AG-1478 (Tyrphostin AG-1478)

製品コードS2728 別名:NSC 693255

AG-1478 (Tyrphostin AG-1478)化学構造

分子量(MW):315.75

AG-1478 (Tyrphostin AG-1478)は一種の選択性的なEGFR阻害剤で、無細胞試験でIC50値が3 nMです。HER2-Neu、PDGFR、Trk、Bcr-AblとInsRに作用する活性が殆どありません。

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カスタマーフィードバック(3)

  • BPA 1 nM, G-1 (a specific agonist of GPR30) alone (10 nM) or after a 90-min pretreatment with G15 (a specific antagonist of GPR30, 1 uM), PD 98059 (an ERK1/2 antagonist, 10 uM), AG-1478 (a potent antagonist of EGFR, 10 uM), or the mixture (G15, PD 98059, and AG-1478). ERK1/2 phosphorylation in TM4 cells exposure to different compounds with the concentrations mentioned above for 15 min. Values shown are expressed in the percentage of control (steroid-free medium) given as the mean ?SD of three independent experiments (n = 3). *p < 0.05 compared with control; **p < 0.01 compared with control.

    Toxicol Lett 2014 226(1), 81-9. AG-1478 (Tyrphostin AG-1478) purchased from Selleck.

    The inhibition of tyrosine kinase activity of EGFR abolished a morphological change associated with EMT (A) and EGF-mediated TACC3 induction (B). Cells were treated with EGF or EGF+AG1478 for 24 h and then subjected to western blot analysis. β-actin was used as a loading control.The intensity of bands was quantified using imageJ software and normalized to β-actin.

    PLoS One, 2013, 8(8): e70353. AG-1478 (Tyrphostin AG-1478) purchased from Selleck.

  • A549 cells were treated with G15 (a specific antagonist of GPR30, 1 uM), AG1478 (a potent antagonist of EGFR, 10 uM), BPA (10-5 M) alone for 15 min or BPA after a 90-min pretreatment with G15 or AG1478 for 15 min. Then the expression of p-ERK1/2 and total ERK1/2 were measured by western blot analysis.

    Biomed Pharmacother 2014 10.1016/j.biopha.2014.09.003. AG-1478 (Tyrphostin AG-1478) purchased from Selleck.

製品安全説明書

EGFR阻害剤の選択性比較

生物活性

製品説明 AG-1478 (Tyrphostin AG-1478)は一種の選択性的なEGFR阻害剤で、無細胞試験でIC50値が3 nMです。HER2-Neu、PDGFR、Trk、Bcr-AblとInsRに作用する活性が殆どありません。
靶点
EGFR [1]
(Cell-free assay)
HER2 [1]
(Cell-free assay)
PDGFR [1]
(Cell-free assay)
3 nM >100 μM >100 μM
In vitro試験

AG-1478 is high selective over ErbB2 and PDGFR with IC50 of >100 μM. [1] AG-1478 preferentially inhibits U87MG cells expressing truncated EGFR with IC50 of 8.7 μM, compared to those expressing endogenous wt EGFR or overexpressing exogenous wt EGFR with IC50 of 34.6 μM and 48.4 μM, respectively, and inhibits the DNA synthesis with IC50 of 4.6 μM, 19.67 μM, and 35.2 μM, respectively. AG-1478 also preferentially inhibits the tyrosine kinase activity and autophosphorylation of the ΔEGFR compared to endogenous or overexpressed exogenous wt EGFR. [2] AG-1478 (0.25 μM) abolishes the MAPK activation induced by Ang II, a Ca2+ ionophore as well as EGF but not by a phorbol ester or platelet-derived growth factor-BB in the VSMC. [3] AG-1478 inhibits EGF-induced mitogenesis of the BaF/ERX and LIM1215 cells with IC50 of 0.07 μM and 0.2 μM, respectively. [6] AG1478 is able to inhibit the function of ATP-binding cassette (ABC) transporters such as ABCB1 and ABCG2, with a more pronounced effect on ABCG2. [7]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
U87MG NX3uRZVpT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M13uNZ4yODBizszN NG\ES|BFVVOR M3;VV2lEPTB;M{SuOkDPxE1? NWnZfWpFQDd3MkG0OS=>
U87MG.ΔEGFR MX;Hdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? Mne1glExOCEQvF2= M2fuOGROW09? Mn3mTWM2OD16Lkeg{txO NX;OemxyQDd3MkG0OS=>
U87MG.wtEGFR. MVjHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NV7hNldThjFyMDFOwG0> M{L3SWROW09? NH;RZ4NKSzVyPUS4MlQh|ryP NXy2S4xsQDd3MkG0OS=>
U87MG NE[3eINMcW6jc3WgZZN{[Xl? MYP+NVAxKM7:TR?= M3\q[mROW09? MWrpcohq[mm2czDFS2ZTKHS7cn;zbY5mKGurbnHz[UBi[3Srdnn0fS=> M4fFOVg4PTJzNEW=
U87MG.ΔEGFR MmTUT4lv[XOnIHHzd4F6 MXr+NVAxKM7:TR?= NIfN[o1FVVOR M4LicYlvcGmkaYTzJGVITlJidInyc5NqdmVia3nuZZNmKGGldHn2bZR6 MWm4O|UzOTR3
U87MG.wtEGFR. NV7Re5N[U2mwYYPlJIF{e2G7 NVf2TIo5hjFyMDFOwG0> M{\4dGROW09? NIK2UXhqdmirYnn0d{BGT0[UIIT5do9{cW6nIHvpcoF{\SCjY4Tpeol1gQ>? NIroOIU5PzV{MUS1
HPV 16-immortalized human keratinocytes MlPFS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? M2D6cJ42OCEQvF2= NEjOW3NFVVOR MorxbY5pcWKrdIOgZ4VtdCCpcn;3eIg> NVrER3F1QTJ6OEe4Ni=>
HPV 16-immortalized human keratinocytes NVXoOGZQTnWwY4Tpc44h[XO|YYm= M4Hyep42OCEQvF2= NYPWO49KTE2VTx?= NYfiblc1cW6mdXPld{BienKnc4SgbY4hfGinIFPlcIwhS3mlbHW= MUG5Nlg5Pzh{
HPV 16-immortalized human keratinocytes NYfocHN[SXCxcITvd4l{KGG|c3H5 NH32XmJ,PTBizszN NEfZNWRFVVOR NFnpdnVqdmS3Y3XzJIFxd3C2b4Ppd{4> MoT4PVI5QDd6Mh?=
A431 MmOwT4lv[XOnIHHzd4F6 NHjsdGl,OTBizszN MonsSG1UVw>? NHzLS3BqdmirYnn0d{B1cGViYnHzZYwh[W6mIGTHSk3PuS2|dHnteYxifGWmIIT5do9{cW6nIIDoc5NxcG:{eXzheIlwdiCxZjD0bIUhTUeIUh?= MWCxNFcxOjJ4Mh?=
MDA-468  NInhPFFMcW6jc3WgZZN{[Xl? M1u0UJ4yOCEQvF2= MWrEUXNQ Mn;abY5pcWKrdIOgeIhmKGKjc3HsJIFv\CCWR1[t{tEue3SrbYXsZZRm\CC2eYLvd4lv\SCyaH;zdIhwenmuYYTpc44hd2ZidHjlJGVITlJ? NFH6e4cyODdyMkK2Ni=>
A431 MYTGeY5kfGmxbjDhd5NigQ>? M1zzWZ4yOCEQvF2= M1nPfGROW09? NEDKdpNqdmS3Y3XzJINmdGxiY4njcIUh[XK{ZYP0 NWrUPJMzOTB5MEKyOlI>
MDA-MB-231 MWjLbY5ie2ViYYPzZZk> NWfCU2NDhjVizszN Ml3USG1UVw>? NWfuSFQ6cW6qaXLpeJMhTUeIIIP0bY12dGG2ZXSgdIhwe3Cqb4L5cIF1cW:wIH;mJGZMUFJ? NHH3fJUyOTB|MEG0Oi=>
CNE2 NUP2bnJUT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M3zYV|ExOCEQvF2= NGfqV3VFVVOR MXXpcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36gZpkhQThwNDW= M3nGXFEyPDFyM{Ky
CNE2 M2rZO2tqdmG|ZTDhd5NigQ>? NHPwO5l,OTByIN88US=> NELHclhFVVOR MX;pcohq[mm2czDFS2ZTKHS7cn;zbY5mKHCqb4PwbI9zgWyjdHnvci=> NVXkZolOOTF2MUCzNlI>
CNE2 MYnGeY5kfGmxbjDhd5NigQ>? NUfwXohjhjFyMDFOwG0> M{PBUWROW09? NWTJcGw4UW6qaXLpeJMhVUGSSzDhcoQhSUuWIHHjeIl3[XSrb36= NVvmdZRLOTF2MUCzNlI>
CNE2 NUHZNFlKTnWwY4Tpc44h[XO|YYm= M2Htbp42OCEQvF2= MUPEUXNQ Ml31ZYZn\WO2czDj[YxtKGO7Y3zlJIRqe3S{aXL1eIlwdg>? MoLmNVE1OTB|MkK=
HSC-2 M2rhUmtqdmG|ZTDhd5NigQ>? NHfZeI05yqEQvF2= MVXEUXNQ NGG1OGRqdmirYnn0d{BxcG:|cHjvdplt[XSrb36gc4YhTUeIUjDhcoQhSWu2 M37nOVE4Pjh7Mki1
HSC-2 M3:ySWFxd3C2b4Ppd{Bie3OjeR?= NXzWT4VbQMLizszN M{THbGROW09? NFX1U4VqdmirYnn0d{BH[XNvbXXkbYF1\WRiYYDvdJRwe2m| MkK1NVc3QDl{OEW=
HEp-2 M{HGXmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NGjMdoZ,OTBizszN MXPEUXNQ Mk[4[Y5p[W6lZYOgc5Jq\G:waX6tbY5lfWOnZDDndo94fGhvaX7obYJqfG:{eR?= NI\rcGYzODJyMke0NS=>
SubG1 NEeySnBCeG:ydH;zbZMh[XO|YYm= MkDtglExKM7:TR?= M17vXWROW09? M3qxcYVvcGGwY3XzJI9zcWSxbnnuMYlv\HWlZXSgZZBweHSxc3nz NWjHVXpCOjB{MEK3OFE>
HEp-2 NUfRNlR[TnWwY4Tpc44h[XO|YYm= NEjRVph,OTBizszN M17MemROW09? NX;wPHg5\W6qYX7j[ZMhV3KrZH;ubY4ucW6mdXPl[EBD[XhiYXP0bZZifGmxbjygRoNtNTJiZHXndoFl[XSrb36gZY5lKFOLUmSxJIlv[WO2aY\heIlwdg>? NW\qSXZSOjB{MEK3OFE>
H508 NYTnSldIT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NXj5PIxNhjFizszN M17EWmROW09? M1nwW41qfGmpYYTld{BEWEZvbXXkbYF1\WRiSEWwPEBk\WyuIHfyc5d1cA>? MnvYNlY2OTR7MkS=

... Click to View More Cell Line Experimental Data

In vivo試験 Administration of AG-1478 blocks phosphorylation of the EGFR at the tumor site and inhibits the growth of A431 xenografts that overexpress the WT EGFR and glioma xenografts expressing the de2-7 EGFR. Even subtherapeutic doses of AG-1478 significantly enhance the efficacy of cytotoxic drugs, with the combination of AG-1478 and temozolomide displaying synergistic antitumor activity against human glioma xenografts. The combination of AG-1478 and an anti-EGFR antibody (mAb 806) displays additive and in some cases synergistic, antitumor activity against tumor xenografts overexpressing the EGFR. [4] The combination of AG-1478 (0.4 mg) with a single dose of 25 μCi 90Y-CHX-A''-DTPA-hu3S193 results in a significant enhancement of efficacy compared with either agent alone. [5]

プロトコル(参考用のみ)

細胞アッセイ:

[2]

+ 展開
  • 細胞株: U87MG
  • 濃度: Dissolved in DMSO, final concentrations ~100 μM
  • 反応時間: 72 hours
  • 実験の流れ:

    Cells are exposed to different concentrations of AG-1478 for 72 hours in 96-well plates. The effects of AG-1478 on cell growth are examined using an Alamar Blue assay. A 20-μL aliquot of Alamar Blue is added to each well, and its absorbance is determined using a Spectromax Scanning Micro plate Reader. The effects of AG-1478 are expressed as percentage of growth inhibition using untreated cells as the control (0% inhibition). Cellular DNA synthesis is determined using a [3H]thymidine incorporation assay.


    (参考用のみ)
動物実験:

[4]

+ 展開
  • 動物モデル: Female BALB/c nu/nu mice inoculated s.c. with A431 or U87MG.Δ2-7 tumor cells
  • 製剤: Dissolved in 100 mM Captisol
  • 投薬量: ~1 mg/kg
  • 投与方法: Injection i.p. three times per week
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 25 mg/mL (79.17 mM)
Ethanol 13 mg/mL (41.17 mM)
Water <1 mg/mL
体内 15% Captisol 30 mg/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 315.75
化学式

C16H14ClN3O2

CAS No. 153436-53-4
保管
in solvent
別名 NSC 693255

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

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

EGFR信号経路図

EGFR Inhibitors with Unique Features

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID