Alectinib (CH5424802)

製品コードS2762 別名:AF-802,RG-7853

Alectinib (CH5424802)化学構造


Alectinib (CH5424802) is a potent ALK inhibitor with IC50 of 1.9 nM in cell-free assays, sensitive to L1196M mutation and higher selectivity for ALK than PF-02341066, NVP-TAE684 and PHA-E429.

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  • Immunoblot analysis of full-length DCTN1-ALK proteins. An expression vector encoding DCTN1-ALK cDNA was introduced into H1299 lung cancer cells, which do not express endogenous ALK. The transfectants were then exposed to crizotinib and alectinib. Levels of phosphorylation at tyrosine 1604 were determined 24 hours after treatment with 0, 0.2, 1.0, or 5.0 μM of each drug.

    Oncologist, 2017, 22(2):158-164. Alectinib (CH5424802) purchased from Selleck.

    Sensitivity of the H3122 cell line to ALK inhibitors (crizotinib and alectinib). To examine the sensitivity of ALK inhibitors, used an MTT assay. The experiment was performed in triplicate. (A) Growth inhibitory effect of crizotinib. The H3122 cell line was sensitive to crizotinib under a normoxic state, compared with a hypoxic state. The graphs, mean of independent triplicate experiments; error bars, SD. (B) IC50 of ALK inhibitors. The IC50 values of both inhibitors in the H3122 cell lines were significantly higher under hypoxia than under normoxia (crizotinib, *P=0.028 and alectinib, *P=0.0035). *P<0.05.

    Int J Oncol 2014 45(4), 1430-6. Alectinib (CH5424802) purchased from Selleck.

  • Western blotting data of NPM/ALK-transformed BaF3 cells, both wild-type and L1196M-mutant, treated with CH5424802 for 4 hours. The blot shows phospho-ALK signal (Y1604), as an indicator of NPM/ALK activation.

    Prof. Gambacorti from Università degli Studi di Milano Bicocc. Alectinib (CH5424802) purchased from Selleck.

    Cell growth data, performed by tritiated thymidine uptake assay, using NPM/ALK wild-type -transformed BaF3 cells.CH5424802 demonstrated a very good ability to block NPM/ALK-transformed BaF3 cells proliferation with an IC50 of 3 nM.

    Prof. Gambacorti from Università degli Studi di Milano Bicocc. Alectinib (CH5424802) purchased from Selleck.




製品説明 Alectinib (CH5424802) is a potent ALK inhibitor with IC50 of 1.9 nM in cell-free assays, sensitive to L1196M mutation and higher selectivity for ALK than PF-02341066, NVP-TAE684 and PHA-E429.
ALK (F1174L) [1]
(Cell-free assay)
ALK [1]
(Cell-free assay)
ALK (R1275Q) [1]
(Cell-free assay)
1 nM 1.9 nM 3.5 nM

The dissociation constant (KD) value of CH5424802 for ALK in an ATP-competitive manner is 2.4 nM. CH5424802 has substantial inhibitory potency against both native ALK and L1196M with Ki of 0.83 nM and 1.56 nM, respectively. CH5424802 prevents autophosphorylation of ALK in NCI-H2228 NSCLC cells expressing EML4-ALK. CH5424802 also suppresses the phosphorylation of STAT3 and AKT, but not of ERK1/2. CH5424802 completely inhibits the phosphorylation of STAT3 at Tyr705. CH5424802 is preferentially efficacious against NCI-H2228 cells expressing EML4-ALK, but not ALK fusion-negative NSCLC cell lines, including HCC827 cells (EGFR exon 19 deletion), A549 cells (KRAS mutant), or NCI-H522 cells (EGFR wild-type, KRAS wild-type, and ALK wild-type) in monolayer culture. CH5424802 elicits an apoptotic marker—caspase-3/7-like activation—in NCI-H2228 spheroid cells. CH5424802 blocks the growth of two lymphoma lines, KARPAS-299 and SR, with NPM-ALK fusion protein but does not influence the growth of an HDLM-2 lymphoma line without ALK fusion. [1] CH5424802 displays high target selectivity and the stronger anti-proliferative activity against KARPAS-299. CH5424802 inhibits KAPRAS-299 with an IC50 of 3 nM, and KDR with IC50 of 1.4 μM. The metabolic stability of CH5424802 is very high.[2]

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NCI-H2228 MX;LbY5ie2ViYYPzZZk> NGHJWFB,OSEQvF2= NGXBR4pxemW4ZX70d{BifXSxcHjvd5Bpd3K7bHH0bY9vKG:oIFHMTy=> Mlf6NlE2PzV6Nk[=
KARPAS-299 M{X4Rmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NXu0UplshjFyIN88US=> NGLScnZKSzVyPUOgcm0> M3TtcFIyPTd3OE[2
SR NWSwdo5kT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NEj6Tml,OTBizszN MVXJR|UxRTZwOTDuUS=> MmjhNlE2PzV6Nk[=
HDLM-2 NHj5NHlIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MV;+NVAh|ryP NHLvXW9KSzVyPkGwMFAxOCCwTR?= NXXuPZBmOjF3N{W4OlY>
NB-1 M{fjfWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NGOxTXd,OTBizszN MYTJR|UxRTRwNTDuUS=> NInEV5QzOTV5NUi2Oi=>
KELLY M1LuWWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MlvrglExKM7:TR?= NIDw[HBKSzVyPU[yJI5O MnSwNlE2PzV6Nk[=
NCI-H2228 NFnUbWtIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NG\x[Yh,OTBizszN NImyUpNKSzVyPUWzJI5O NHryWGQzOTV5NUi2Oi=>
Calu-3 NHjjXpJIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= Ml3xglExKM7:TR?= M3nmUGlEPTB;PkGwMFAxOCCwTR?= M3u0TlIyPTd3OE[2
PC-1 NHHzWlNIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NIj0eJh,OTBizszN MWnJR|UxRjFyLECwNEBvVQ>? MkP4NlE2PzV6Nk[=
NCI-H23 M{LaVmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 Mlz6glExKM7:TR?= NEDD[VZKSzVyPUO2NFAhdk1? Mlq5NlE2PzV6Nk[=
Calu-1 NX7YeFJYT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MkDFglExKM7:TR?= MnnpTWM2OD5zMDywNFAhdk1? NH2zdXUzOTV5NUi2Oi=>
NCI-H2009 M2DtdWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MmjlglExKM7:TR?= M17yWmlEPTB-MUCsNFAxKG6P NFjiWVYzOTV5NUi2Oi=>
NCI-H1993 NVvjR2prT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MWD+NVAh|ryP NYS3ZpdjUUN3ME6xNEwxODBibl2= NXuydHlyOjF3N{W4OlY>
MKN-45 MoP1S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NGXmVmp,OTBizszN NVftW5d5UUN3ME6xNEwxODBibl2= NVHkUHd[OjF3N{W4OlY>
SNU-5 MoLoS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? M1jtSJ4yOCEQvF2= NEDjbXhKSzVyPUG4NFAhdk1? MV:yNVU4PTh4Nh?=
KATO-III NYW5XHBNT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M2nUbZ4yOCEQvF2= NIXiZ2xKSzVyPUe5NFAhdk1? M4foSFIyPTd3OE[2
SK-BR-3 MXTHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? Mlf2glExKM7:TR?= NVXuWVJ4UUN3ME6xNEwxODBibl2= MUeyNVU4PTh4Nh?=
BT-483 NH;MeFJIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NEi4TFV,OTBizszN NXOwXo1EUUN3ME6xNEwxODBibl2= MX[yNVU4PTh4Nh?=
PC-3 NFLGWFRIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= M1TZTp4yOCEQvF2= NXXMWGxbUUN3ME6xNEwxODBibl2= MXGyNVU4PTh4Nh?=
22Rv1 MUHHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MUn+NVAh|ryP NV\wN3NMUUN3ME6xNEwxODBibl2= MnPoNlE2PzV6Nk[=
U-87 MG NEH2UJZIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NEnibol,OTBizszN M{fq[GlEPTB-MUCsNFAxKG6P NH;NPZczOTV5NUi2Oi=>
H3122 M170bmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MkDzglExKM7:TR?= MV3JR|UxRTN|IH7N NFPIWY4zPTB7NkSwNC=>
LC-2/ad MYHBdI9xfG:|aYOgZZN{[Xl? NGfHUXF,OSEQvF2= MUHEUXNQ MUjpcoR2[2W|IHHwc5B1d3Orcx?= NU\IZlMzOjV|NEmzNFc>
LC-2/ad MXrGeY5kfGmxbjDhd5NigQ>? NUjYXFk1hjFizszN NEDwWIpFVVOR M13ENIlvcGmkaYTzJJRp\SCPQWDLJJNq\26jbHnu[{Bx[XSqd3H5 NWPKWIkyOjV|NEmzNFc>
Ba/F3 MYPGeY5kfGmxbjDhd5NigQ>? MnrzglEh|ryP MlrGSG1UVw>? NXjvRYh7e3WycILld5NmeyCyaH;zdIhwenmuYYTpc44hd2ZiRWLLJIFv\CCrbnPy[YF{\XNidHjlJIFjfW6mYX7j[UBw\iCESV2= MmDENlU{PDl|MEe=
SNU-2535 MVXHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MoKxglExKM7:TR?= Mk[2TWM2OD1|Mz6xJI5O NWXPbWhvOjZ6NEm2N|c>
SNU-2535 MVLLbY5ie2ViYYPzZZk> MlnkglEh|ryP M1XvVolvcGmkaYTzJJRp\SCyaH;zdIhwenmuYYTpc44hd2ZiQVzLJIFv\CCrdIOg[I94dnO2cnXhcUBud2ynY4Xs[ZMhTVKNMT:yJIFv\CCDS2S= NV3Dd2FVOjZ6NEm2N|c>


体内試験 Oral administration of CH5424802 dose-dependently inhibits tumor growth with an ED50 of 0.46 mg/kg and tumor regression. Treatment of 20 mg/kg CH5424802 reveals rapid tumor regression by 168%, the tumor volume in any mouse is <30 mm3 after 11 days of treatment (at day 28), a potent antitumor effect is maintained, and tumor regrowth does not occur throughout the 4-week drug-free period. The half-life and the oral bioavailability of CH5424802 in mice are 8.6 hours and 70.8%, respectively. At a repeated dose of 6 mg/kg, the mean plasma levels reached 1.7, 1.5, and 0.3 nM at 2, 7, and 24 hours post-dose, respectively. Administration of CH5424802 leads to tumor growth prevention and tumor regression. Tumor growth inhibition at 20 mg/kg is 119% for KARPAS-299 and 104% for NB-1 on day 20. CH5424802 inhibits the phosphorylation of STAT3 in a dose-dependent manner (2–20 mg/kg). A partial decrease in AKT phosphorylation is also observed in CH5424802-treated xenograft tumors. [1]


+ 展開

Kinase inhibitory assays in Vitro:

The inhibitory ability against each kinase except for MEK1 and Raf-1 is evaluated by examining their ability to phosphorylate various substrate peptides in the presence of CH5424802 using time-resolved fluorescence resonance energy transfer (TR-FRET) assay or fluorescence polarization (FP) assay. The inhibitory activity against MEK1 is evaluated by quantitative analysis of the phosphorylation of a substrate peptide by a recombinant ERK2 protein in the presence of CH5424802. The inhibitory activity against Raf-1 is evaluated by examining the ability of the kinases to phosphorylate MEK1 in the presence of CH5424802.
細胞試験: [1]
+ 展開
  • 細胞株: NSCLC, A549 and HCC827 cell lines
  • 濃度: 0-1 μM
  • 反応時間: 5 days
  • 実験の流れ: Cells including NSCLC, A549 and HCC827 are seeded in 96-well plates overnight and incubated with various concentrations of CH5424802 for the indicated time. For spheroid cell growth inhibition assay, cells are seeded on spheroid plates, incubated overnight, and then treated with compound for the indicated times. The viable cells are measured by the Luminescent Cell Viability Assay. Caspase-3/7 assay is evaluated using the Caspase-Glo 3/7 Assay Kit.
+ 展開
  • 動物モデル: SCID or nude mice bearing NCI-H2228
  • 製剤: 0.02 N HCl, 10% DMSO, 10% Cremophor EL, 15% PEG400, and 15% HPCD (2-hydroxypropyl-β-cyclodextrin)
  • 投薬量: 20 mg/kg
  • 投与方法: Oral administration

溶解度 (25°C)

体外 DMSO 0.5 mg/mL (1.03 mM) warming
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):
30% PEG400+0.5% Tween80+5% propylene glycol
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。


分子量 482.62


CAS No. 1256580-46-7
in solvent
別名 AF-802,RG-7853





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


  • 質量





開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1



  • 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):




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


質量 濃度 体積 分子量


NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02314481 Not yet recruiting Non-small Cell Lung Cancer University College, London|Hoffmann-La Roche January 2017 Phase 2
NCT02838420 Recruiting Anaplastic Lymphoma Kinase-positive Non-small Cell Lung Cancer Hoffmann-La Roche August 2016 Phase 3
NCT02621047 Recruiting Hepatic Impairment Hoffmann-La Roche December 2015 Phase 1
NCT02604342 Recruiting Anaplastic Lymphoma Kinase-positive Non-small Cell Lung Cancer Hoffmann-La Roche November 2015 Phase 3
NCT02521051 Recruiting Non-Small Cell Lung Cancer (NSCLC) Massachusetts General Hospital|Genentech, Inc. October 2015 Phase 1|Phase 2
NCT02271139 Completed Non-Small Cell Lung Cancer Genentech, Inc. December 2014 --



Handling Instructions


  • * 必須


ALK 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