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) is a selective EGFR inhibitor with IC50 of 3 nM in cell-free assays, almost no activity on HER2-Neu, PDGFR, Trk, Bcr-Abl and InsR.

サイズ 価格(税別)  
JPY 10624.00
JPY 11620.00
JPY 18260.00
JPY 36520.00
JPY 61420.00

カスタマーフィードバック(3)

  • 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.

    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.

  • 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.

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) is a selective EGFR inhibitor with IC50 of 3 nM in cell-free assays, almost no activity on HER2-Neu, PDGFR, Trk, Bcr-Abl and InsR.
ターゲット
EGFR [1]
(Cell-free assay)
3 nM
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
U87MG MUHHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NGrpRVB,OTByIN88US=> MojvSG1UVw>? NX7GR|ZCUUN3ME2zOE43KM7:TR?= NVvxbXJRQDd3MkG0OS=>
U87MG.ΔEGFR M3S5WGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MU\+NVAxKM7:TR?= NInuT5lFVVOR Mnv0TWM2OD16Lkeg{txO M4jGZVg4PTJzNEW=
U87MG.wtEGFR. M2XNTmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NVXMNpZbhjFyMDFOwG0> MYnEUXNQ NVLKOVFHUUN3ME20PE41KM7:TR?= MoDSPFc2OjF2NR?=
U87MG NGfUZpRMcW6jc3WgZZN{[Xl? MVT+NVAxKM7:TR?= M{LJd2ROW09? NHTMXolqdmirYnn0d{BGT0[UIIT5do9{cW6nIHvpcoF{\SCjY4Tpeol1gQ>? MmLhPFc2OjF2NR?=
U87MG.ΔEGFR MXXLbY5ie2ViYYPzZZk> NWLvZpF3hjFyMDFOwG0> MmHGSG1UVw>? Ml63bY5pcWKrdIOgSWdHWiC2eYLvd4lv\SCtaX7hd4Uh[WO2aY\peJk> Mo\jPFc2OjF2NR?=
U87MG.wtEGFR. MWHLbY5ie2ViYYPzZZk> MV7+NVAxKM7:TR?= MofJSG1UVw>? NInGcVNqdmirYnn0d{BGT0[UIIT5do9{cW6nIHvpcoF{\SCjY4Tpeol1gQ>? MUm4O|UzOTR3
HPV 16-immortalized human keratinocytes NVLtWZlDT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NYTFPGFbhjVyIN88US=> NHXMPYlFVVOR M2Gzd4lvcGmkaYTzJINmdGxiZ4Lve5Rp MWm5Nlg5Pzh{
HPV 16-immortalized human keratinocytes MY\GeY5kfGmxbjDhd5NigQ>? NUL0fnpbhjVyIN88US=> MXLEUXNQ M1rPeYlv\HWlZYOgZZJz\XO2IHnuJJRp\SCFZXzsJGN6[2yn NVnJfJlyQTJ6OEe4Ni=>
HPV 16-immortalized human keratinocytes MYjBdI9xfG:|aYOgZZN{[Xl? M1PuR542OCEQvF2= MWDEUXNQ MWjpcoR2[2W|IHHwc5B1d3Orcz6= NEK0elU6Ojh6N{iy
A431 NVnCbJhMU2mwYYPlJIF{e2G7 NYTzS45XhjFyIN88US=> Mmr3SG1UVw>? NHric5RqdmirYnn0d{B1cGViYnHzZYwh[W6mIGTHSk3PuS2|dHnteYxifGWmIIT5do9{cW6nIIDoc5NxcG:{eXzheIlwdiCxZjD0bIUhTUeIUh?= NXHGOGdKOTB5MEKyOlI>
MDA-468  MVrLbY5ie2ViYYPzZZk> MXj+NVAh|ryP NFe3[IxFVVOR NXXNSpZScW6qaXLpeJMhfGinIHLhd4FtKGGwZDDUS2Yu|rFvc4TpcZVt[XSnZDD0fZJwe2mwZTDwbI9{eGixconsZZRqd25ib3[geIhmKEWJRmK= NEjBNI4yODdyMkK2Ni=>
A431 MWDGeY5kfGmxbjDhd5NigQ>? M1XGWJ4yOCEQvF2= NWPCcYtWTE2VTx?= MV7pcoR2[2W|IHPlcIwh[3mlbHWgZZJz\XO2 NWHwOGFjOTB5MEKyOlI>
MDA-MB-231 MXTLbY5ie2ViYYPzZZk> Mke2glUh|ryP MYrEUXNQ NH\HOZpqdmirYnn0d{BGT0Zic4TpcZVt[XSnZDDwbI9{eGixconsZZRqd25ib3[gSmtJWg>? NYG1eWQ1OTFyM{CxOFY>
CNE2 NY[4R2JRT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MVexNFAh|ryP MlTmSG1UVw>? MoDJbY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;uJIJ6KDl6LkSl M1W4RlEyPDFyM{Ky
CNE2 MkP2T4lv[XOnIHHzd4F6 NV;sWmV4hjFyMDFOwG0> MYPEUXNQ MlPmbY5pcWKrdIOgSWdHWiC2eYLvd4lv\SCyaH;zdIhwenmuYYTpc44> MnPSNVE1OTB|MkK=
CNE2 M{H2dWZ2dmO2aX;uJIF{e2G7 MV3+NVAxKM7:TR?= MkDOSG1UVw>? MWLJcohq[mm2czDNRXBMKGGwZDDBT3Qh[WO2aY\heIlwdg>? Ml\hNVE1OTB|MkK=
CNE2 NYe0cZRZTnWwY4Tpc44h[XO|YYm= M{T1Z542OCEQvF2= NGjrcopFVVOR NVnESFN6[W[oZXP0d{Bk\WyuIHP5Z4xmKGSrc4TybYJ2fGmxbh?= MYixNVQyODN{Mh?=
HSC-2 MYPLbY5ie2ViYYPzZZk> MWW4xsDPxE1? NX7VZld7TE2VTx?= NEDGN29qdmirYnn0d{BxcG:|cHjvdplt[XSrb36gc4YhTUeIUjDhcoQhSWu2 MUexO|Y5QTJ6NR?=
HSC-2 MVzBdI9xfG:|aYOgZZN{[Xl? MYq4xsDPxE1? M17Y[2ROW09? MnHLbY5pcWKrdIOgSoF{NW2nZHnheIVlKGGyb4D0c5Nqew>? MnP3NVc3QDl{OEW=
HEp-2 M3vXUmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NFPrfY5,OTBizszN NHXB[W5FVVOR M3Ta[YVvcGGwY3XzJI9zcWSxbnnuMYlv\HWlZXSg[5Jwf3SqLXnubIljcXSxcom= NXO2WZVYOjB{MEK3OFE>
SubG1 NXG3NmVmSXCxcITvd4l{KGG|c3H5 NY\RNopIhjFyIN88US=> NFj4UnZFVVOR MUHlcohidmOnczDvdolld26rbj3pcoR2[2WmIHHwc5B1d3Orcx?= NUXBd4lMOjB{MEK3OFE>
HEp-2 MlrISpVv[3Srb36gZZN{[Xl? NYfnRYJQhjFyIN88US=> Mnm3SG1UVw>? NUfQXJhi\W6qYX7j[ZMhV3KrZH;ubY4ucW6mdXPl[EBD[XhiYXP0bZZifGmxbjygRoNtNTJiZHXndoFl[XSrb36gZY5lKFOLUmSxJIlv[WO2aY\heIlwdg>? Mk\zNlAzODJ5NEG=
H508 NIrHSGVIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NXvHcFJMhjFizszN Ml;QSG1UVw>? M2rOOY1qfGmpYYTld{BEWEZvbXXkbYF1\WRiSEWwPEBk\WyuIHfyc5d1cA>? MXqyOlUyPDl{NB?=

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

体内試験 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]

お薦めの試験操作(参考用のみ)

細胞試験:

[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)
動物試験:

[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 Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
15% Captisol
混合させたのち直ちに使用することを推奨します。
30 mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程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

求めたい質量、体積または濃度を計算してください。

質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    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

貯蔵液を準備するために必要な希釈率を計算してください。Selleck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 ( 入力 出力 )

  • 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

質量 濃度 体積 分子量

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

EGFRシグナル伝達経路

EGFR Inhibitors with Unique Features

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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID