Cat. No.: HY-109566

Elrelesertib

Name: Elrelesertib
Brand: MedChemExpress
SKU: HY-109566
Price: 100.00 USD
Availability: InStock
Rating: 5 (13 reviews)

(Synonyms: AZD1390)

13 Cited Publications

Customer Review

Based on 13 publication(s) in Google Scholar

Elrelesertib (AZD1390) is an orally active, brain-penetrant ATM kinase inhibitor with IC₅₀ values of 0.78 nM. Elrelesertib blocks ATM-dependent DNA damage response, inhibits ATM autophosphorylation and downstream Chk2, Rad50 phosphorylation, and accumulates at DNA breaks. Elrelesertib acts as a radiosensitizer, induces apoptosis, genomic instability, G2-M cell cycle arrest, ROS elevation, and mitochondrial membrane potential alteration. Elrelesertib has low efflux liability against P-gp and BCRP. Elrelesertib can be used for the research of central nervous system malignancies, glioblastoma multiforme, glioma, lung cancer brain metastases, and breast cancer.

For research use only. We do not sell to patients.

Purity: 99.22%
CAS No.: 2089288-03-7
Formula: C₂₇H₃₂FN₅O₂
Molecular Weight:477.57

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 1 year , -20°C, 6 months

Elrelesertib Chemical Structure

CAS No.: 2089288-03-7

Size

Price

Stock

Quantity

Amount: USD 0.00

* Please select Quantity before adding items.

Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
- Clinical Trial
Chemical Information
Publications (13)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]

ATM

0.78 nM (IC₅₀)

Chk2

All ATM/ATR Isoforms :

All Checkpoint Kinase (Chk) Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
NCI-H2228	IC50	0.78 nM	Inhibition of cellular ATM activity in human NCI-H2228 p53 mutant lung cancer cells, measured via high-content immunofluorescence imaging assay of DDR biomarkers with 1-hour pre-incubation and analysis up to 48 hours post-irradiation. Inhibition of cellular ATM activity in human NCI-H2228 p53 mutant lung cancer cells, measured via high-content immunofluorescence imaging assay of DDR biomarkers with 1-hour pre-incubation and analysis up to 48 hours post-irradiation.	29938225
MCF7	IC50	16.143 μM	Reduction in cell viability against human breast cancer MCF-7 cells incubated for 12 hrs by WST-1 assay. Reduction in cell viability against human breast cancer MCF-7 cells incubated for 12 hrs by WST-1 assay.	39681282
MDA-MB-231	IC50	5.524 μM	Reduction in cell viability against human breast cancer MDA-MB-231 cells incubated for 12 hrs by WST-1 assay. Reduction in cell viability against human breast cancer MDA-MB-231 cells incubated for 12 hrs by WST-1 assay.	39681282
MCF7	IC50	10.685 μM	Reduction in cell viability against human breast cancer MCF-7 cells incubated for 24 hrs by WST-1 assay. Reduction in cell viability against human breast cancer MCF-7 cells incubated for 24 hrs by WST-1 assay.	39681282
MDA-MB-231	IC50	2.563 μM	Reduction in cell viability against human breast cancer MDA-MB-231 cells incubated for 24 hrs by WST-1 assay. Reduction in cell viability against human breast cancer MDA-MB-231 cells incubated for 24 hrs by WST-1 assay.	39681282

In Vitro

Elrelesertib (AZD1390) (3-300 nM; 1 h pre-incubation, 4 h post-irradiation) dose-dependently inhibits ATM target engagement in LN18 p53 mutant GBM cells, with strong inhibition of phospho-ATM Ser1981 observed at 3 nM^[1].
Elrelesertib (10-100 nM; 1 h pre-incubation, 1 h/6 h post-irradiation, 6 h post-washout) dose-dependently modulates ATM pathway activity in NCI-H2228 p53 mutant lung cancer cells, with pathway reactivation observed 6 hours after washout^[1].
Elrelesertib (0.125-1250 nM; 1 h pre-incubation, 1/6/24/48 h post-irradiation) inhibits DDR biomarkers in NCI-H2228 p53^G12C mutant lung cancer cells, with an XC₅₀ of 2.7 nM for discrete phospho-ATM foci, and dose-dependently increases micronuclei formation when combined with radiation^[1].
Elrelesertib (10 nM; 1 h pre-incubation, 12-14 days post-irradiation) potently radiosensitizes p53 mutant GBM and lung cancer cell lines more effectively than p53 wild-type cell lines in clonogenic survival assays^[1].
Elrelesertib (10 nM; 1 h pre-incubation, 5 days post-irradiation) potently radiosensitizes p53 mutant GBM cell lines more effectively than p53 wild-type GBM cell lines in a high-throughput Live/Dead antiproliferation assay^[1].
Elrelesertib (0.125-100 nM; 1 h pre-incubation, 24/48 h post-irradiation) in combination with radiation causes dose-dependent G₂ phase accumulation and apoptosis (sub-G₁ population) in NCI-H2228 p53 mutant lung cancer cells^[1].
Elrelesertib (0.2-2 nM; 24 h) completely abrogates clonogenic capacity in MCF-7, MDA-MB-231, and RPE-1 cells^[3].
Elrelesertib (0.2-5 μM; 24 h) dose-dependently inhibits proliferation in MCF-7, MDA-MB-231, and RPE-1 cells over a 24-h period, with significant effects at higher concentrations^[3].
Elrelesertib (0.2-5 μM; 24 h) dose-dependently elevates intracellular ROS levels in MCF-7, MDA-MB-231, and RPE-1 cells after 24 h of treatment^[3].
Elrelesertib (0.2-5 μM; 24 h) dose-dependently reduces mitochondrial membrane potential in MCF-7, MDA-MB-231, and RPE-1 cells after 24 h of treatment^[3].
Elrelesertib (0.2-5 μM; 24 h) dose-dependently induces DNA damage in MCF-7, MDA-MB-231, and RPE-1 cells after 24 h of treatment, as measured by increased comet % Tail DNA and tail length^[3].
Elrelesertib (0.2-5 μM; 24 h) dose-dependently arrests MCF-7, MDA-MB-231, and RPE-1 cells in the G₂-M phase of the cell cycle after 24 h of treatment^[3].
Elrelesertib (0.2-5 μM; 24 h) dose-dependently induces apoptosis and necrosis in MCF-7, MDA-MB-231, and RPE-1 cells after 24 h of treatment, with significant increases in apoptotic cell percentages in breast cancer cell lines^[3].
Elrelesertib (0.2-5 μM) dose-dependently inhibits ATM phosphorylation (reduces p-ATM levels without altering total ATM) and modulates apoptosis-related protein expression (increases PARP, Beclin-1, BAX; decreases Bcl-2) in MCF-7 and MDA-MB-231 cells^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[1]

Cell Line:

LN18 glioblastoma (GBM) cells (p53 mutant)
Concentration:

3, 10, 300 nM
Incubation Time:

1 h (pre-incubation); 4 h (post-irradiation)
Result:

Dose-dependently inhibited ATM autophosphorylation (phospho-ATM Ser1981) at 4 hours post-treatment, with strong inhibition observed at 3 nM.
Did not affect phosphorylation of non-ATM pathway markers including KAP1, CDK1, or p53.

Western Blot Analysis^[1]

Cell Line:

NCI-H2228 lung cancer cells (p53 mutant)
Concentration:

10, 100 nM
Incubation Time:

1 h (pre-incubation); 1, 6 h (post-irradiation); 6 h (post-washout)
Result:

Dose-dependently inhibited phospho-KAP1 Ser824 and phospho-Chk2 Thr68 at 1 and 6 hours post-treatment.
Began to rise phospho-Chk2 levels at 6 hours after washout.

Immunofluorescence^[1]

Cell Line:

NCI-H2228 lung cancer cells (p53 mutant)
Concentration:

0.125, 0.3125, 1, 3, 12.5, 31.25, 100, 300, 1250 nM
Incubation Time:

1 h (pre-incubation); 1, 6, 24, 48 h (post-irradiation)
Result:

Achieved XC₅₀ values of 0.78 nM for inhibition of total nuclear phospho-ATM and γH2AX staining, and 2.7 nM for inhibition of discrete nuclear phospho-ATM foci.
Dose-dependently increased micronuclei formation when combined with radiation.

Cell Cycle Analysis^[1]

Cell Line:

NCI-H2228 lung cancer cells (p53 mutant)
Concentration:

0.125, 0.3125, 1, 3, 12.5, 31.25,100 nM
Incubation Time:

1 h (pre-incubation); 24, 48 h (post-irradiation)
Result:

Combined with 2 Gy IR, caused a dose-dependent increase in G₂ phase accumulation at 24 hours.
Combined with 2 Gy IR, caused a dose-dependent increase in sub-G₁ population at 48 hours, indicating induction of apoptosis.

Cell Proliferation Assay^[1]

Cell Line:

GBM and lung cancer cell lines (LN18, T98G, NCI-H2228, A172, DDBRTG-05MG, U87MG)
Concentration:

10 nM
Incubation Time:

1 h (pre-incubation); 12-14 days (post-irradiation)
Result:

Radiosensitized p53 mutant cell lines more potently than p53 wild-type lines.

Cell Proliferation Assay^[1]

Cell Line:

GBM cell lines (LN18, T98G, HS683T, SW1088, SW1783, DDBRTG-05MG, CCF-STTG1, A172, U87-MG)
Concentration:

10 nM
Incubation Time:

1 h (pre-incubation); 5 days (post-irradiation)
Result:

Radiosensitized p53 mutant cell lines more potently than p53 wild-type lines.

Cell Proliferation Assay^[3]

Cell Line:

human breast cancer cell lines MCF-7, MDA-MB-231, human non-transformed epithelial cell line RPE-1
Concentration:

0.2, 0.4, 0.6, 0.8, 1 μM (MDA-MB-231, RPE-1); 1, 2, 3, 4, 5 μM (MCF-7)
Incubation Time:

24 h
Result:

Caused a dose-dependent reduction in cell proliferation in all three cell lines over 24 h.
Induced significant effects at the highest three concentrations for each cell line compared to controls.

Cell Cycle Analysis^[3]

Cell Line:

human breast cancer cell lines MCF-7, MDA-MB-231, human non-transformed epithelial cell line RPE-1
Concentration:

0.2, 0.6, 1 μM (MDA-MB-231, RPE-1); 1, 3, 5 μM (MCF-7)
Incubation Time:

24 h
Result:

Caused a dose-dependent increase in the proportion of cells in the G2-M phase and a corresponding decrease in the S phase in all three cell lines compared to untreated controls.
Indicated cell cycle arrest at the G2-M checkpoint.

Apoptosis Analysis^[3]

Cell Line:

human breast cancer cell lines MCF-7, MDA-MB-231, human non-transformed epithelial cell line RPE-1
Concentration:

0.2, 0.6, 1 μM (RPE-1); 0.2, 0.65, 1 μM (MDA-MB-231); 1, 3, 5 μM (MCF-7)
Incubation Time:

24 h
Result:

Caused a dose-dependent increase in early and late apoptotic cells, as well as necrotic cells, in all three cell lines compared to DMSO-treated controls.
Induced statistically significant increases in apoptotic cell percentage in breast cancer cell lines.

Parmacokinetics

Species	Dose	Route	CL	V_ss	T_1/2	Bioavailability
Rat^[1]	10 mg/kg	p.o.	16.3 mL/min/kg	3.0 L/kg	2.4 h	74 %

In Vivo

Elrelesertib (AZD1390) (5-20 mg/kg; p.o.; q.d or b.i.d; 4 days) combined with daily 2.5 Gy IR significantly inhibits tumor growth and improves survival in a mouse model of intracranial lung cancer brain metastasis^[1].
Elrelesertib (2-20 mg/kg; p.o.; single dose) inhibits IR-induced ATM pathway activation in a dose- and time-dependent manner and induces apoptosis in a mouse model of intracranial lung cancer brain metastasis, with free brain exposure correlating with pharmacodynamic activity^[1].
Elrelesertib (5-15 mg/kg; p.o.; q.d; 5 days) combined with daily 2 Gy IR and TMZ provides additive tumor growth inhibition and survival benefit in a mouse model of intracranial lung cancer brain metastasis^[1].
Elrelesertib (2-20 mg/kg; p.o.; q.d; 4 days) combined with daily 2.5 Gy IR provides dose-dependent tumor growth inhibition and survival benefit in a mouse model of lung cancer brain metastasis established via intracarotid artery injection^[1].
Elrelesertib (5-20 mg/kg; p.o.; q.d) combined with stereotactic IR significantly improves survival in an immunocompetent mouse model of intracranial glioblastoma, with a dose-dependent efficacy response observed^[1].
Elrelesertib (20 mg/kg; p.o.; q.d; 5 days) combined with daily 2 Gy IR produces robust tumor growth inhibition and survival benefit in a panel of subcutaneous glioblastoma PDX models, with p53 mutant models showing particularly strong responses^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Immunodeficient nude mice (6-8 weeks old)^[1]
Dosage:

5, 20 mg/kg
Administration:

p.o.; q.d for 4 days; b.i.d for 4 days
Result:

Showed marginal tumor growth inhibition (TGI) at 5 mg/kg q.d plus IR.
Produced superior TGI and significantly improved survival compared to IR alone at 20 mg/kg q.d or b.i.d plus IR.
Induced a statistically significant increase in the apoptotic biomarker cleaved caspase-3 (CC3) compared to IR alone.

Animal Model:

Immunodeficient nude mice (6-8 weeks old)^[1]
Dosage:

5, 15 mg/kg
Administration:

p.o.; q.d for 5 days
Result:

The triplet combination of 15 mg/kg q.d, 2 Gy ×5 IR, and 25 mg/kg TMZ q.d was well-tolerated, provided additive TGI and survival benefit over the 15 mg/kg plus IR doublet arm.

Animal Model:

Immunodeficient nude mice (6-8 weeks old)^[1]
Dosage:

2, 5, 20 mg/kg
Administration:

p.o.; q.d for 4 days
Result:

Produced dose-dependent TGI and survival benefit compared to IR alone.
Showed the most pronounced efficacy in reducing tumor growth and extending survival at 20 mg/kg dose.

Animal Model:

C57 Black 6 mice^[1]
Dosage:

5, 20 mg/kg
Administration:

p.o.; q.d for the duration of IR dosing
Result:

Significantly improved survival compared to IR or Elrelesertib alone at 20 mg/kg q.d combined with two 5-Gy IR fractions.
Significantly improved survival compared to IR alone at 5 mg/kg q.d combined with ten 2-Gy IR fractions, though efficacy was reduced compared to the 20 mg/kg dose.

Animal Model:

NMRI nude mice (female, 7-11 weeks old)^[1]
Dosage:

20 mg/kg
Administration:

p.o.; q.d for 5 days
Result:

Produced robust tumor growth inhibition and survival benefit across the PDX panel.
Showed particularly strong responses in p53 mutant models (ST108, ST112), while the least responsive model was p53 wild-type (ST2473).
Several p53 wild-type models also showed meaningful responses to the combination.

Animal Model:

Immunodeficient nude mice^[1]
Dosage:

2, 5, 20 mg/kg
Administration:

p.o.; single dose
Result:

Inhibited IR-induced phospho-ATM (Ser¹⁹⁸¹) in a dose- and time-dependent manner, with 20 mg/kg producing the highest and most sustained inhibition (peaking at approximately 95% inhibition at 3 hours post-IR).
Reduced IR-induced phospho-Rad50 (Ser⁶³⁵) by up to 86% and induced statistically significant increases in apoptotic biomarker CC3 compared to IR alone.
Free brain concentrations peaked within 1 hour of dosing and correlated with ATM inhibition activity.

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS No. 2089288-03-7
Appearance Solid
Molecular Weight 477.57
Formula C₂₇H₃₂FN₅O₂
Color White to off-white
SMILES

O=C(N1C(C)C)N(C)C2=C1C3=CC(C4=CC=C(OCCCN5CCCCC5)N=C4)=C(F)C=C3N=C2
Synonyms

AZD1390
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	1 year
	-20°C	6 months

Publications (13)

All WBIPCell Imaging/StainingOthersIn Vivo Efficacy Study

Sort by:

Journal Impact Factor

Signal Transduct Target Ther

Dual ENPP1/ATM depletion blunts DNA damage repair boosting radioimmune efficacy to abrogate triple-negative breast cancer. [Abstract]

2025 Jun 13;10(1):185. PMID: 40506449

Elrelesertib purchased from MedChemExpress. Usage Cited in: Signal Transduct Target Ther. 2025 Jun 13;10(1):185. [Abstract]

Immunoblot analysis was performed on cell lysates extracted from ANV5-OE cells at different time points after treatment with IR (2 Gy), IR/ENPP1i (5 µM), IR/ATMi (AZD1390: 5 µM), or triple therapy to detect the protein expression levels of γHA2X, PARP1, cleaved PARP1 (c-PARP), ENPP1, RAD51, GAPDH, and Tubulin.

Elrelesertib purchased from MedChemExpress. Usage Cited in: Signal Transduct Target Ther. 2025 Jun 13;10(1):185. [Abstract]

The number of positive cells labeled with anti-γH2AX antibody was quantitatively assessed. Cells were incubated with ENPP1i (5 µM) and ATMi (AZD1390: 5 µM) for 24 h.

Elrelesertib purchased from MedChemExpress. Usage Cited in: Signal Transduct Target Ther. 2025 Jun 13;10(1):185. [Abstract]

After orthotopic transplantation of OE-ANV5 cells, mice were treated with FD (6.2 Gy × 4) alone, or in combination with ENPP1i (6 mg/kg, twice daily), ATMi (AZD1390: 5 mg/kg, once daily), or triple therapy (n = 8 mice per group), and changes in tumor volume were observed.
Nat Nanotechnol

Therapeutically reprogrammed nutrient signalling enhances nanoparticulate albumin bound drug uptake and efficacy in KRAS-mutant cancer. [Abstract]

2021 Jul;16(7):830-839. PMID: 33958764
Sci Adv

53BP1 orchestrates sequence feature of RAG targets to balance DNA repair outcomes during V(D)J recombination. [Abstract]

2026 May 22;12(21):eaec2231. PMID: 42172328
EMBO J

DNA-PKcs and ATM modulate mitochondrial ADP-ATP exchange as an oxidative stress checkpoint mechanism. [Abstract]

2023 Mar 15;42(6):e112094. PMID: 36727301

Elrelesertib purchased from MedChemExpress. Usage Cited in: EMBO J. 2023 Mar 15;42(6):e112094. [Abstract]

HeLa cells expressing Flag‐tagged VDAC2 and V5‐tagged ANT2 were subjected to Co‐IP using anti‐Flag antibody and analyzed by western blot as indicated. ANT2, but not VDAC2, temporarily dissociated from DNA‐PKcs after treatment of 10 Gy IR. ATM knockdown and inhibition (AZD1390, 10 nM) disrupted the dissociation.

Elrelesertib purchased from MedChemExpress. Usage Cited in: EMBO J. 2023 Mar 15;42(6):e112094. [Abstract]

Primary mouse embryonic fibroblasts (MEF) RPE-1 were analyzed for ADP-ATP exchange activity at different time points (up to 16 hours) in response to 100 μM H₂O₂. The ATM inhibitor (AZD1390, 10 nM) was also included in the parallel analysis.
Int J Radiat Oncol Biol Phys

Radiation-Induced Remodeling of the Tumor Microenvironment Through Tumor Cell-Intrinsic Expression of cGAS-STING in Esophageal Squamous Cell Carcinoma. [Abstract]

2023 Mar 15;115(4):957-971. PMID: 36368436
J Med Chem

Discovery of a Meisoindigo-Derived PROTAC as the ATM Degrader: Revolutionizing Colorectal Cancer Therapy via Synthetic Lethality with ATR Inhibitors. [Abstract]

2024 May 9;67(9):7620-7634. PMID: 38634707
Mol Cancer Ther

2026 Jul 15:10.1158/1535-7163.MCT-26-0182. PMID: 42456172
CNS Neurosci Ther

AZD1390, an ataxia telangiectasia mutated inhibitor, attenuates microglia-mediated neuroinflammation and ischemic brain injury. [Abstract]

2024 Apr;30(4):e14696. PMID: 38668740
Cancers (Basel)

2026 Jul 23;18(15):2381. PMID: 42588601
Shock

ATAXIA TELANGIECTASIA MUTATED PROTECTS AGAINST LIPOPOLYSACCARIDE-INDUCED BLOOD-BRAIN BARRIER DISRUPTION BY REGULATING ATK/DRP1-MEDIATED MITOCHONDRIAL HOMEOSTASIS. [Abstract]

2023 Jul 1;60(1):100-109. PMID: 37141173
EANM Innovation

2026 May 19;3:100274.
University of Califomia San Francisco

2026.
bioRxiv

2025 Jul 31.

Solvent & Solubility

In Vitro:

DMSO : 5 mg/mL (10.47 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.0939 mL

10.4697 mL

20.9393 mL

5 mM

0.4188 mL

2.0939 mL

4.1879 mL

10 mM

0.2094 mL

1.0470 mL

2.0939 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

In Vivo:

Working Solution

For the following dissolution methods, please prepare the working solution directly:

It is recommended to prepare fresh solutions and use them promptly within a short period of time.

The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 50% PEG300 50% Saline

Solubility: 5 mg/mL (10.47 mM); Suspended solution; Need ultrasonic

Protocol 2

Add each solvent one by one: 0.5% CMC-Na/saline water

Solubility: 5 mg/mL (10.47 mM); Suspended solution; Need ultrasonic

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (292 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Durant ST, et al. The brain-penetrant clinical ATM inhibitor AZD1390 radiosensitizes and improves survival of preclinical brain tumor models. Science advances. 2018 Jun;4(6):eaat1719. [Content Brief]

[2]. Jucaite A, et al. Brain exposure of the ATM inhibitor AZD1390 in humans-a positron emission tomography study. Neuro-oncology. 2021 Apr 12;23(4):687-696.

[3]. Özdemir D, et al. AZD1390, an Ataxia telangiectasia mutated inhibitor, enhances cisplatin mediated apoptosis in breast cancer cells. Experimental cell research. 2025 Jan 15;444(2):114382.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.0939 mL	10.4697 mL	20.9393 mL	52.3483 mL
	5 mM	0.4188 mL	2.0939 mL	4.1879 mL	10.4697 mL
	10 mM	0.2094 mL	1.0470 mL	2.0939 mL	5.2348 mL

Bioz

Elrelesertib

13 Cited Publications

100 mg Get Quote

Subscribe to the

MedChemExpress

Newsletter

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent:

Product Name:
CAS No.:
Species:
Purity:
Quantity:

Elrelesertib

Ceralasertib

Berzosertib

AZD0156

KU-55933

Olaparib

AZD-7648

Elimusertib

KU-60019

Adavosertib

AZ20

Tuvusertib

Nedisertib

Publications Citing Use of MedChemExpress (MCE) Elrelesertib

All ATM/ATR Isoforms

All Checkpoint Kinase (Chk) Isoforms

Biological Activity

Chemical Information

Publications (13)

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

Bioz

Elrelesertib

Ceralasertib

Berzosertib

AZD0156

KU-55933

Olaparib

AZD-7648

Elimusertib

KU-60019

Adavosertib

AZ20

Tuvusertib

Nedisertib

Publications Citing Use of MedChemExpress (MCE) Elrelesertib

All ATM/ATR Isoforms

All Checkpoint Kinase (Chk) Isoforms

Biological Activity

Chemical Information

Publications (13)

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

Elrelesertib Related Classifications

HY-109566 Related Classifications

Bioz