AZD6738

目录号：S7693

Molecular Weight(MW): 412.51

AZD6738是一种口服具有活性的，选择性 ATR 激酶抑制剂，IC50 为 1 nM。Phase 1/2。

规格

价格

库存

购买数量

5mg	RMB 1615.57	现货
25mg	RMB 5700.55	现货
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客户使用Selleck该产品发表文献9篇：

Nature, 2019, 10.1038/s41586-019-1607-3

PubMed: 31578521 ( click the link to review the publication )

Cancer Cell, 2017, 32(5):624-638

PubMed: 29056426 ( click the link to review the publication )

Cell Rep, 2019, 26(6):1518-1532

PubMed: 30726735 ( click the link to review the publication )

Clin Cancer Res, 2018, 10.1158/1078-0432.CCR-18-1346

PubMed: 30087144 ( click the link to review the publication )

J Exp Clin Cancer Res, 2018, 37(1):205

PubMed: 30157958 ( click the link to review the publication )

Am J Cancer Res, 2018, 8(7):1307-1316

PubMed: 30094103 ( click the link to review the publication )

Radiat Oncol, 2018, 13(1):76

PubMed: 29685176 ( click the link to review the publication )

Sci Rep, 2017, 7:41950

PubMed: 28176818 ( click the link to review the publication )

J Dermatol Sci, 2016, 84(3):239-247

PubMed: 27743911 ( click the link to review the publication )

客户使用该产品的4个实验数据：

Number of γH2AX foci per cell of irradiated (2 Gy) SAS cells treated with inhibitors against ATM (ATMi, KU55933), DNA-PK (DNA-PKi, KU57788), or ATR (ATRi, AZD6738) with or without LY364947.

Clin Cancer Res, 2018, doi:10.1158/1078-0432.CCR-18-1346. AZD6738 purchased from Selleck.

Histograms showing the analysis results of RPMI8226 (transfection with control shRNA or HMGB1 shRNA) apoptosis induced by Dex (100 μM) in presence of AZD6738 (2 μM, an ATR inhibitor) (*P<0.05,**P<0.01,***P<0.001)

J Exp Clin Cancer Res, 2018, 37(1):205. AZD6738 purchased from Selleck.
AZD6738 (AZD) synergizes with cytarabine (ara-C) to induce apoptosis and proliferation inhibition in AML cells. (a) OCI-AML3 cells were treated with cytarabine and AZD6738, alone or in combination, for 24 h and then subjected to annexin V-FITC/PI staining and flow cytometry analyses. CI values were calculated using CompuSyn software. Combined drug treatments were compared to single drug treatment using 1-way ANOVA with Bonferroni post hoc test. ***indicates p < 0.001. (b and c) OCI-AML3 cells were treated with cytarabine and AZD-6738, alone or in combination, for 24 h. Whole cell lysates were subjected to Western blotting and probed with the indicated antibodies.

Sci Rep, 2017, 7:41950. AZD6738 purchased from Selleck.

MyLa2000 cells were irradiated with UVA at dose 1.6 J/cm2. Kinase inhibitors were added at the following concentrations: 10 μM VE-821, 1 μM VE-822, 1.6 μM Chir-124, 1 μM AZD6738, 1 μM MK8776 (selected basing on toxicity studies performed previously; data not shown) 30 minutes before irradiation (30 min before UVA), immediately before irradiation (0 min before UVA) or immediately after irradiation (0 min after UVA). Cell viability was analyzed 48 hours after treatment by PI exclusion assay.

J Dermatol Sci, 2016, 84(3):239-247. AZD6738 purchased from Selleck.

产品安全说明书

ATM/ATR抑制剂选择性比较

生物活性

产品描述

AZD6738是一种口服具有活性的，选择性 ATR 激酶抑制剂，IC50 为 1 nM。Phase 1/2。

靶点

ATR ^[1]
(Cell-free assay)

1 nM

体外研究

在四个Kras突变细胞系：H23，H460，A549，和H358中，AZD6738抑制ATR激酶活性，并损害细胞活性。在ATM缺失的H23细胞中，AZD6738强烈增强顺铂诱导快速细胞死亡的作用。^[1]在p53 或 ATM缺失的细胞中，AZD6738治疗引起复制叉停滞和未修复DNA损伤的积累，导致有丝分裂障碍，从而使细胞死亡。^[2]

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Activity Description	PMID
LICR-LON-HN4 and LICR-LON-HN5 cells	Mo\qSpVv[3Srb36gZZN{[Xl?	MnvJNE4xOyxiMD6xMEAxNjNuIEGsJFMtKDFyIN88US=>		MnrxRXpFPjd\|ODDpcohq[mm2aX;uJI9nKEGWUjD0bJJwfWeqIHzvd5Mhd2ZiZH;3cpN1emWjbTDwbI9{eGixconsZZRqd25ib3[gR2hMOSCxbjDT[ZI{PDVw	MVizNFA2Pzh7MB?=
K8484 cells	NYnyZnNNTnWwY4Tpc44h[XO\|YYm=	M1v2VFIh\|ryP	NVXKSmFUPyCqb4Xydy=>	MnnxTY4hUzh2OESgZ4VtdHNuIFHaSFY4OzhiYYSgNkDDvU1iY3;tdIxmfGWueTDwdoV3\W62ZXSg[4Vu[2m2YXLpcoUucW6mdXPl[EBEcGtzIIDoc5NxcG:{eXzheIlwdiCxbjDT[ZJqdmViM{S1MEB1cGViZH;3cpN1emWjbTDBWHIhfGG{Z3X0Mi=>	MoXNNlk5QTF2OEi=
SNU-601 cells	Ml\DR4VtdCCpcn;3eIghcW6qaXLpeIlwdiCjc4PhfS=>	NHrxWGQxNTFizsztc4wwVA>?	MWO1JIRigXN?	MknPWIhmKFNiYX7kJJN2[i2JMTDwc5B2dGG2aX;ud{Bw\iCVTmWtOlAyKGOnbHzzJJdmemViZILhcYF1cWOjbHz5JIFv\CCmb4PlMYRmeGWwZHXueIx6KGmwY4LlZZNm\CCkeTDBXmQ3PzN6Lh?=	M2G4V\|I5OTN6MEO0
breast cancer cell lines	M4nKcWNmdGxiZ4Lve5RpKGmwaHnibZRqd25iYYPzZZk>	MoPiNE4yOjVuIECuNlUtKDBwNTDhcoQhOS5yIN88US=>	NXHmXo5LPSCmYYnz	MVfJR\|UxKH[jbIXld{Bz[W6pZXSg[pJwdSByLkOgeI8hRjFizsztc4wwVA>?	NGPpO4gzPzVyMUGxNy=>
LoVo cells	M{m5PWZ2dmO2aX;uJIF{e2G7		NGTm[YczPCCq	Mn;CVoVlfWO2aX;uJIlvKGOnbHygZ492dnR9IHGgdJJweG:{dHnvckBw\iC2aHWgZ4VtdCCyb4D1cIF1cW:wIHHy[UApcW5iYXTkbZRqd25idH:gZ4VtdCCleXPs[UBienKnc4SpJJVv\GW{Z3;pcoch[XCxcITvd4l{KHeqZX6g[Zhxd3OnZDD0c{BlenWpIHH0JINwdmOnboTyZZRqd26\|IHfy[YF1\XJidHjhckA{6oDLzszN	NVjIS\|ZEOjZ\|MUCzNVI>

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	pCHK1 / pCDC25c / pRPA32 / γH2AX / pHH3 / cleaved caspase-3 / RAD51; PubMed: 29605721 Neoplasia MDA-231 or Hs578t cells were treated with 50 nM or 100 nM of AZD1775 with or without 500 nM of AZD6738 for 24 h. After treatment, western blot was performed using anti-γH2AX, anti-pCHK1 (S345), anti-CHK1, anti-pCDC25c (S216), anti-CDC25c, anti-pHH3, anti-RAD51 anti-pRPA32 (S4/S8), anti-cleaved-caspase 3, and anti-GAPDH antibodies. ATM pSer1981 / ATM / ATR / Chk1 pSer345 / Chk1 / Chk2 pThr68 / Chk2; PubMed: 26563132 Blood TP53/ATM wild-type (TP53/ATM-wt) primary CLL cells cocultured with and CLL cells, both CII-GFPsh and CII-ATMsh were treated with AZD6738 (1 μM) for 2 hours, or left untreated, prior to exposure to HU (1 mM) or IR (6 Gy) for a further 5 hours. AZD6738 treatment inhibited ATR signaling as indicated by a reduction in HU-induced Chk1 phosphorylation (lanes 3 vs 4 and 9 vs 10). In ATM-proficient CLL cells, this also led to ATM activation as evidenced by ATM phosphorylation and Chk2 phosphorylation (lane 3 vs 4).	29605721 26563132
Immunofluorescence	γH2AX / RAD51; PubMed: 29605721 Neoplasia MDA-231 cells were treated with 50 nM or 100 nM of AZD1775 with or without 500 nM of AZD6738 for 24 h. Cells were probed with anti-γH2AX and anti-RAD51 antibodies. Scale bar: 5 μm. 53BP1; PubMed: 26563132 Blood Cells treated with AZD6738 (1 μM) for 48 hours were labeled with anti-53BP1 antibodies, and at least 200 cells were then analyzed in each sample using a ×60 lens. AZD6738 treatment led to an accumulation of 53BP1 foci in Mec1 and ATMi pretreated CII cells and an accumulation of 53BP1 bodies in CII cells without ATMi pretreatment.	29605721 26563132
Growth inhibition assay	Cell viability; PubMed: 26563132 Blood CII-GFPsh, CII-ATMsh (ATM-deficient), and Mec1 (p53-defective) cells were treated with AZD6738 for 4 days, and viability was measured using the CellTiter-Glo assay. Surviving fraction is expressed relative to untreated controls. AZD6738 induced significantly greater dose-dependent cytotoxicity with significantly lower AZD6738 EC50 in CII-ATMsh and Mec1 cells compared with CII-GFPsh cells. IC50; PubMed: 28062704 Mol Cancer Ther Cell line IC50 values assessed for growth inhibition in a 72-hour MTT assay	26563132 28062704

体内研究

在负荷H460和H23肿瘤的裸鼠中，AZD6738 (50 mg/kg, p.o.)导致肿瘤生长抑制(TGI)，结合顺铂引起ATM缺失的H23肿瘤快速退化。^[1]在负荷LoVo异种移植物的裸鼠中，AZD6738 (50 mg/kg) + IR (2 Gy)的组合避免了毒性，同时仍保持疗效。^[3]

细胞实验：^[1]	+ 展开 Cell lines: H23，H460，A549，和 H358 细胞 Concentrations: ~30 μM Incubation Time: 48小时 Method: 细胞在白色壁，透明底的96孔板中与指示剂量的AZD6738，cisplatin，gemcitabine，或它们的组合处理48小时。ATP水平通过CellTiter-Glo发光细胞活性试验和Safire2酶标仪测量代替品活性评估。进一步分析之前，原始数据对本底发光进行校正。对于AZD6738治疗，在GraphPad Prism 6中将对数转化(x=log(x))的数据归一化为未处理对照组的平均值，通过非线性回归(log(抑制剂) vs. 对可变斜率的响应值) 生成对数剂量响应曲线。GI50值，定义为Y = 50%时，X的剂量，根据剂量反应曲线推导得出。 (Only for Reference)
动物实验： ^[1]	+ 展开 Animal Models: 负荷 H23 或 H460 异种移植物的雌性无胸腺裸鼠 Formulation: 10% DMSO，40% 丙二醇，和 50% 无菌 dH₂O Dosages: 25 或 50 mg/kg Administration: p.o. (Only for Reference)

参考文献

溶解度 (25°C)

体外	DMSO	82 mg/mL (198.78 mM)
	Ethanol	41 mg/mL warmed (99.39 mM)
	Water	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)： 10% DMSO+40% propylene glycol+ddH2O	10mg/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 Download AZD6738 SDF

分子量	412.51
化学式	C₂₀H₂₄N₆O₂S
CAS号	1352226-88-0
储存条件	3 years -20°C powder
储存条件	2 years -80°C in solvent
别名	N/A

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

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
初始浓度:
稀释倍数:

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

通过输入化合物的化学式来计算其分子量：

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 (data from https://clinicaltrials.gov, updated on )

NCT Number	Recruitment	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT03669601	Not yet recruiting	Cancer	CCTU- Cancer Theme\|AstraZeneca\|Cambridge University Hospitals NHS Foundation Trust	September 30 2019	Phase 1
NCT03770429	Recruiting	Leukemia\|Myelodysplastic Syndrome	Massachusetts General Hospital\|AstraZeneca	August 5 2019	Phase 1
NCT02630199	Recruiting	Refractory Cancer	Samsung Medical Center	December 2015	Phase 1
NCT02223923	Recruiting	Solid Tumour Refractory to Conventional Treatment	Royal Marsden NHS Foundation Trust\|AstraZeneca\|Cancer Research UK\|RM/ICR Biomedical Research Centre	July 2014	Phase 1
NCT01955668	Completed	11q-deleted Relapsed/Refractory Chronic Lymphocytic Leukaemia (CLL)\|Prolymphocytic Leukaemia (PLL)\|B Cell Lymphomas	AstraZeneca\|CLL Consortium	November 2013	Phase 1

技术支持

在订购、运输、储存和使用我们的产品的任何阶段，您遇到的任何问题，均可以通过拨打我们的热线电话400-668-6834，或者技术支持邮箱tech@selleck.cn，直接联系到我们。我们会在24小时内尽快联系您。

操作手册

如果有其他问题，请给我们留言。

研究领域

产品类型

AZD6738

客户使用Selleck该产品发表文献9篇：

客户使用该产品的4个实验数据：

产品安全说明书

ATM/ATR抑制剂选择性比较

生物活性

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)

参考文献

溶解度 (25°C)

化学数据 Download AZD6738 SDF

计算器

摩尔浓度计算器

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

稀释计算器

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

连续稀释计算器方程

连续稀释

计算结果

分子量计算器

总分子量：g/mol

摩尔浓度计算器

临床试验信息 (data from https://clinicaltrials.gov, updated on )

技术支持

ATM/ATR Signaling Pathway Map

相关ATM/ATR产品