Rociletinib (CO-1686, AVL-301)

製品コードS7284 別名:CNX-419

Rociletinib (CO-1686, AVL-301)化学構造

分子量(MW):555.55

Rociletinib (CO-1686, AVL-301) is an irreversible, mutant-selective EGFR inhibitor with Ki of 21.5 nM and 303.3 nM for EGFRL858R/T790M and EGFRWT in cell-free assays, respectively. Phase 2.

サイズ 価格(税別)  
JPY 49302.00
JPY 161020.00

カスタマーフィードバック(5)

  • Immunohistochemical studies reveal the tumor cells to be negative for chromogranin and synaptophysin pre-rociletinib and positive for both neuroendocrine markers in the post-rociletinib liver biopsy. The results, in conjunction with the morphology, are consistent with the diagnosis of small cell carcinoma in the rociletinib-resistant specimen. H&E, hematoxylin and eosin.

    Cancer Discov, 2015, 5(7): 713-22. Rociletinib (CO-1686, AVL-301) purchased from Selleck.

    Lysates from MGH700 cells treated with DMSO or 1 μmol/L of gefi tinib, afatinib, or rociletinib for 6 hours were probed with the indicated antibodies.

    Cancer Discov, 2015, 5(7): 713-22. Rociletinib (CO-1686, AVL-301) purchased from Selleck.

  • Lysates from MGH121 parental cells treated with 1 μM of the indicated TKIs except for AZD9291 (160 nM) for 6 hours were probed with the indicated antibodies.

    Clin Cancer Res, 2015, 10.1158/1078-0432.CCR-15-0560 . Rociletinib (CO-1686, AVL-301) purchased from Selleck.

    Western blot analysis of H1975 mock and H1975 EGFR cells treated with the indicated concentrations of EGF and rociletinib for phosphorylated (p-) and total (t-) EGFR, AKT, ERK1/2, and b-actin.

    Cancer Res, 2017, 77(8):2078-2089. Rociletinib (CO-1686, AVL-301) purchased from Selleck.

  • Inhibition of the phosphorylation of EGFR and downstream proteins by EGFR-TKIs in BaF3 cells harboring EGFR mutations. The results of immunoblotting for Ba/F3 cells with EGFR exon 19 deletion, L858R, exon 19 deletion+T790M, and L858R+T790M are shown. The cells were treated with the indicated concentrations of EGFR-TKIs for 4 h. Erlotinib, afatinib, osimertinib, and rociletinib were used as EGFR-TKIs. pEGFR, pAKT, and pERK indicate the phosphorylated form of EGFR, AKT, and ERK, respectively. Actin was used as a loading control.

    Oncotarget, 2015, 6(36):38789-803. . Rociletinib (CO-1686, AVL-301) 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 Rociletinib (CO-1686, AVL-301) is an irreversible, mutant-selective EGFR inhibitor with Ki of 21.5 nM and 303.3 nM for EGFRL858R/T790M and EGFRWT in cell-free assays, respectively. Phase 2.
ターゲット
EGFR (L858R/T790M) [1]
(Cell-free assay)
EGFR (wt) [1]
(Cell-free assay)
21.5 nM(Ki) 303.3 nM(Ki)
体外試験

CO-1686 inhibits p-EGFR with IC50 ranging from 62 to 187 nM in the mutant EGFR–expressing cells, while inhibits EGFR phosphorylation with IC50 of > 2,000 nM in the three WT EGFR–expressing cells. CO-1686 selectively inhibits growth of NSCLC cells expressing mutant EGFR with GI50 ranging from 7 to 32 nM, and induces apoptosis. CO-1686–resistant NSCLC cell lines exhibits signs of epithelial-mesenchymal transition and increased sensitivity to AKT inhibitors. [1]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NCI-H1975 MWDLbY5ie2ViYYPzZZk> NEjhNIh,PSEQvF2= NVj6VpZrTE2VTx?= M2LiOolvcGmkaYTzJJBGT0[UIIfpeIghUUN3MDDv[kA3OiCwTR?= MXeyOFA3PTd|MR?=
HCC827 MnfVT4lv[XOnIHHzd4F6 M{HJTZ42KM7:TR?= MX\EUXNQ NIOxS|RqdmirYnn0d{BxTUeIUjD3bZRpKEmFNUCgc4YhOTh5IH7N MnSzNlQxPjV5M{G=
HCC827-EPR MnqyT4lv[XOnIHHzd4F6 NUPhVmlxhjVizszN MoOzSG1UVw>? NWXCcHk2cW6qaXLpeJMheEWJRmKge4l1cCCLQ{WwJI9nKDF6MDDuUS=> NEjGcGMzPDB4NUezNS=>
PC9 MmLnT4lv[XOnIHHzd4F6 NU\p[lk5hjVizszN NGm4SZhFVVOR M1XpeolvcGmkaYTzJJBGT0[UIIfpeIghUUN3MDDv[kAzOTFibl2= Mn\ZNlQxPjV5M{G=
A431 MnP6T4lv[XOnIHHzd4F6 NX3hU2lnhjVizszN NUnseWdqTE2VTx?= NV\hWYIzcW6qaXLpeJMheEWJRmKge4l1cCCLQ{WwJI9nKD52M{OxJI5O NXjHdZpYOjRyNkW3N|E>
NCI-H1299 NV7FelVJU2mwYYPlJIF{e2G7 MYT+OUDPxE1? M{XHXWROW09? MnHFbY5pcWKrdIOgdGVITlJid3n0bEBKSzVyIH;mJF4zODByIH7N M4D1WVI1ODZ3N{Ox
NCI-H358 M2rpV2tqdmG|ZTDhd5NigQ>? NVrac|hlhjVizszN MXjEUXNQ NFy3TJFqdmirYnn0d{BxTUeIUjD3bZRpKEmFNUCgc4YhRjJyMECgcm0> NFyybHgzPDB4NUezNS=>
NCI-H1975 NYH1fW9MT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M{DTWZ42KM7:TR?= M37EfmROW09? NYrPS|V2T0l3ME2zNkBvVQ>? MUmyOFA3PTd|MR?=
HCC827 M2fxc2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MoSyglUh|ryP M3S2TmROW09? MoX1S2k2OD15IH7N M{jNO|I1ODZ3N{Ox
HCC827-EPR MkD4S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NYLhPJl3hjVizszN MnfCSG1UVw>? MonxS2k2OD1{MDDuUS=> NIjofHEzPDB4NUezNS=>
PC9 M{DiZ2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NHjJZXJ,PSEQvF2= NVjhWpYzTE2VTx?= NVTnVoNWT0l3ME2yOkBvVQ>? MUGyOFA3PTd|MR?=
A431 NIfac4JIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NEjsdG5,PSEQvF2= MonUSG1UVw>? MkO1S2k2OD13NEegcm0> MWKyOFA3PTd|MR?=
NCI-H1299 NULGS2wzT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NELQeZB,PSEQvF2= M1:4ZWROW09? NE\lc4NIUTVyPUSyO|Uhdk1? MonFNlQxPjV5M{G=
NCI-H358 M37FNWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NGDxW5F,PSEQvF2= Mk\ySG1UVw>? MlTpS2k2OD1zOEC2JI5O MYqyOFA3PTd|MR?=
PC-9 (exon 19del) MUjHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MoHxglExKM7:TR?= MXTEUXNQ NGLoV3FKSzVyPUi0JI5O MX[yOlUyPTR4NB?=
H3255 (L858R) NES4SmVIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NGPMVmZ,OTBizszN MlvOSG1UVw>? M{XjeGlEPTB;M{Wgcm0> MYSyOlUyPTR4NB?=
PC-9ER (exon 19del+T790M) M{PnVGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MonIglExKM7:TR?= NWTwOpJUTE2VTx?= M3;mdmlEPTB;M{egcm0> M2n4VFI3PTF3NE[0
H1975 (L858R+T790M) MlXzS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MnjPglExKM7:TR?= M4TD[mROW09? NF3PR4FKSzVyPUKzJI5O NFjOblkzPjVzNUS2OC=>
BID007 (A763_Y764insFQEA) NGHKXphIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MWP+NVAh|ryP Mn7tSG1UVw>? M4DqU2lEPTB;MUK3PEBvVQ>? NUjvcopkOjZ3MUW0OlQ>
Ba/F3 (FQEA) MXTHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NYGyTHJ3hjFyIN88US=> NGPhe3ZFVVOR MnjlTWM2OD14N{Ogcm0> NWjHOm9DOjZ3MUW0OlQ>
Ba/F3 (HH) NEfBUI9Iem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MnO3glExKM7:TR?= NEO0WlFFVVOR MYfJR|UxRTF5M{Cgcm0> MVKyOlUyPTR4NB?=
Ba/F3 (ASV) MX7Hdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MWL+NVAh|ryP NGfvSlVFVVOR MXzJR|UxRTV{OUCgcm0> MknpNlY2OTV2NkS=
Ba/F3 (FQEA) Mn;OS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NWDtbHBMhjFyIN88US=> MXjEUXNQ Mn3QTWM2OD1{NkKgcm0> NHjZc5IzPjVzNUS2OC=>

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 CO-1686 causes dose-dependent and significant tumor growth inhibition in all EGFR-mutant models as well as human EGFRL858R- and EGFRL858R/T790M-expressing transgenic mice. [1]

お薦めの試験操作(参考用のみ)

キナーゼ試験:[1]
+ 展開

Inhibition Kinetics Studies:

Recombinant human wild-type and T790M/L858R double mutant EGFR, both Nterminal GST-tagged, are used in the assay. The Omnia continuous read assay is performed as described by the vendor.
細胞試験: [1]
+ 展開
  • 細胞株: NSCLC cell lines expressing mutant EGFR (HCC827, PC9, HCC827-EPR, and NCI-H1975) and cell lines expressing WT EGFR (A431, NCI-H1299, and NCI-H358)
  • 濃度: ~10 μM
  • 反応時間: 72 hours
  • 実験の流れ: Cells are seeded at 3,000 cells per well in growth media supplemented with 5% FBS, 2 mmol/L, L-glutamine, and 1% penicillin–streptomycin, allowed to adhere overnight, and treated with a dilution series of test compounds for 72 hours. Cell viability is determined by CellTiter-Glo, and results are represented as background-subtracted relative light units normalized to a dimethyl sulfoxide (DMSO)–treated control. Growth inhibition (GI 50) values are determined by GraphPad Prism 5.04. MK-2206 and XL-880 compounds are obtained from Selleck Chemical. CI data are generated using CalcuSyn.
    (参考用のみ)
動物試験:[1]
+ 展開
  • 動物モデル: Human EGFRL858R- and EGFRL858R/T790M-expressing transgenic mice.
  • 製剤: DMSO: Solutol HS15: PBS (5:15:80; v:v:v)
  • 投薬量: ~50 mg/kg
  • 投与方法: Oral gavage
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 100 mg/mL (180.0 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):
1% DMSO+30% polyethylene glycol+1% Tween 80
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 555.55
化学式

C27H28F3N7O3

CAS No. 1374640-70-6
保管
in solvent
別名 CNX-419

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
NCT02705339 Withdrawn Carcinoma Non-Small-Cell Lung|Non-Small Cell Lung Cancer|Nonsmall Cell Lung Cancer Washington University School of Medicine|Clovis Oncology Inc. May 2016 Phase 2
NCT02630186 Completed Non-small Cell Lung Cancer Clovis Oncology Inc.|Genentech Inc. January 2016 Phase 1|Phase 2
NCT02580708 Terminated Non-small Cell Lung Cancer Clovis Oncology Inc.|Novartis Pharmaceuticals September 30 2015 Phase 1|Phase 2
NCT02322281 Terminated Non-small Cell Lung Cancer Clovis Oncology Inc. February 2015 Phase 3
NCT02186301 Terminated Non-Small Cell Lung Cancer Clovis Oncology Inc. November 2014 Phase 2|Phase 3
NCT02147990 Active not recruiting Non-small Cell Lung Cancer Clovis Oncology Inc. April 2014 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

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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