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AZD1390 {[allProObj[0].p_purity_real_show]}

货号：A775616

AZD1390是一种ATM 抑制剂，具有脑渗透性，细胞中对 ATM的 IC50 为 0.78 nM。

AZD1390 化学结构 CAS号：2089288-03-7
AZD1390 化学结构
CAS号：2089288-03-7
AZD1390 3D分子结构
CAS号：2089288-03-7
AZD1390 化学结构 CAS号：2089288-03-7
AZD1390 3D分子结构 CAS号：2089288-03-7
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AZD1390 纯度/质量文件 产品仅供科研

货号：A775616 标准纯度： {[allProObj[0].p_purity_real_show]}
批次查询： 批次纯度:

全球学术期刊中引用的产品

• Nature, 2025, 645, 793-800. Ambeed. [ A201204 , A444152 , A344107 , A952055 ]
• Cell, 2025. Ambeed. [ A122167 ]
• Science, 2025, 387(6729): eadp5637. Ambeed. [ A875019 ]
• Sig. Transduct. Target. Ther., 2025, 10, 257. Ambeed. [ A104916 ]
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产品名称 ATM ↓ ATR ↓ 其他靶点 纯度
Wortmannin ++

ATM, IC50: 150 nM

 		PI3K,MLCK,DNA-PK 99%+
CP-466722 +

ATM, IC50: 410 nM

 		99%+
Torin 2 ++

ATM, EC50: 28 nM

 		++

ATR, EC50: 35 nM

 		mTOR,DNA-PK 99%+
KU-55933 +++

ATM, IC50: 12.9 nM

 		96%
ETP-46464 +

ATM, IC50: 545 nM

 		+++

ATR, IC50: 14 nM

 		mTOR,DNA-PK 98%
CGK733 ++

ATM, IC50: 200 nM

 		++

ATR, IC50: 200 nM

 		99%+
AZD0156 ✔ 99%+
Dactolisib +++

ATR, IC50: 21 nM

 		98+%
Ceralasertib ++++

ATR, IC50: 1 nM

 		99%+
Berzosertib +++

ATR, IC50: 19 nM

 		99%+
VE-821 +++

ATR, Ki: 13 nM

 		99%+
AZ20 ++++

ATR, IC50: 5 nM

 		mTOR 99%+
Schizandrin B +

ATR, IC50: 7.25 μM

 		P-gp 98%
m-PEG25-NHS ester ++++

ATR, IC50: 7 nM

 		95%
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多，抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用，但抑制强度暂时没有相关数据。

AZD1390 生物活性

描述 The ataxia-telangiectasia mutated (ATM) protein kinase is a master regulator of the DNA damage response (DDR), and it coordinates checkpoint activation, DNA repair, and metabolic changes in eukaryotic cells in response to DNA double-strand breaks and oxidative stress[1]. AZD1390 is a potent, highly selective, orally bioavailable, brain-penetrant ATM inhibitor with an IC50 of 0.78 nM in cell[2]. AZD1390 blocks ATM-dependent DDR pathway activity and combines with radiation to induce G2 cell cycle phase accumulation, micronuclei, and apoptosis. AZD1390 radiosensitizes glioma and lung cancer cell lines, with p53 mutant glioma cells generally being more radiosensitized than wild type[2]. In in vivo syngeneic and patient-derived glioma as well as orthotopic lung-brain metastatic models, AZD1390 dosed in combination with daily fractions of ionizing radiation (IR) (whole-brain or stereotactic radiotherapy) significantly induced tumor regressions and increased animal survival compared to IR treatment alone[2].

AZD1390 细胞实验

Cell Line
Concentration Treated Time Description References
SF295 100 nM 1 hour To evaluate the inhibitory effect of AZD1390 on HR and MMEJ, results showed that AZD1390 significantly inhibited HR and MMEJ Nat Commun. 2024 Jun 21;15(1):5294.
HNSCC cell lines 10 nM 1 hour To observe the effect of AZD1390 on clonogenic survival of HNSCC cells following X-ray and proton irradiation, results showed that AZD1390 significantly decreased clonogenic survival of HNSCC cell lines. Cell Death Discov. 2024 Jun 12;10(1):282.
3D spheroid HNSCC cells 0.2 µM 1 hour To observe the effect of AZD1390 on the growth inhibition of 3D spheroid HNSCC cells following X-ray irradiation, results showed that AZD1390 significantly suppressed spheroid growth. Cell Death Discov. 2024 Jun 12;10(1):282.
Panc1 cells 30 nM 3 days To evaluate the effect of AZD1390 on radiation-induced T1IFN expression, results showed that AZD1390 combined with radiotherapy significantly increased T1IFN reporter activity JCI Insight. 2024 Feb 20;9(6):e168824.
LN18 GBM cells 0-300 nM 4 hours AZD1390 significantly inhibited ATM autophosphorylation in LN18 GBM cells after 4 hours, indicating its ability to effectively block ATM-dependent DDR pathway. Sci Adv. 2018 Jun 20;4(6):eaat1719.
A431/CCKBR cells 5 µM 48 hours AZD1390 inhibits ATM kinase, significantly enhancing the cytotoxicity of 225Ac-PP-F11N on A431/CCKBR cells, reducing cell viability from 14% to 8%. J Nucl Med. 2023 Jun;64(6):873-879.
SJ-DIPG7 cells 100 nM 6 days To assess the impact of AZD1390 on radiation-induced DNA damage, results showed that AZD1390 exacerbated DNA damage Neuro Oncol. 2023 Oct 3;25(10):1828-1841.
H157 4 µM 6 days To evaluate the effect of ATM inhibition on Gal-9 expression, results showed a significant increase in Gal-9 levels. Int J Biol Sci. 2023 Jan 16;19(3):981-993.
A549 4 µM 6 days To evaluate the effect of ATM inhibition on Gal-9 expression, results showed a significant increase in Gal-9 levels. Int J Biol Sci. 2023 Jan 16;19(3):981-993.
B16-F10 10 µM 6 days To evaluate the effect of ATM inhibition on Gal-9 expression, results showed a significant increase in Gal-9 levels. Int J Biol Sci. 2023 Jan 16;19(3):981-993.
MC-38 10 µM 6 days To evaluate the effect of ATM inhibition on Gal-9 expression, results showed a significant increase in Gal-9 levels. Int J Biol Sci. 2023 Jan 16;19(3):981-993.
U251 cells 30 nM 6 hours AZD1390 suppressed radiation-induced ATM signaling, abrogated G0-G1 arrest, and promoted a proapoptotic response specifically in p53-mutant GBM cells. Sci Transl Med. 2024 Feb 14;16(734):eadj5962.
GBM12 cells 30 nM 6 hours AZD1390 suppressed RT-induced ATM signaling in GBM12 cells, exhibiting even greater potency. Sci Transl Med. 2024 Feb 14;16(734):eadj5962.
SU-DIPGXIII cells 4 nM 7 days To evaluate the synergy of AZD1390 with radiation, results showed that AZD1390 significantly enhanced the efficacy of radiation Neuro Oncol. 2023 Oct 3;25(10):1828-1841.
KB1P-G3 2 µM 72 hours AZD1390 inhibits ATM signaling, showing BRCA1-deficient cells are more sensitive to ATM inhibition Breast Cancer Res. 2022 Jun 17;24(1):41.
KB1P-B11 2 µM 72 hours AZD1390 inhibits ATM signaling, showing BRCA1-deficient cells are more sensitive to ATM inhibition Breast Cancer Res. 2022 Jun 17;24(1):41.
KP-3.33 2 µM 72 hours AZD1390 inhibits ATM signaling, showing BRCA1-deficient cells are more sensitive to ATM inhibition Breast Cancer Res. 2022 Jun 17;24(1):41.
KP-6.3 2 µM 72 hours AZD1390 inhibits ATM signaling, showing BRCA1-deficient cells are more sensitive to ATM inhibition Breast Cancer Res. 2022 Jun 17;24(1):41.
SU-DIPGXIII ATM KO cells 100 nM To verify the target specificity of AZD1390, results showed that ATM KO cells did not show further radiosensitization with AZD1390 Neuro Oncol. 2023 Oct 3;25(10):1828-1841.
SJ-DIPG29 cells 100 nM To assess the impact of AZD1390 on radiation-induced cytotoxicity, results showed that AZD1390 did not significantly enhance radiation-induced cytotoxicity Neuro Oncol. 2023 Oct 3;25(10):1828-1841.
Dorsal Root Ganglion Neurons (DRGN) 1-10 nM AZD1390 significantly reduced ATM activation levels (pATM levels), with 5 nM being the lowest effective dose, promoting significant increases in DRGN survival, neurite outgrowth, and longest neurite length Clin Transl Med. 2022 Jul;12(7):e962.

AZD1390 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
CD-1 Nude mice SJ-DIPG7 and SJ-DIPG37 orthotopic xenograft models Oral 20 mg/kg Once daily for 7 days To evaluate the tolerability and efficacy of AZD1390 in combination with radiation, results showed that AZD1390 significantly prolonged the survival of mice Neuro Oncol. 2023 Oct 3;25(10):1828-1841.
Nude mice Orthotopic GBM xenograft model Oral 20 mg/kg Once daily for 5 days AZD1390 combined with RT significantly prolonged survival in TP53-mutant GBM models, but no significant survival benefit was observed in TP53-WT models. Sci Transl Med. 2024 Feb 14;16(734):eadj5962.
Mice Orthotopic brain tumor model Oral 20 mg/kg Once daily for 5 days AZD1390 combined with daily fractions of IR (whole-brain or stereotactic radiotherapy) significantly induced tumor regressions and increased animal survival compared to IR treatment alone. Sci Adv. 2018 Jun 20;4(6):eaat1719.
Mice Spinal Cord Injury Model Oral 20 mg/kg Once daily, for 4 weeks AZD1390 significantly suppressed ATM levels, promoted axon regeneration and functional recovery, and improved sensory and motor function Clin Transl Med. 2022 Jul;12(7):e962.
C57BL/6 mice Pancreatic cancer model Oral 20 mg/kg Once daily for 11 days To evaluate the antitumor efficacy of AZD1390 in combination with radiotherapy and anti-PD-L1, results showed that the triplet combination significantly inhibited tumor growth and delayed tumor volume doubling JCI Insight. 2024 Feb 20;9(6):e168824.
Mice BRCA1-deficient mammary tumor model Oral gavage 20 mg/kg Twice daily for 28 consecutive days Combination of AZD1390 with GSK126 significantly increased anti-tumor activity and prolonged progression-free survival Breast Cancer Res. 2022 Jun 17;24(1):41.
Mice Patient-derived xenograft (PDX) models Oral gavage 20 mg/kg/day Once daily for 4 days To evaluate the efficacy of AZD1390 combined with radiation therapy in treating breast cancer CNS metastasis. Results showed that pretreatment with AZD1390 followed by radiation significantly inhibited the growth of PDX tumors and improved animal survival. Clin Cancer Res. 2023 Nov 1;29(21):4492-4503
BALB/c mice CT26 subcutaneous tumor model 5 mg/kg 9 times To evaluate the effect of AZD1390 combined with anti-Gal-9 antibody on tumor growth, results showed that the combination therapy significantly suppressed tumor growth and prolonged survival. Int J Biol Sci. 2023 Jan 16;19(3):981-993.
Mice GBM PDX model Oral 66 mg/kg Once daily for 5 days To evaluate the effect of AZD1390 in combination with TMZ, results showed that AZD1390 significantly enhanced the efficacy of TMZ Nat Commun. 2024 Jun 21;15(1):5294.

AZD1390 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT03215381 Healthy Volunteer Male Subject... 展开 >>s 收起 << Phase 1 Completed - Sweden ... 展开 >> Research Site Stockholm, Sweden, 171 76 收起 <<
NCT03423628 Recurrent Glioblastoma Multifo... 展开 >>rme Primary Glioblastoma Multiforme Brain Neoplasms, Malignant Leptomeningeal Disease (LMD) 收起 << Phase 1 Recruiting April 5, 2021 United States, Massachusetts ... 展开 >> Research Site Recruiting Boston, Massachusetts, United States, 02215 United States, New York Research Site Recruiting New York, New York, United States, 10065 United States, Pennsylvania Research Site Recruiting Pittsburgh, Pennsylvania, United States, 15232 United States, Virginia Research Site Recruiting Richmond, Virginia, United States, 23294 United Kingdom Research Site Recruiting Cambridge, United Kingdom, CB2 0QQ Research Site Recruiting Glasgow, United Kingdom, G12 0YN Research Site Recruiting Leeds, United Kingdom 收起 <<

AZD1390 参考文献

[1]Paull TT. Mechanisms of ATM Activation. Annu Rev Biochem. 2015;84:711-38. doi: 10.1146/annurev-biochem-060614-034335. Epub 2015 Jan 12. PMID: 25580527.

[2]Durant ST, Zheng L, Wang Y, Chen K, Zhang L, Zhang T, Yang Z, Riches L, Trinidad AG, Fok JHL, Hunt T, Pike KG, Wilson J, Smith A, Colclough N, Reddy VP, Sykes A, Janefeldt A, Johnström P, Varnäs K, Takano A, Ling S, Orme J, Stott J, Roberts C, Barrett I, Jones G, Roudier M, Pierce A, Allen J, Kahn J, Sule A, Karlin J, Cronin A, Chapman M, Valerie K, Illingworth R, Pass M. The brain-penetrant clinical ATM inhibitor AZD1390 radiosensitizes and improves survival of preclinical brain tumor models. Sci Adv. 2018 Jun 20;4(6):eaat1719. doi: 10.1126/sciadv.aat1719. PMID: 29938225; PMCID: PMC6010333.

AZD1390 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

2.09mL

0.42mL

0.21mL

10.47mL

2.09mL

1.05mL

20.94mL

4.19mL

2.09mL

AZD1390 技术信息

CAS号2089288-03-7
分子式C27H32FN5O2
分子量 477.57
SMILES Code O=C(N1C(C)C)N(C)C2=C1C3=CC(C4=CC=C(OCCCN5CCCCC5)N=C4)=C(F)C=C3N=C2
MDL No. MFCD31619275
别名
运输蓝冰
InChI Key VQSZIPCGAGVRRP-UHFFFAOYSA-N
Pubchem ID 126689157
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Sealed in dry,2-8°C
溶解方案

DMSO: 4 mg/mL(8.38 mM)，配合低频超声，并水浴加热至45℃助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的方式配制澄清的储备液，再依次添加助溶剂：
——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议现用现配，当天使用； 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶
方案 一
方案 二

Tags: AZD1390 | 2089288-03-7 | AZD 1390 | AZD-1390 | ATM Inhibitor | Cell Cycle/DNA Damage | PI3K/Akt/mTOR | ATM/ATR | 仅供科研使用 | AmBeed-信号通路专用抑制剂 | AZD1390 纯度/质量文件 | AZD1390 亚型比较 | AZD1390 生物活性 | AZD1390 临床数据 | AZD1390 参考文献 | AZD1390 实验方案 | AZD1390 技术信息

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