Afatinib (BIBW2992) Dimaleate

製品コードS7810

Afatinib (BIBW2992) Dimaleate化学構造

分子量(MW):717.18

Afatinib (BIBW2992) Dimaleate irreversibly inhibits EGFR/HER2 including EGFR(wt), EGFR(L858R), EGFR(L858R/T790M) and HER2 with IC50 of 0.5 nM, 0.4 nM, 10 nM and 14 nM, respectively; 100-fold more active against Gefitinib-resistant L858R-T790M EGFR mutant.

サイズ 価格(税別)  
JPY 16102.00
JPY 21082.00
JPY 42662.00

文献中Selleckの製品使用例(30)

カスタマーフィードバック(4)

  • (F) Stably transduced MCF10A cells were treated with the indicated drugs at 100 nM for 4 h in EGF- and serum-free media. Cell lysates were subjected to immunoblot analyses with the indicated antibodies.

    Cancer Discov, 2017, 7(6):575-585. Afatinib (BIBW2992) Dimaleate purchased from Selleck.

    Immunoblotting of lysates from EGFR L858R and EGFR L858M/L861Q NIH-3T3 cells treated with the indicated concentrations of gefitinib, osimertinib, or afatinib. The ratio of phospho-EGFR in treated vs. untreated samples was quantified by densitometry for each cell line.

    J Thorac Oncol, 2017, 12(5):884-889. Afatinib (BIBW2992) Dimaleate purchased from Selleck.

  • Inhibition of signaling pathway activation in lung tumor cell lines by kinase inhibitors. Lung tumor cells were cultured in 10% FBS until reaching ∼80% confluence and then the cells were starved in serum-free medium for overnight, followed by 4-hour treatment with the inhibitors. Cell lysates were then prepared and used for determination of the pathway activation signals by the CEER assay.

    Int J Proteomics 2011 215496. Afatinib (BIBW2992) Dimaleate purchased from Selleck.

    Inhibition of anchorage-independent growth of lung tumor cell lines by selected inhibitors. Each selected cell line was treated with the indicated inhibitor at 0.1 μM and 1 μM concentrations for two weeks and cell colony size formation was scored under the Nikon inverted-phase microscope.

    Int J Proteomics 2011 215496. Afatinib (BIBW2992) Dimaleate 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 Afatinib (BIBW2992) Dimaleate irreversibly inhibits EGFR/HER2 including EGFR(wt), EGFR(L858R), EGFR(L858R/T790M) and HER2 with IC50 of 0.5 nM, 0.4 nM, 10 nM and 14 nM, respectively; 100-fold more active against Gefitinib-resistant L858R-T790M EGFR mutant.
ターゲット
EGFR (L858R) [1]
(Cell-free assay)
EGFR (wt) [1]
(Cell-free assay)
EGFR (L858R/T790M) [1]
(Cell-free assay)
HER2 [1]
(Cell-free assay)
0.4 nM 0.5 nM 10 nM 14 nM
体外試験

BIBW2992 is more effective than erlotinib, gefitinib, or lapatinib in inhibiting survival of lung cancer cell lines harboring wild-type (H1666) or L858R/T790M (NCI-H1975) EGFR. BIBW2992 is similarly effective against NSCLC lines expressing HER2 776insV (NCI-H1781) or EGFR E746_A750del (HCC827), but shows no activity toward A549 cells, which express wild-type EGFR and HER2.[1] Afatinib enhances cytotoxicity of topotecan and mitoxantrone to SP cells, and increases the apoptosis induced by topotecan and mitoxantrone in SP cells.[2]

体内試験 In the MDA-MB-453 xenograft model, BIBW2992 (20 mg/kg, p.o.) results in dramatic tumor regression with a cumulative treated/control tumor volume ratio (T/C ratio) of 2%, and downregulation of EGFR and AKT phosphorylation.[1] In A7, A431, FaDu, UT-SCC-14 and UT-SCC-15 xenograft models, application of BIBW 2992 (30 mg/kg, p.o.) leads to a significant prolongation of tumour growth time.[3] In HER2-amplified xenograft medel, Afatinib (30 mg/kg, p.o.) results a markedly inhibition in tumor growth and a significant improvement in the duration of overall survival.[4] In HER2-positive gastric cancer NCI-N87 xenograft, afatinib (25 mg/kg, p.o.) leads to dramatic tumor volume regression within 4 d and near-complete tumor resolution after 21 d of treatment.[5]

お薦めの試験操作(参考用のみ)

キナーゼ試験:[1]
+ 展開

In vitro kinase activity assay:

EGFR kinase: Each 100 µL enzyme reaction contained 10 μL of inhibitor in 50% Me2SO, 20 μL of substrate solution (200 mM HEPES pH 7.4, 50 mM Mg-acetate, 2.5 mg/mL poly (EY), 5 μg/mL bio-pEY) and 20 µL enzyme preparation. The enzymatic reaction is started by addition of 50 µL of a 100 µM ATP solution made in 10 mM MgCl2. Assays are carried out at room temperature for 30 min and terminated by the addition of 50 µL of stop solution (250 mM EDTA in 20 mM HEPES pH 7.4). 100 µL are transferred to a streptavidin coated microtiterplate, after an incubation time of 60 min at room temperature the plate is washed with 200 µL of wash solution (50 mM Tris, 0.05% Tween20). A 100 µL aliquot of a HRPO- labeled anti-PY antibody (PY20H Anti-Ptyr:HRP ) 250 ng/mL are added to the wells. After 60 min of incubation, the plate is washed three times with a 200 µL wash solution. The samples are then developed with a 100µL TMB Peroxidase Solution (A:B= 1:1). The reaction is stopped after 10 min. The plate is transferred to an ELISA reader and extinction is measured at OD450nm. HER2-IC enzyme: Enzyme activity is assayed in the presence or absence of serial inhibitor dilutions performed in 50 % Me2SO. Each 100 µL reaction contains similar components as described for EGFR kinase assay with addition of 1000 µM Na3VO4. The enzymatic reaction is started by addition of 50µL of 500 µM ATP solution made in 10 mM Mg-acetate. The dilution of the enzyme is set so that incorporation of phosphate into bio-pEY is linear with respect to time and amount of enzyme. The enzyme preparation is diluted in 20 mM HEPES pH 7.4, 130 mM NaCl, 0.05% Triton X-100, 1 mM DTT and 10% glycerol. Assays are carried out at room temperature for 30 min and terminated by the addition of 50 µL of stop solution. Src kinase assays: Each 100 µL reaction contained 10 µL of inhibitor in 50 % Me2SO, 20µL of enzyme preparation, 20 µL of substrate solution supplemented with 1000 µM Na3VO4. The enzymatic reaction is started by addition of 50 µL of a 1000 µM ATP solution made in 10 mM Mg-acetate. BIRK kinase assay: 250 mM Tris pH 7.4, 10mM DTT, 2.5 mg/mL poly(EY), 5 mg/mL bio-pEY is used as substrate solution and enzymatic reaction is started by addition of 50 µL of a 2 mM ATP solution made in 8 mM MnCl2, 20 mM Mg-acetate. VEGF2 and HGFR kinase assays: Assays are carried out at room temperature for 20 minutes and terminated by the addition of 10 µL of 5 % H3PO4. The precipitate is then trapped onto GF/B filters using a 96 well filter mate universal harvester. After extensive washing the filter plate is dried for 1 h at 50°C, sealed and incorporated radioactivity is determined by scintillation counting using a TopCount™ or a Microbeta b counter™.
細胞試験: [2]
+ 展開
  • 細胞株: SP and NSP cell lines
  • 濃度: 1 μM
  • 反応時間: 48 h
  • 実験の流れ: Cytotoxicity is determined using MTT assay. The IC 50 value is defined as the drug concentration resulting in 50% cell death. Both the fitted sigmoidal dose response curve and IC50 are calculated by Bliss method.
    (参考用のみ)
動物試験:[4]
+ 展開
  • 動物モデル: SCID mice harbouring ARK2 xenografts
  • 製剤: DMSO
  • 投薬量: 25 mg/kg
  • 投与方法: p.o.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 100 mg/mL (139.43 mM)
Water Insoluble
Ethanol 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):
5% DMSO+30% PEG 300+ddH2O
混合させたのち直ちに使用することを推奨します。
28mg/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 717.18
化学式

C24H25ClFN5O3.2C4H4O4

CAS No. 850140-73-7
保管
in solvent
別名 N/A

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

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03727724 Not yet recruiting Carcinoma Non-Small-Cell Lung The Netherlands Cancer Institute|Boehringer Ingelheim|Merck Serono International SA November 2018 Phase 2
NCT03695510 Not yet recruiting Head and Neck Neoplasms National Taiwan University Hospital November 2018 Phase 2
NCT03652233 Not yet recruiting Recurrent Squamous Cell Carcinoma of the Head or Neck|Platinum- and Cetuximab-Refractory Squamous Cell Carcinoma of the Head or Neck|Metastatic Squamous Cell Carcinoma of the Head or Neck|Squamous Cell Carcinoma Vanderbilt-Ingram Cancer Center|National Comprehensive Cancer Network|Boehringer Ingelheim November 2018 Phase 1
NCT03711422 Not yet recruiting Non-small Cell Lung Cancer|Leptomeningeal Disease|Central Nervous System Metastases National Cancer Centre Singapore October 2018 Phase 1
NCT03574402 Not yet recruiting Carcinoma Non-Small-Cell Lung Guangdong Association of Clinical Trials July 1 2018 Phase 2
NCT03083678 Recruiting Chordoma Leiden University Medical Center|Chordoma Foundation|Boehringer Ingelheim June 21 2018 Phase 2

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

相関EGFR製品

Tags: Afatinib (BIBW2992) Dimaleateを買う | Afatinib (BIBW2992) Dimaleate ic50 | Afatinib (BIBW2992) Dimaleate供給者 | Afatinib (BIBW2992) Dimaleateを購入する | Afatinib (BIBW2992) Dimaleate費用 | Afatinib (BIBW2992) Dimaleate生産者 | オーダーAfatinib (BIBW2992) Dimaleate | Afatinib (BIBW2992) Dimaleate化学構造 | Afatinib (BIBW2992) Dimaleate分子量 | Afatinib (BIBW2992) Dimaleate代理店
×

平素は、格別のご愛顧を賜り厚く御礼申し上げます。
誠に勝手ながら、弊社では下記の期間を年末年始による休業とさせていただきます。
【休業期間】
2018年12月29日(土)から2019年1月6日(日)
休業期間中にいただきましたお問合せ等につきましては、2019年1月7日(月)以降の対応とさせていただきます。また、年内の出荷業務は2018年12月26日(水)までとさせていただきます。
ご不便をお掛けいたしますが、ご了承のほど何卒よろしくお願いいたします。

×
細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID