Bzd2yrZnXyZZRqd25iYYPzZZk> M3vydGlvcGmkaYTpc44hd2ZiTVzGJI1wfXOnIHz1coch\mmkcn;icIF{fCClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PzJibl2= MUexNlE6ODNzMx?=
human NCI60 cells M{LlOnBzd2yrZnXyZZRqd25iYYPzZZk> NUXmWos{PzJiaB?= NUTnbYVESW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDOR2k3OCClZXzsd{Bi\nSncjC3NkBpenNiYomgd5Vt\m:{aH;kZY1qdmViQjDhd5NigSxiR1m1NF04PC55IH7N NWO5UIlVOjFyOEC3NFM>
LX-1 human lung carcinoma NXjrfIhkWHKxbHnm[ZJifGmxbjDhd5NigQ>? NHzMcHRKdmirYnn0bY9vKG:oIFzYMVEhcHWvYX6gcJVv\yClYYLjbY5wdWFicILvcIln\XKjdHnvckwhUUN3ME23OUBvVQ>? NGfaNVYyOjF7MEOxNy=>
A431 human squamous cell NGTQbWdRem:uaX\ldoF1cW:wIHHzd4F6 M{PHRWlvcGmkaYTpc44hd2ZiQUSzNUBpfW2jbjDzdZVidW:3czDj[YxtKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:PzVibl2= M2DOXFEzOTlyM{Gz
SKBR-3 human breast carcinoma cell Mmn5VJJwdGmoZYLheIlwdiCjc4PhfS=> NVLBfnZMUW6qaXLpeIlwdiCxZjDTT2JTNTNiaIXtZY4h[nKnYYP0JINiemOrbn;tZUBk\WyuIIDyc4xq\mW{YYTpc44tKEmFNUC9O|chdk1? Mn;vNVIyQTB|MUO=
A2780/TAX-R human ovarian carcinoma cell M1TzPHBzd2yrZnXyZZRqd25iYYPzZZk> NYLzWpNzUW6qaXLpeIlwdiCxZjDBNlc5OC:WQWitVkBpfW2jbjDveoFzcWGwIHPhdoNqdm:vYTDj[YxtKHC{b3zp[oVz[XSrb36sJGlEPTB;N{igcm0> NGTTVmQyOjF7MEOxNy=>
M109 mouse lung carcinoma cell MonOVJJwdGmoZYLheIlwdiCjc4PhfS=> M4PJdWlvcGmkaYTpc44hd2ZiTUGwPUBud3W|ZTDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QDBibl2= MnH1NVIyQTB|MUO=
CACO-2 human colon carcinoma cell MnrWVJJwdGmoZYLheIlwdiCjc4PhfS=> MofwTY5pcWKrdHnvckBw\iCFQVPPMVIhcHWvYX6gZ49td25iY3HyZ4lvd22jIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD16NjDuUS=> NF7obVcyOjF7MEOxNy=>
A549 human lung carcinoma cell NITLZXlRem:uaX\ldoF1cW:wIHHzd4F6 M{XhTGlvcGmkaYTpc44hd2ZiQUW0PUBpfW2jbjDseY5oKGOjcnPpco9u[SClZXzsJJBzd2yrZnXyZZRqd25uIFnDOVA:QTZibl2= M2rrN|EzOTlyM{Gz
MIP human colon carcinoma cell NYm5OHRyTnWwY4Tpc44h[XO|YYm= NWj0c|ljUW6qaXLpeIlwdiCxZjDNTXAhcHWvYX6gZ49td25iY3HyZ4lvd22jIHPlcIwhdGmwZTygTWM2OD1yLkGyJO69VQ>? NIHRVocyOjF7MEOxNy=>
K562 human leukemia cell NH7VV4pRem:uaX\ldoF1cW:wIHHzd4F6 MlXJTY5pcWKrdHnvckBw\iCNNU[yJIh2dWGwIHzleYtmdWmjIHPlcIwheHKxbHnm[ZJifGmxbjygTWM2OD1yLkGzJO69VQ>? MWqxNlE6ODNzMx?=
MCF-7 tumor cell MofJVJJwdGmoZYLheIlwdiCjc4PhfS=> MX\Jcohq[mm2aX;uJI9nKE2FRj23JJR2dW:{IHPlcIwheHKxbHnm[ZJifGmxbh?= NUPsOXBNOTB6NEOyNVE>
human NCI60 cells NHnCdIhRem:uaX\ldoF1cW:wIHHzd4F6 MYi3NkBp MX3BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE6FSU[wJINmdGy|IHHzd4V{e2WmIHHzJIxmfGijbDDl[oZm[3RiYX\0[ZIhPzJiaILzJIJ6KHO3bH\vdohw\GGvaX7lJGIh[XO|YYmsJGxEPTB;MD65NFQh|ryP NHHnUoUzOTB6MEewNy=>
PC3 cell NIX2c4ZHfW6ldHnvckBie3OjeR?= MXfJcohq[mm2aX;uJI9nKFCFMzDj[YxtKGOub37v[4VvcWNiYYPzZZktKEmFNUC9NVAh|ryP NHrlXI4yOTB4M{[wPS=>
HCT116 cell MXPGeY5kfGmxbjDhd5NigQ>? MmX6TY5pcWKrdHnvckBw\iCKQ2SxNVYh[2WubDDjcI9vd2enbnnjJIF{e2G7LDDJR|UxRTF|IN88US=> M{\YRlEyODZ|NkC5
A2780 cell MoLrSpVv[3Srb36gZZN{[Xl? M2\pOWlvcGmkaYTpc44hd2ZiQUK3PFAh[2WubDDjcI9vd2enbnnjJIF{e2G778{MJGlEPTB;MUWg{txO MWSxNVA3OzZyOR?=
Mia PaCa-2 cell MnLTSpVv[3Srb36gZZN{[Xl? M4TC[GlvcGmkaYTpc44hd2ZiTXnhJHBiS2FvMjDj[YxtKGOub37v[4VvcWNiYYPzZZktKEmFNUC9N|Yh|ryP NIXzR|UyOTB4M{[wPS=>
human A2780 cells MY\GeY5kfGmxbjDhd5NigQ>? MWjJcohq[mm2aX;uJI9nKGOmaz3t[YRq[XSnZDDOVG0heGixc4Doc5J6dGG2aX;uJIF1KHSqckG5PUBqdiCqdX3hckBCOjd6MDDj[Yxtew>? NFX1dmIyQDR4OUiwPS=>
human A2780 cells NVnCOYViTnWwY4Tpc44h[XO|YYm= M2Pod|I1KGh? MXTJcohq[mm2aX;uJI9nKGOmaz3t[YRq[XSnZDDSZkBxcG:|cHjvdplt[XSrb36gZZQhfGi{OEKxJIlvKGi3bXHuJGEzPzhyIHPlcIx{KGGodHXyJFI1KGi{cx?= MoDDNVg1Pjl6MEm=

多くの細胞株試験データを見る場合、クリックしてください

体内試験 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]

お薦めの試験操作(参考用のみ)

キナーゼ試験:

[1]

+ 展開

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.
細胞試験:

[5]

+ 展開
  • 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)
動物試験:

[5]

+ 展開
  • 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 Insoluble
体内 順序で溶剤を入れること:
5% DMSO+30% PEG 300+ddH2O
2.5mg/mL

* 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
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

相関CDK製品

Tags: Flavopiridol (Alvocidib)を買う | Flavopiridol (Alvocidib) ic50 | Flavopiridol (Alvocidib)供給者 | Flavopiridol (Alvocidib)を購入する | Flavopiridol (Alvocidib)費用 | Flavopiridol (Alvocidib)生産者 | オーダーFlavopiridol (Alvocidib) | Flavopiridol (Alvocidib)化学構造 | Flavopiridol (Alvocidib)分子量 | Flavopiridol (Alvocidib)代理店
×
細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID