Ceralasertib (AZD6738)

For research use only. Not for use in humans.

製品コードS7693

Ceralasertib (AZD6738)化学構造

CAS No. 1352226-88-0

Ceralasertib (AZD6738) is an orally active, and selective ATR kinase inhibitor with IC50 of 1 nM. Phase 1/2.

サイズ 価格(税別)  
JPY 34700
JPY 117700
JPY 246000
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バルク問合せ

文献中Selleckの製品使用例(62)

製品安全説明書

ATM/ATR阻害剤の選択性比較

生物活性

製品説明 Ceralasertib (AZD6738) is an orally active, and selective ATR kinase inhibitor with IC50 of 1 nM. Phase 1/2.
ターゲット
ATR [1]
(Cell-free assay)
1 nM
体外試験

In four Kras mutant cell lines: H23, H460, A549, and H358, AZD6738 inhibits ATR kinase activity and impairs cell viability. In ATM-deficient H23 cells, AZD6738 strongly synergizes with cisplatin to induce rapid cell death. [1] In p53 or ATM defective cells, AZD6738 treatment results in replication fork stalls and accumulation of unrepaired DNA damage, resulting in cell death by mitotic catastrophe. [2]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
LICR-LON-HN4 and LICR-LON-HN5 cells NHvnfIZHfW6ldHnvckBie3OjeR?= Mk\GNE4xOyxiMD6xMEAxNjNuIEGsJFMtKDFyIN88US=> MknIRXpFPjd|ODDpcohq[mm2aX;uJI9nKEGWUjD0bJJwfWeqIHzvd5Mhd2ZiZH;3cpN1emWjbTDwbI9{eGixconsZZRqd25ib3[gR2hMOSCxbjDT[ZI{PDVw NG\FWI49[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MEC1O|g6OCd-M{CwOVc5QTB:L3G+
K8484 cells M2DDV2Z2dmO2aX;uJIF{e2G7 MW[yJO69VQ>? M4jPWFchcG:3coO= NXu2THJTUW5iS{i0PFQh[2WubIOsJGFbTDZ5M{igZZQhOiEEtV2gZ49ueGyndHXsfUBxemW4ZX70[YQh\2WvY3n0ZYJqdmVvaX7keYNm\CCFaHuxJJBpd3OyaH;yfYxifGmxbjDvckBU\XKrbnWgN|Q2NCC2aHWg[I94dnO2cnXhcUBCXFJidHHy[4V1Ng>? Mnm1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl6OUG0PFgoRjJ7OEmxOFg5RC:jPh?=
SNU-601 cells NYTYdmFqS2WubDDndo94fGhiaX7obYJqfGmxbjDhd5NigQ>? MnuxNE0yKM7:bX;sM2w> NGXIV3Y2KGSjeYO= M4C2fHRp\SCVIHHu[EB{fWJvR{GgdI9xfWyjdHnvcpMhd2ZiU17VMVYxOSClZXzsd{B4\XKnIHTyZY1ifGmlYXzsfUBidmRiZH;z[U1l\XCnbnTlcpRtgSCrbnPy[YF{\WRiYomgRXpFPjd|OD6= MV[8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQDF|OECzOEc,OjhzM{iwN|Q9N2F-
breast cancer cell lines Mke3R4VtdCCpcn;3eIghcW6qaXLpeIlwdiCjc4PhfS=> NGPCS4IxNjF{NTygNE4zPSxiMD61JIFv\CBzLkCg{txO MmTrOUBl[Xm| M4O1U2lEPTBidnHseYV{KHKjbnfl[EBnem:vIECuN{B1dyB-MTFOwI1wdC:O M{G4XFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ5NUCxNVE{Lz5{N{WwNVEyOzxxYU6=
LoVo cells M3W4WGZ2dmO2aX;uJIF{e2G7 M1fhVlI1KGh? NWC3U5VNWmWmdXP0bY9vKGmwIHPlcIwh[2:3boS7JIEheHKxcH;yeIlwdiCxZjD0bIUh[2WubDDwc5B2dGG2aX;uJIFz\SBqaX6gZYRlcXSrb36geI8h[2WubDDjfYNt\SCjcoLld5QqKHWwZHXy[49qdmdiYYDvdJRwe2m|IIfo[Y4h\Xiyb4Pl[EB1dyCmcoXnJIF1KGOxbnPlcpRz[XSrb37zJIdz\WG2ZYKgeIhidiB|4pEJ{txO MnS1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ|MUCzNVIoRjJ4M{GwN|EzRC:jPh?=
HT29 cells M2jtWGZ2dmO2aX;uJIF{e2G7 MUi2NEBucW6| MlzVTWM2OCB;IECuNFc1KM7:TR?= M{P6eFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyM{S2O|czLz5|MEO0Olc4OjxxYU6=
LoVo cells NH3rXGxEgXSxdH;4bYNqfHliYYPzZZk> NHvYOYw4OiCqcoO= NIHmeXFIUTVyIE2gNE41PCEQvF2= MonOQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOzB|NE[3O|IoRjNyM{S2O|czRC:jPh?=
LoVo cells MmDWSpVv[3Srb36gZZN{[Xl? NVm5UJRwOjVibXevb4c> NF7tfow5KGi{cx?= MVrDdEA:KDBwN{Sg{txO NEfqNIk9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MEO0Olc4Oid-M{CzOFY4PzJ:L3G+
LoVo cells MoPsSpVv[3Srb36gZZN{[Xl? MV[1NEBu\y:tZx?= M1vtWFghcHK| MoTSR5AhRSB{LkKg{txO M4fVVFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyM{S2O|czLz5|MEO0Olc4OjxxYU6=
HT-29 cells MXjDfZRwfG:6aXPpeJkh[XO|YYm= NUTJUmFwPzJiaILz MlflS2k2OCB;IEKuOkDPxE1? NI\4WGM9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MEO0Olc4Oid-M{CzOFY4PzJ:L3G+
LoVo cells MUPGeY5kfGmxbjDhd5NigQ>? MoTaO|UhdWdxa3e= MlP4PEBpenN? MnHER5AhRSB{Lk[g{txO NF7mXXc9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MEO0Olc4Oid-M{CzOFY4PzJ:L3G+
MDA-MB-468 cells MV;GeY5kfGmxbjDhd5NigQ>? NX;HRpg4UUN3MDC9JFUvPyEQvF2= M4f3OVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyM{S2O|czLz5|MEO0Olc4OjxxYU6=

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アッセイ
Methods Test Index PMID
Western blot
ATM pSer1981 / ATM / ATR / Chk1 pSer345 / Chk1 / Chk2 pThr68 / Chk2; 

PubMed: 26563132     


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). 

pCHK1 / pCDC25c / pRPA32 / γH2AX / pHH3 / cleaved caspase-3 / RAD51; 

PubMed: 29605721     


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. 

26563132 29605721
Immunofluorescence
53BP1; 

PubMed: 26563132     


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.

γH2AX / RAD51; 

PubMed: 29605721     


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. 

26563132 29605721
Growth inhibition assay
IC50; 

PubMed: 28062704     


Cell line IC50 values assessed for growth inhibition in a 72-hour MTT assay

Cell viability; 

PubMed: 26563132     


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.

28062704 26563132
体内試験 In nude mice bearing H460 and H23 tumors, AZD6738 (50 mg/kg, p.o.) results in tumor growth inhibition (TGI), and the the combination with cisplatin causes rapid regression of ATM-deficient H23 tumors. [1] In nude mice bearing LoVo xenografts, a combination of AZD6738 (50 mg/kg) + IR (2 Gy) avoids toxicity while still maintaining efficacy. [3]

お薦めの試験操作(参考用のみ)

細胞試験: [1]
- 合併
  • 細胞株: H23, H460, A549, and H358 cells
  • 濃度: ~30 μM
  • 反応時間: 48 h
  • 実験の流れ: Cells are treated in white walled, clear bottom 96-well plates with the indicated doses of AZD6738, cisplatin, gemcitabine, or combination for 48 h. ATP levels are assessed as surrogate measure of viability is assessed using the CellTiter-Glo Luminescent Cell Viability Assay and Safire2 plate reader. Raw data are corrected for background luminescence prior to further analysis. For AZD6738 treatment, log dose response curves are generated in GraphPad Prism 6 by nonlinear regression (log(inhibitor) vs. response with variable slope) of log-transformed (x = log(x)) data normalized to the mean of untreated controls. GI50 values, defined as the dose X at which Y = 50%, were extrapolated from dose response curves.
    (参考用のみ)
動物試験: [1]
- 合併
  • 動物モデル: Female athymic nude mice bearing H23 or H460 xenografts
  • 投薬量: 25 or 50 mg/kg
  • 投与方法: p.o.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 82 mg/mL (198.78 mM)
Water Insoluble
Ethanol '41 mg/mL warmed '41
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):
5% DMSO+40% propylene glycol+ddH2O
混合させたのち直ちに使用することを推奨します。
10mg/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 412.51
化学式

C20H24N6O2S

CAS No. 1352226-88-0
Storage powder
in solvent
別名 N/A
Smiles CC1COCCN1C2=NC(=NC(=C2)C3(CC3)S(=N)(=O)C)C4=C5C=CNC5=NC=C4

投与溶媒組成計算器(クリア溶液)

ステップ1:実験データを入力してください。(実験操作によるロスを考慮し、動物数を1匹分多くして計算・調製することを推奨します)
投与量 mg/kg 動物平均体重 g 投与体積(動物毎) ul 動物数
ステップ2:投与溶媒の組成を入力してください。(ロット毎に適した溶解組成が異なる場合があります。詳細については弊社までお問い合わせください)
% DMSO % % Tween 80 % ddH2O
計算リセット

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 (mg) = 濃度 (mM) x 体積 (mL) 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SDS/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SDS/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 interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04704661 Recruiting Drug: Ceralasertib|Biological: Trastuzumab Deruxtecan Advanced Breast Carcinoma|Advanced Colon Carcinoma|Advanced Colorectal Carcinoma|Advanced Endometrial Carcinoma|Advanced Gastric Carcinoma|Advanced Gastroesophageal Junction Adenocarcinoma|Advanced Malignant Solid Neoplasm|Advanced Salivary Gland Carcinoma|Anatomic Stage III Breast Cancer AJCC v8|Anatomic Stage IIIA Breast Cancer AJCC v8|Anatomic Stage IIIB Breast Cancer AJCC v8|Anatomic Stage IIIC Breast Cancer AJCC v8|Anatomic Stage IV Breast Cancer AJCC v8|Clinical Stage III Gastric Cancer AJCC v8|Clinical Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IV Gastric Cancer AJCC v8|Clinical Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVA Gastric Cancer AJCC v8|Clinical Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVB Gastric Cancer AJCC v8|Clinical Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|HER2 Positive Breast Carcinoma|Liver and Intrahepatic Bile Duct Carcinoma|Metastatic Breast Carcinoma|Metastatic Gastroesophageal Junction Adenocarcinoma|Metastatic Malignant Solid Neoplasm|Pathologic Stage III Gastric Cancer AJCC v8|Pathologic Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIA Gastric Cancer AJCC v8|Pathologic Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIB Gastric Cancer AJCC v8|Pathologic Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIC Gastric Cancer AJCC v8|Pathologic Stage IV Gastric Cancer AJCC v8|Pathologic Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|Prognostic Stage III Breast Cancer AJCC v8|Prognostic Stage IIIA Breast Cancer AJCC v8|Prognostic Stage IIIB Breast Cancer AJCC v8|Prognostic Stage IIIC Breast Cancer AJCC v8|Prognostic Stage IV Breast Cancer AJCC v8|Stage III Colon Cancer AJCC v8|Stage III Colorectal Cancer AJCC v8|Stage III Major Salivary Gland Cancer AJCC v8|Stage III Uterine Corpus Cancer AJCC v8|Stage IIIA Colon Cancer AJCC v8|Stage IIIA Colorectal Cancer AJCC v8|Stage IIIA Uterine Corpus Cancer AJCC v8|Stage IIIB Colon Cancer AJCC v8|Stage IIIB Colorectal Cancer AJCC v8|Stage IIIB Uterine Corpus Cancer AJCC v8|Stage IIIC Colon Cancer AJCC v8|Stage IIIC Colorectal Cancer AJCC v8|Stage IIIC Uterine Corpus Cancer AJCC v8|Stage IIIC1 Uterine Corpus Cancer AJCC v8|Stage IIIC2 Uterine Corpus Cancer AJCC v8|Stage IV Colon Cancer AJCC v8|Stage IV Colorectal Cancer AJCC v8|Stage IV Major Salivary Gland Cancer AJCC v8|Stage IV Uterine Corpus Cancer AJCC v8|Stage IVA Colon Cancer AJCC v8|Stage IVA Colorectal Cancer AJCC v8|Stage IVA Major Salivary Gland Cancer AJCC v8|Stage IVA Uterine Corpus Cancer AJCC v8|Stage IVB Colon Cancer AJCC v8|Stage IVB Colorectal Cancer AJCC v8|Stage IVB Major Salivary Gland Cancer AJCC v8|Stage IVB Uterine Corpus Cancer AJCC v8|Stage IVC Colon Cancer AJCC v8|Stage IVC Colorectal Cancer AJCC v8|Stage IVC Major Salivary Gland Cancer AJCC v8|Unresectable Colorectal Carcinoma|Unresectable Gastroesophageal Junction Adenocarcinoma|Unresectable Malignant Solid Neoplasm National Cancer Institute (NCI) March 5 2021 Phase 1
NCT04361825 Enrolling by invitation Drug: Durvalumab Small Cell Lung Cancer Samsung Medical Center|AstraZeneca June 17 2020 Phase 2
NCT04298008 Recruiting Drug: AZD6738|Drug: Durvalumab Bile Duct Cancer|Chemotherapy Effect Seoul National University Hospital June 25 2020 Phase 2
NCT04298021 Recruiting Drug: AZD6738|Drug: Durvalumab|Drug: Olaparib Bile Duct Cancer|Chemotherapy Effect Seoul National University Hospital June 25 2020 Phase 2
NCT03669601 Recruiting Drug: AZD6738|Drug: Gemcitabine Cancer CCTU- Cancer Theme|AstraZeneca|Cambridge University Hospitals NHS Foundation Trust October 15 2019 Phase 1

技術サポート

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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

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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