Alectinib (CH5424802)

For research use only. Not for use in humans.

製品コードS2762 別名:AF-802,RG-7853

Alectinib (CH5424802)化学構造

CAS No. 1256580-46-7

Alectinib (CH5424802, AF-802, RG-7853) 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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製品説明 Alectinib (CH5424802, AF-802, RG-7853) 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 MWfLbY5ie2ViYYPzZZk> M1nufp4yKM7:TR?= NXSwNI1ZeHKndnXueJMh[XW2b4Doc5NxcG:{eXzheIlwdiCxZjDBUGs> NUnZO|BCOjF3N{W4OlY>
KARPAS-299 NFrGN|NIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NVT1e2ZlhjFyIN88US=> NGT1eohKSzVyPUOgcm0> NVLkbmEyOjF3N{W4OlY>
SR M2PheGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M4npTJ4yOCEQvF2= NGrCelVKSzVyPU[uPUBvVQ>? NIHMUoozOTV5NUi2Oi=>
HDLM-2 MUfHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NUPGXGJjhjFyIN88US=> MWPJR|UxRjFyLECwNEBvVQ>? NXGzWoh6OjF3N{W4OlY>
NB-1 M1ryfWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M37Q[J4yOCEQvF2= MknJTWM2OD12LkWgcm0> NVfHcFNQOjF3N{W4OlY>
KELLY NXXCT3Q2T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M4LRc54yOCEQvF2= NHHFNohKSzVyPU[yJI5O Mlf5NlE2PzV6Nk[=
SK-N-FI NFLkOVVIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NEO0R2J,OTBizszN MmXtTWM2OD5zMDywNFAhdk1? NXf1Tox2OjF3N{W4OlY>
NCI-H2228 NWHXVIFrT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M3PS[54yOCEQvF2= M4S2RWlEPTB;NUOgcm0> MXSyNVU4PTh4Nh?=
Calu-3 NETkTGFIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MlrVglExKM7:TR?= M37kb2lEPTB;PkGwMFAxOCCwTR?= NVHiWJlZOjF3N{W4OlY>
PC-1 MVfHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NGnrUGJ,OTBizszN NIGzfnZKSzVyPkGwMFAxOCCwTR?= NIrEWZEzOTV5NUi2Oi=>
NCI-H23 NHuxSZpIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MWL+NVAh|ryP NXPhTZh2UUN3ME2zOlAxKG6P M2GxNlIyPTd3OE[2
Calu-1 MkT4S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NXTzWpB[hjFyIN88US=> NFT5cnpKSzVyPkGwMFAxOCCwTR?= M{HNblIyPTd3OE[2
NCI-H2009 M1nwRWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MoK2glExKM7:TR?= MULJR|UxRjFyLECwNEBvVQ>? MWWyNVU4PTh4Nh?=
NCI-H1993 M1GyWWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MojaglExKM7:TR?= NWLZbIdJUUN3ME6xNEwxODBibl2= NVjqdVZCOjF3N{W4OlY>
MKN-45 NYjkV5MzT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NELNTop,OTBizszN MUDJR|UxRjFyLECwNEBvVQ>? NET4UpkzOTV5NUi2Oi=>
SNU-5 NX[xbmxQT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M{j0dp4yOCEQvF2= NEH0S5FKSzVyPUG4NFAhdk1? MlP6NlE2PzV6Nk[=
KATO-III M4jBNGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M1f5UZ4yOCEQvF2= NV7sUmlyUUN3ME23PVAxKG6P NFXkcpczOTV5NUi2Oi=>
SK-BR-3 NIiyTo5Iem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NULqOYJUhjFyIN88US=> MlG0TWM2OD5zMDywNFAhdk1? M1XKSlIyPTd3OE[2
BT-483 NXriSoFWT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NXe0d4I{hjFyIN88US=> MlryTWM2OD5zMDywNFAhdk1? MX2yNVU4PTh4Nh?=
PC-3 MV7Hdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NWjOPYJ3hjFyIN88US=> MmnOTWM2OD5zMDywNFAhdk1? MW[yNVU4PTh4Nh?=
22Rv1 MWjHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NUSyUYtYhjFyIN88US=> MWLJR|UxRjFyLECwNEBvVQ>? NXy4TYk{OjF3N{W4OlY>
U-87 MG M{LwO2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M3HVZ54yOCEQvF2= NWjPblZTUUN3ME6xNEwxODBibl2= NWW0U3B2OjF3N{W4OlY>
H3122 NYDxV|Z4T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M{H0OZ4yOCEQvF2= M37BXGlEPTB;M{Ogcm0> NYqwfpBxOjVyOU[0NFA>
LC-2/ad MX\BdI9xfG:|aYOgZZN{[Xl? M{ToRZ4yKM7:TR?= NHvqWFdFVVOR Mki0bY5lfWOnczDhdI9xfG:|aYO= NXjaPZpYOjV|NEmzNFc>
LC-2/ad NHPpZnJHfW6ldHnvckBie3OjeR?= M1e3NJ4yKM7:TR?= M3zOO2ROW09? MlfabY5pcWKrdIOgeIhmKE2DUFugd4lodmGuaX7nJJBifGi5YYm= MXSyOVM1QTNyNx?=
Ba/F3 MWrGeY5kfGmxbjDhd5NigQ>? MUX+NUDPxE1? NXvKS5BjTE2VTx?= MnHUd5VxeHKnc4Pld{BxcG:|cHjvdplt[XSrb36gc4YhTVKNIHHu[EBqdmO{ZXHz[ZMhfGinIHHieY5l[W6lZTDv[kBDUU1? MnP6NlU{PDl|MEe=
SNU-2535 NWrnRmhJT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= Moq4glExKM7:TR?= M1fxfGlEPTB;M{OuNUBvVQ>? NWnNcoF1OjZ6NEm2N|c>
SNU-2535 MkfDT4lv[XOnIHHzd4F6 Mlq2glEh|ryP MXPpcohq[mm2czD0bIUheGixc4Doc5J6dGG2aX;uJI9nKEGOSzDhcoQhcXS|IHTve45{fHKnYX2gcY9t\WO3bHXzJGVTUzFxMjDhcoQhSUuW M2XtT|I3QDR7NkO3


Methods Test Index PMID
Western blot
pALK / ALK / pAKT / AKT / pERK / ERK / pS6 / S6 ; 

PubMed: 25228534     

Parental H3122 and CHR-A1 cells were treated with alectinib at the indicated concentrations for 6 hrs. Cell extracts were immunoblotted to detect the indicated proteins.

PARP / cleaved PARP / Akt / caspase 3 / Cleaved caspase 3; 

PubMed: 28455243     

Alectinib inhibits PI3K/Akt/mTOR signaling and induces apoptosis in NB cells. NB-19, Kelly, IMR-32, SH-SY5Y, SK-N-AS and LA-N-6 cells were treated with 10 μM alectinib for various time points as indicated. The anti-β-Actin antibody was used as a loading c䲧疝Ỵ疞㧀疜膉痘 瘿⟸෕ᾰƌ

pROS1 / ROS1 / pSTAT3 / STAT3; 

PubMed: 25351743     

Inhibition of phospho-ROS1 by various ALK inhibitors in Ba/F3 models. CD74-ROS1 expressing Ba/F3 cells were exposed to increasing concentrations of crizotinib, ceritinib, AP26113, or ASP3026 for 3 h. Cell lysates were immunoblotted to detect the indicated䲧疝Ỵ疞㧀

p-EGFR Tyr1068 / EGFR / p-HER3 Tyr1222 / HER3 / p-IGF-1R Tyr1135 / IGF-1R; 

PubMed: 26992917     

Cells were treated with indicated drugs for 1 hour; immunoblotting for RTKs in both resistant cell lines showed upregulation of phosphor-EGFR and phosphor-HER3 when compared with parental cells.

25228534 28455243 25351743 26992917
Growth inhibition assay
Cell viability ; 

PubMed: 25228534     

(A) Cells were seeded in 96-well black plates and treated with increasing concentrations of alectinib for 72 hrs. Cell survival was analyzed using the CellTiter-Glo assay. While H3122 cells showed high sensitivity to alectinib (red line), H3122 CHR-A1 cel䲧疝Ỵ疞㧀疜膉痘 瘿�෋ᾰƌ෋à 㺣痖帉痖Ѐ瑖堘𢡄빢᎒෋à鑸᎒彿堙奋堙巫堙᎒ﻺ᎒彿堙ﻮ᎒塚堙ﻺ᎒ꍈ堞빢᎒學堙漸堞圔堙빢᎒圞堙圭堙𢡄玚Wᾰƌ ᾰƌ戤瘯Ɖ⟸෕䐺痖暼瘿⟸෕ᾰƌ

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]


- 合併

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]
- 合併
  • 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.
- 合併
  • 動物モデル: SCID or nude mice bearing NCI-H2228
  • 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

* 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
Storage powder
in solvent
別名 AF-802,RG-7853
Smiles CCC1=CC2=C(C=C1N3CCC(CC3)N4CCOCC4)C(C5=C(C2=O)C6=C(N5)C=C(C=C6)C#N)(C)C


投与量 mg/kg 動物平均体重 g 投与体積(動物毎) ul 動物数
% DMSO % % Tween 80 % ddH2O





質量 (mg) = 濃度 (mM) x 体積 (mL) 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 interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04644315 Not yet recruiting Drug: Alectinib Solid Tumors Hoffmann-La Roche January 4 2021 Phase 2
NCT04111705 Recruiting Drug: Lorlatinib Non Small Cell Lung Cancer Metastatic Intergroupe Francophone de Cancerologie Thoracique August 5 2020 Phase 2
NCT03445000 Recruiting Drug: Alectinib Non-small Cell Lung Cancer|Non-small Cell Lung Cancer Metastatic|Non-small Cell Lung Cancer Recurrent European Thoracic Oncology Platform|Hoffmann-La Roche November 6 2018 Phase 2



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