Alectinib (CH5424802)

目录号:S2762 别名: AF-802,RG-7853

Alectinib (CH5424802) Chemical Structure

Molecular Weight(MW): 482.62

Alectinib (CH5424802)是一种有效的ALK抑制剂,在无细胞试验中IC50为1.9 nM,对L1196M突变型敏感,对ALK比PF-02341066, NVP-TAE684和PHA-E429选择性高。

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客户使用Selleck该产品发表文献13篇:

客户使用该产品的4个实验数据:

  • 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.

  • 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.

产品安全说明书

ALK抑制剂选择性比较

生物活性

产品描述 Alectinib (CH5424802)是一种有效的ALK抑制剂,在无细胞试验中IC50为1.9 nM,对L1196M突变型敏感,对ALK比PF-02341066, NVP-TAE684和PHA-E429选择性高。
靶点
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
体外研究

CH5424802作用于ALK 为ATP竞争性的,解离常数(KD)为2.4 nM。CH5424802对ALK 和L1196M 具有强大的抑制效果,Ki分别为0.83 和1.56 nM。 CH5424802 作用于表达EML4-ALK的NCI-H2228 NSCLC细胞,抑制ALK自磷酸化。 CH5424802 也抑制STAT3 和AKT,而不是 ERK1/2的磷酸化。CH5424802 完全抑制STAT3在Tyr705位点的磷酸化。CH5424802优先有效作用于表达EML4-ALK的 NCI-H2228细胞,而不作用于融合ALK的阴性 NSCLC细胞系,包括单层培养的HCC827细胞(EGFR外显子19缺失), A549细胞(KRAS突变), 或NCI-H522细胞(EGFR 野生型, KRAS 野生型, 和ALK野生型)。CH5424802作用于 NCI-H2228球体细胞,引起凋亡标记—caspase-3/7样激活。CH5424802抑制含NPM-ALK融合蛋白的两种淋巴瘤细胞, KARPAS-299和SR生长,为不影响不含ALK融合的 HDLM-2淋巴瘤细胞生长。[1] CH5424802 作用于KARPAS-299具有高度靶向选择性和更强的抗增殖活性。CH5424802抑制KAPRAS-299,IC50为3 nM, 抑制KDR, IC50为1.4 μM。CH5424802代谢稳定性很高。[2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NCI-H2228 MojNT4lv[XOnIHHzd4F6 M4raNJ4yKM7:TR?= NITtbFFxemW4ZX70d{BifXSxcHjvd5Bpd3K7bHH0bY9vKG:oIFHMTy=> NVfMPGNkOjF3N{W4OlY>
KARPAS-299 MYHHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MmHaglExKM7:TR?= NEjpVolKSzVyPUOgcm0> NHPSOXkzOTV5NUi2Oi=>
SR NF[5T2RIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= M3fuOJ4yOCEQvF2= NV:yXpFqUUN3ME22Mlkhdk1? MlyzNlE2PzV6Nk[=
HDLM-2 NEm1[3VIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NVPpTWx2hjFyIN88US=> MljsTWM2OD5zMDywNFAhdk1? M2ThUFIyPTd3OE[2
NB-1 MnzJS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NInsT|N,OTBizszN NGW2Uo1KSzVyPUSuOUBvVQ>? MnnHNlE2PzV6Nk[=
KELLY MWPHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MYn+NVAh|ryP MUXJR|UxRTZ{IH7N NE\GO5MzOTV5NUi2Oi=>
SK-N-FI NXXjTnF5T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M2HnO54yOCEQvF2= M1raOGlEPTB-MUCsNFAxKG6P MWqyNVU4PTh4Nh?=
NCI-H2228 M1S0Xmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NHf1UoJ,OTBizszN M2PkPWlEPTB;NUOgcm0> NUXm[FJ{OjF3N{W4OlY>
Calu-3 MWDHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NGDxSlV,OTBizszN M2rXT2lEPTB;PkGwMFAxOCCwTR?= M2rOclIyPTd3OE[2
PC-1 MUjHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MWn+NVAh|ryP NYTPNJFLUUN3ME6xNEwxODBibl2= NYfSdI1HOjF3N{W4OlY>
NCI-H23 MmTRS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MX\+NVAh|ryP MoP1TWM2OD1|NkCwJI5O M2m1OlIyPTd3OE[2
Calu-1 NHjzVFVIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NUjrdlRphjFyIN88US=> MmLnTWM2OD5zMDywNFAhdk1? M2TZRlIyPTd3OE[2
NCI-H2009 M4\zPGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M{XmcJ4yOCEQvF2= NIq4SpVKSzVyPkGwMFAxOCCwTR?= NVvwdlJJOjF3N{W4OlY>
NCI-H1993 M{\zc2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MmjJglExKM7:TR?= NIDpS3ZKSzVyPkGwMFAxOCCwTR?= NUPnSGt5OjF3N{W4OlY>
MKN-45 MkPtS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? M1riUJ4yOCEQvF2= NHfDXmRKSzVyPkGwMFAxOCCwTR?= NX;JOnVIOjF3N{W4OlY>
SNU-5 NI\yNlFIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MWn+NVAh|ryP MWXJR|UxRTF6MECgcm0> MWOyNVU4PTh4Nh?=
KATO-III NYK5OFdKT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= M4DGdJ4yOCEQvF2= M3fNdmlEPTB;N{mwNEBvVQ>? MYiyNVU4PTh4Nh?=
SK-BR-3 M{\DTmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M3[2O54yOCEQvF2= M4LiVWlEPTB-MUCsNFAxKG6P M33ySFIyPTd3OE[2
BT-483 M3rNZmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MYX+NVAh|ryP M3zIUGlEPTB-MUCsNFAxKG6P MmjLNlE2PzV6Nk[=
PC-3 MWjHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MmftglExKM7:TR?= M1fmW2lEPTB-MUCsNFAxKG6P M1XNU|IyPTd3OE[2
22Rv1 MlWzS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MlG4glExKM7:TR?= M17PTWlEPTB-MUCsNFAxKG6P MYqyNVU4PTh4Nh?=
U-87 MG MnXYS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MonLglExKM7:TR?= NHz0SVhKSzVyPkGwMFAxOCCwTR?= M3;tZlIyPTd3OE[2
H3122 M1fWcmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M2fPS54yOCEQvF2= NHLVTpVKSzVyPUOzJI5O NGHNPIgzPTB7NkSwNC=>
LC-2/ad MnnmRZBweHSxc3nzJIF{e2G7 NXvD[|hQhjFizszN M4n2ZWROW09? MkPibY5lfWOnczDhdI9xfG:|aYO= NFPFWXUzPTN2OUOwOy=>
LC-2/ad M2rIcGZ2dmO2aX;uJIF{e2G7 M3qwTZ4yKM7:TR?= MnPPSG1UVw>? MlTRbY5pcWKrdIOgeIhmKE2DUFugd4lodmGuaX7nJJBifGi5YYm= M{jq[FI2OzR7M{C3
Ba/F3 MlzxSpVv[3Srb36gZZN{[Xl? NFnkW2l,OSEQvF2= NHjVT5RFVVOR NV\mXHJGe3WycILld5NmeyCyaH;zdIhwenmuYYTpc44hd2ZiRWLLJIFv\CCrbnPy[YF{\XNidHjlJIFjfW6mYX7j[UBw\iCESV2= NHn3Z4gzPTN2OUOwOy=>
SNU-2535 MYXHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NY\tNI1ohjFyIN88US=> NInNblJKSzVyPUOzMlEhdk1? MVGyOlg1QTZ|Nx?=
SNU-2535 NILuUopMcW6jc3WgZZN{[Xl? NHrMfJp,OSEQvF2= NHHjN49qdmirYnn0d{B1cGVicHjvd5Bpd3K7bHH0bY9vKG:oIFHMT{BidmRiaYTzJIRwf26|dILlZY0hdW:uZXP1cIV{KEWUS{GvNkBidmRiQVvU NUTY[plmOjZ6NEm2N|c>

... Click to View More Cell Line Experimental Data

Assay
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

25228534
体内研究 CH5424802口服处理,抑制肿瘤生长,这种作用存在剂量依赖性,ED50为0.46 mg/kg。CH5424802按20 mg/kg剂量处理,引起肿瘤快速衰退,衰退达168%,处理11天后(在第28天)每个鼠中的肿瘤体积<30 mm3, 维持有效的抗肿瘤效果,且在4周的无药处理期间,不会出现肿瘤再生长。CH5424802 处理小鼠的半衰期和口服生物有效性分别为8.6 小时和 70.8%。按6 mg/kg重复剂量处理,在2,7,和24小时后,平均血浆水平达到1.7,1.5,和0.3 nM。CH5424802处理抑制肿瘤生长。CH5424802按20 mg/kg剂量处理 KARPAS-299 和 NB-1,在第20天,肿瘤生长抑制达 119% 和104%。CH5424802 抑制STAT3磷酸化,这种作用存在剂量依赖性(2-20 mg/kg)。CH5424802处理的移植瘤中,观察到AKT磷酸化部分降低。[1]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:[1]
+ 展开

体外激酶抑制检测:

在CH5424802存在时,通过时间分辨荧光共振能量转移(TR-FRET)分析或荧光偏振(FP)法测量磷酸化各种底物肽的能力,而测评抑制各种激酶(除了MEK1和 Raf-1)的能力。在CH5424802存在时,通过定量分析重组ERK2 蛋白对底物的磷酸化而测评对MEK1的抑制活性。在 CH5424802存在时,通过测定激酶磷酸化MEK1的能力而测评对Raf-1的抑制活性。
细胞实验:[1]
+ 展开
  • Cell lines: NSCLC, A549 和 HCC827 细胞
  • Concentrations: 0-1 μM
  • Incubation Time: 5天
  • Method: NSCLC, A549 和HCC827细胞接种在96孔板中过夜,与不同浓度CH5424802按指定时间温育。球体细胞生长抑制实验中,细胞接种在球板上,温育过夜,然后在指定时间用化合物处理。通过发光细胞活性检测存活细胞。使用Caspase-Glo 3/7 检测试剂盒进行Caspase-3/7检测。
    (Only for Reference)
动物实验:[1]
+ 展开
  • Animal Models: 携带NCI-H2228细胞的 SCID 或裸鼠
  • Formulation: 0.02 N HCl, 10% DMSO, 10% Cremophor EL, 15% PEG400, 和 15% HPCD (2 - 羟丙基-β-环糊精)
  • Dosages: 20 mg/kg
  • Administration: 口服处理
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 0.5 mg/mL warmed (1.03 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
30% PEG400+0.5% Tween80+5% propylene glycol
30 mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 482.62
化学式

C30H34N4O2

CAS号 1256580-46-7
储存条件 powder
in solvent
别名 AF-802,RG-7853

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03737994 Not yet recruiting ALK Gene Rearrangement|ALK Positive|Lung Non-Squamous Non-Small Cell Carcinoma|Stage IV Lung Cancer AJCC v8|Stage IVA Lung Cancer AJCC v8|Stage IVB Lung Cancer AJCC v8 National Cancer Institute (NCI) April 1 2019 Phase 2
NCT03737994 Not yet recruiting ALK Gene Rearrangement|ALK Positive|Lung Non-Squamous Non-Small Cell Carcinoma|Stage IV Lung Cancer AJCC v8|Stage IVA Lung Cancer AJCC v8|Stage IVB Lung Cancer AJCC v8 National Cancer Institute (NCI) April 1 2019 Phase 2
NCT03779191 Not yet recruiting ALK Gene Rearrangement Positive|Non-Squamous Non-Small Cell Neoplasm of Lung Instituto Nacional de Cancerologia de Mexico|Roche Pharma AG March 20 2019 Phase 2
NCT03779191 Not yet recruiting ALK Gene Rearrangement Positive|Non-Squamous Non-Small Cell Neoplasm of Lung Instituto Nacional de Cancerologia de Mexico|Roche Pharma AG March 20 2019 Phase 2
NCT03596866 Not yet recruiting ALK-positive Advanced NSCLC Ariad Pharmaceuticals|Takeda February 15 2019 Phase 3
NCT03596866 Not yet recruiting ALK-positive Advanced NSCLC Ariad Pharmaceuticals|Takeda February 15 2019 Phase 3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID