Cat. No.: HY-111783

AZD-7648

Name: AZD-7648
Brand: MedChemExpress
SKU: HY-111783
Price: 100.00 USD
Availability: InStock
Rating: 5 (57 reviews)

57 Cited Publications

Customer Review

Based on 57 publication(s) in Google Scholar

AZD-7648 is a potent, orally active, selective DNA-PK inhibitor with an IC₅₀ of 0.6 nM. AZD-7648 induces apoptosis and shows antitumor activity.

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

Purity : 99.86%
CAS No.: 2230820-11-6
Formula: C₁₈H₂₀N₈O₂
Molecular Weight:380.40

Storage:

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

AZD-7648 Chemical Structure

CAS No.: 2230820-11-6

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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
- In Vivo
Chemical Information
Publications (57)
Solvent & Solubility
- In Vitro
- In Vivo
Protocols (6)
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

AZD-7648 is a potent, orally active, selective DNA-PK inhibitor with an IC₅₀ of 0.6 nM. AZD-7648 induces apoptosis and shows antitumor activity^[1].

IC₅₀ & Target

^[1]

PI3Kγ

1.37 μM (IC₅₀)

ATM

17.93 μM (IC₅₀)

DNA-PKcs

91.3 nM (IC₅₀)

All ATM/ATR Isoforms :

All PI3K Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A549	IC₅₀	0.091 μM Compound: Example 16; AZD7648	Inhibition of DNA-PK in human A549 cells assessed as reduction in irradiation-induced autophosphorylation at S2056 residue preincubated for 1 hr followed by 8 Gy irradiation and measured after 1 hr by ELISA Inhibition of DNA-PK in human A549 cells assessed as reduction in irradiation-induced autophosphorylation at S2056 residue preincubated for 1 hr followed by 8 Gy irradiation and measured after 1 hr by ELISA	[PMID: 31851518]
B16-F10	IC₅₀	11.4 μM Compound: AZD-7648	Synergistic antiproliferative activity against mouse B16-F10 cells assessed as reduction in cell viability incubated for 48 hrs in presence of doxorubicin by CCK-8 assay Synergistic antiproliferative activity against mouse B16-F10 cells assessed as reduction in cell viability incubated for 48 hrs in presence of doxorubicin by CCK-8 assay	[PMID: 38587857]
B16-F10	IC₅₀	33.6 μM Compound: AZD-7648	Antiproliferative activity against mouse B16-F10 cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay Antiproliferative activity against mouse B16-F10 cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay	[PMID: 38587857]
CHO	IC₅₀	>198 μM Compound: Example 16; AZD7648	Inhibition of human ERG stably expressed in CHO cells at -90 mV holding potential by electrophysiological assay Inhibition of human ERG stably expressed in CHO cells at -90 mV holding potential by electrophysiological assay	[PMID: 31851518]
CT26	IC₅₀	18.8 μM Compound: AZD-7648	Antiproliferative activity against mouse CT26 cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay Antiproliferative activity against mouse CT26 cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay	[PMID: 38587857]
CT26	IC₅₀	6.74 μM Compound: AZD-7648	Synergistic antiproliferative activity against mouse CT26 cells assessed as reduction in cell viability incubated for 48 hrs in presence of doxorubicin by CCK-8 assay Synergistic antiproliferative activity against mouse CT26 cells assessed as reduction in cell viability incubated for 48 hrs in presence of doxorubicin by CCK-8 assay	[PMID: 38587857]
HCT-116	IC₅₀	19.5 μM Compound: AZD-7648	Antiproliferative activity against human HCT-116 cells assessed as inhibition of cell growth incubated for 48 hrs in presence of 100 nM doxorubicin by MTT assay Antiproliferative activity against human HCT-116 cells assessed as inhibition of cell growth incubated for 48 hrs in presence of 100 nM doxorubicin by MTT assay	[PMID: 35468512]
HCT-116	IC₅₀	35.3 μM Compound: AZD-7648	Antiproliferative activity against human HCT-116 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay Antiproliferative activity against human HCT-116 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	[PMID: 35468512]
HCT-116	IC₅₀	38.08 nM Compound: 4; AZD7648	Inhibition of colony formation in human HCT-116 cells preincubated with compound for 1 hr followed by exposure to 2 Gy gamma irradiation and measured after 7 days by crystal violet staining based chemiluminescence assay Inhibition of colony formation in human HCT-116 cells preincubated with compound for 1 hr followed by exposure to 2 Gy gamma irradiation and measured after 7 days by crystal violet staining based chemiluminescence assay	[PMID: 38117951]
HeLa	IC₅₀	0.6 nM Compound: Example 16; AZD7648	Inhibition of human HeLa cell-derived full length DNA-PK catalytic subunit using fluorescein-EPPLSQEAFADLWKK as substrate preincubated for 30 mins followed by substrate addition and measured after 40 mins TR-FRET assay Inhibition of human HeLa cell-derived full length DNA-PK catalytic subunit using fluorescein-EPPLSQEAFADLWKK as substrate preincubated for 30 mins followed by substrate addition and measured after 40 mins TR-FRET assay	[PMID: 31851518]
HT-29	IC₅₀	>29 μM Compound: Example 16; AZD7648	Inhibition of ATR in human HT-29 cells assessed as reduction in 4NQO-induced CHK1 phosphorylation at S345 residue preincubated for 1 hr followed by 4NQO addition and measured after 1 hr by Hoechst staining-based imaging analysis Inhibition of ATR in human HT-29 cells assessed as reduction in 4NQO-induced CHK1 phosphorylation at S345 residue preincubated for 1 hr followed by 4NQO addition and measured after 1 hr by Hoechst staining-based imaging analysis	[PMID: 31851518]
HT-29	IC₅₀	17.9 μM Compound: Example 16; AZD7648	Inhibition of ATM in human HT-29 cells assessed as reduction in irradiation-induced autophosphorylation at Ser1981 residue preincubated for 1 hr followed by 6 Gy irradiation and measured after 1 hr by Hoechst staining-based imaging analysis Inhibition of ATM in human HT-29 cells assessed as reduction in irradiation-induced autophosphorylation at Ser1981 residue preincubated for 1 hr followed by 6 Gy irradiation and measured after 1 hr by Hoechst staining-based imaging analysis	[PMID: 31851518]
Jurkat	IC₅₀	0.09 μM Compound: AZD-7648	Synergistic antiproliferative activity against human Jurkat cells assessed as reduction in cell viability incubated for 48 hrs in presence of doxorubicin by CCK-8 assay Synergistic antiproliferative activity against human Jurkat cells assessed as reduction in cell viability incubated for 48 hrs in presence of doxorubicin by CCK-8 assay	[PMID: 38587857]
Jurkat	IC₅₀	12.3 μM Compound: AZD-7648	Antiproliferative activity against human Jurkat cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay Antiproliferative activity against human Jurkat cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay	[PMID: 38587857]
MDA-MB-231	IC₅₀	>30 μM Compound: Example 16; AZD7648	Inhibition of mTOR/PI3Kalpha in human MDA-MB-231 cells assessed as reduction in AKT phosphorylation at S473 residue measured after 2 hrs by Hoechst staining-based imaging analysis Inhibition of mTOR/PI3Kalpha in human MDA-MB-231 cells assessed as reduction in AKT phosphorylation at S473 residue measured after 2 hrs by Hoechst staining-based imaging analysis	[PMID: 31851518]
MDA-MB-468	IC₅₀	>30 μM Compound: Example 16; AZD7648	Inhibition of PI3Kbeta in human MDA-MB-468 cells assessed as reduction in AKT phosphorylation at T208 residue measured after 2 hrs by QuantaBlu substrate based fluorescence assay Inhibition of PI3Kbeta in human MDA-MB-468 cells assessed as reduction in AKT phosphorylation at T208 residue measured after 2 hrs by QuantaBlu substrate based fluorescence assay	[PMID: 31851518]

In Vitro

AZD7648 (0-30 μM) is a potent radiosensitizer^[1].
AZD7648 (3 μM) increases sensitivity to Doxorubicin (HY-15142A)^[1].
AZD7648 (0.6 μM) enhances the activity of PARP inhibitor Olaparib (HY-10162)^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

Cell Cycle Analysis^[1]

View Protocol

Cell Line:

IR (ionizing radiation)-treated A549 cells or A549 cells
Concentration:

0-30 μM
Incubation Time:

48 h
Result:

Arrested cell cycle at G2/M phase.

Western Blot Analysis^[1]

View Protocol

Cell Line:

IR (ionizing radiation)-treated A549 cells or OAW42 cells treated with Doxorubicin
Concentration:

0.03, 0.1, 0.3, 1, 3, 10 and 30 μM for A549; 3 μM for OAW42
Incubation Time:

1 h for A549; 0.5, 2, 4, 8 and 16 h for OAW42
Result:

Potently inhibited DNA-PKcs autophosphorylation at Ser2056. Downregulated pDNA-PKcs Ser2056, γH2AX Ser139 and pRPA32 Ser4/Ser8 phosphorylation at early time points (at 30 min, 2 h and 4 h).
Resulted in increased levels of γH2AX and the apoptosis marker cleaved PARP1 compared with doxorubicin treatment alone at later time points (8 and 16 h).

In Vivo

AZD-7648 (100 mg/kg; p.o.; once daily for 5 days) induces tumour growth inhibition and tumour regression^[1].

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

Animal Model:

Nude mice, A549 xenografts and NCI-H1299 xenografts^[1]
Dosage:

100 mg/kg
Administration:

Oral administration, once daily for 5 days
Result:

Induced tumour growth inhibition in combination with IR in A549 xenografts and induced tumour regression in combination with IR in NCI-H1299 xenografts.

Chemical Information

CAS No. 2230820-11-6
Appearance Solid
Molecular Weight 380.40
Formula C₁₈H₂₀N₈O₂
Color White to yellow
SMILES

CC1=CC2=NC=NN2C=C1NC3=NC=C(N(C)C(N4C5CCOCC5)=O)C4=N3
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

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

Publications (57)

All Flow CytometryCell Proliferation/Viability AssayApoptosis AnalysisCell Imaging/Staining

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Journal Impact Factor

Signal Transduct Target Ther

Phosphoproteomics distinguishes disease-specific mechanisms for human phospholamban cardiomyopathy reversible by RNA therapy. [Abstract]

2026 May 28;11(1):199. PMID: 42204136
Cell

Engineered nucleocytosolic vehicles for loading of programmable editors. [Abstract]

2025 May 15;188(10):2637-2655.e31. PMID: 40209705
Nat Methods

Exonuclease-enhanced prime editors. [Abstract]

2024 Mar;21(3):455-464. PMID: 38302659
Nat Cell Biol

Intron-encoded cistronic transcripts for minimally invasive monitoring of coding and non-coding RNAs. [Abstract]

2022 Nov;24(11):1666-1676. PMID: 36344775
Nat Commun

Unveiling the cut-and-repair cycle of designer nucleases in human stem and T cells via CLEAR-time dPCR. [Abstract]

2025 Nov 3;16(1):9571. PMID: 41184307
Nat Commun

Refined DNA repair manipulation enables a universal knock-in strategy in mouse embryos. [Abstract]

2025 Jul 15;16(1):6502. PMID: 40664653
Nat Commun

Dual inhibition of DNA-PK and Polϴ boosts precision of diverse prime editing systems. [Abstract]

2025 May 8;16(1):4290. PMID: 40341582
Nat Commun

Multi-pathway DNA-repair reporters reveal competition between end-joining, single-strand annealing and homologous recombination at Cas9-induced DNA double-strand breaks. [Abstract]

2022 Sep 8;13(1):5295. PMID: 36075911

AZD-7648 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2022 Sep 8;13(1):5295. [Abstract]

HEK 293T DSB-Spectrum_V3 cells were transfected with Cas9 and an sgRNA targeting either AAVS1 or BFP, followed by treatment with the DNA-PKcs inhibitors M3841 (2 µM) or AZD7648 (2 µM). At 72h after Cas9 transfection cells were analyzed by flow cytometry (n=4; mean ± SEM; One-way ANOVA, post-hoc Dunnett's).
Nat Commun

Harnessing DSB repair to promote efficient homology-dependent and -independent prime editing. [Abstract]

2022 Mar 24;13(1):1240. PMID: 35332138
Trends Biotechnol

Highly efficient prime editors for mammalian genome editing based on porcine retrovirus reverse transcriptase. [Abstract]

2025 Aug 30:S0167-7799(25)00314-2. PMID: 40885667
Nucleic Acids Res

Gene editing in hematopoietic stem cells by co-delivery of Cas9/sgRNA ribonucleoprotein and templates for homology-directed repair in 'all-in-one' lentivirus-derived nanoparticles. [Abstract]

2025 Aug 11;53(15):gkaf767. PMID: 40808298

AZD-7648 purchased from MedChemExpress. Usage Cited in: Nucleic Acids Res. 2025 Aug 11;53(15):gkaf767. [Abstract]

AZD7648 (1 µM; 48 h) showed less cytotoxicity in HSPCs relative to M3814 (2 µM; 48 h).
Nucleic Acids Res

Single-stranded DNA with internal base modifications mediates highly efficient knock-in in primary cells using CRISPR-Cas9. [Abstract]

2024 Dec 11;52(22):13561-13576. PMID: 39569586
Theranostics

A genome-wide CRISPR/Cas9 screen identifies DNA-PK as a sensitiser to 177Lutetium-DOTA-octreotate radionuclide therapy. [Abstract]

2023 Aug 28;13(14):4745-4761. PMID: 37771787

AZD-7648 purchased from MedChemExpress. Usage Cited in: Theranostics. 2023 Aug 28;13(14):4745-4761. [Abstract]

Cell growth response at Day 14, shown as % relative growth as compared to control of H1299-7 cells treated with 0, 5 or 10 MBq/mL LuTate alone, or in combination with 0.5 μM or 1 μM of AZD-7648.
Adv Sci (Weinh)

EccDNA-Driven VPS41 Amplification Alleviates Genotoxic Stress via Lysosomal KAI1 Degradation. [Abstract]

2025 Jul;12(25):e2501934. PMID: 40271553
Sci Adv

Patient-derived organoids across cancers reveal conserved tumor heterogeneity and actionable therapeutic vulnerabilities. [Abstract]

2026 Jun 26;12(26):eadz3351. PMID: 42361179
Mol Ther

2026 Jul 20:S1525-0016(26)00602-7. PMID: 42478045
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
Cell Rep

Dual α-globin-truncated erythropoietin receptor knockin restores hemoglobin production in α-thalassemia-derived erythroid cells. [Abstract]

2025 Jan 3;44(1):115141. PMID: 39754719
Mol Cancer Ther

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

Radiation and chemo-sensitizing effects of DNA-PK inhibitors are proportional in tumors and normal tissues. [Abstract]

2024 Sep 4;23(9):1230-1240. PMID: 38781104
Int J Mol Sci

AZD-7648, a DNA-PK Inhibitor, Induces DNA Damage, Apoptosis, and Cell Cycle Arrest in Chronic and Acute Myeloid Leukemia Cells. [Abstract]

2023 Oct 18;24(20):15331. PMID: 37895013

AZD-7648 purchased from MedChemExpress. Usage Cited in: Int J Mol Sci. 2023 Oct 18;24(20):15331. [Abstract]

Log dose–response viability curve of AZD-7648 after 24 or 48 (KG-1*) hours of treatment.

AZD-7648 purchased from MedChemExpress. Usage Cited in: Int J Mol Sci. 2023 Oct 18;24(20):15331. [Abstract]

Analysis of cell death induced by AZD-7648 (AZD，50-200 μM) in CML and AML cell lines after 24 or 48 (KG-1) hours of treatment.The type of cell death was identified using annexin V/propidium iodide staining and analyzed using flow cytometry. Data are expressed as a percentage (%) of viable, early apoptosis, late apoptosis/necrotic, and necrotic cells and represent mean ± SEM of 5 independent experiments. Statistical analyses were performed by comparison with control, using one-way ANOVA and Dunnett’s multiple comparisons test, Kruskal–Wallis and Dunn’s multiple comparisons test, unpaired t-test, or Mann–Whitney test.

AZD-7648 purchased from MedChemExpress. Usage Cited in: Int J Mol Sci. 2023 Oct 18;24(20):15331. [Abstract]

Analysis of cell death induced by AZD-7648 (AZD, 50-200 μM) in CML and AML cell lines after 24 or 48 (KG-1) hours of treatment. Cell morphology was observed by light microscopy (amplification: 1000×), and the most representative image was selected.
Sci Rep

DNA-PK inhibition extends the therapeutic effects of Top2 poisoning to non-proliferating cells, increasing activity at a cost. [Abstract]

2023 Aug 1;13(1):12429. PMID: 37528151
J Cell Mol Med

BNIP3L/BNIP3-Mediated Mitophagy Contributes to the Maintenance of Ovarian Cancer Stem Cells. [Abstract]

2025 Oct;29(19):e70704. PMID: 41078116
CRISPR J

CRISPR-Cas9-Mediated Correction of TSC2 Pathogenic Variants in iPSCs from Patients with Tuberous Sclerosis Complex Type 2. [Abstract]

2025 Feb;8(1):60-70. PMID: 39654514
DNA Repair

Contributions of DNA double strand break repair pathways to DNA crosslink repair. [Abstract]

2025 Sep:153:103889. PMID: 40913914
DNA Repair

DNA-PK inhibitor AZD7648 is a more portent radiosensitizer than PARP inhibitor Olaparib in BRCA1/2 deficient tumors. [Abstract]

2024 Jul:139:103689. PMID: 38749239
PLoS One

Omics-aided design genome editing strategy for challenging human immortalized cell models. [Abstract]

2026 Feb 12;21(2):e0341124. PMID: 41678468
Technical University of Munich

2026.
bioRxiv

2026 Jul 10:2026.07.10.737056. PMID: 42465403
bioRxiv

2026 Jun 22.
SSRN

2026 Jun 22.
EANM Innovation

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

2026.
bioRxiv

2026 Mar 11.
bioRxiv

2026 Feb 17.
bioRxiv

2026 Jan 24.
bioRxiv

2025 Nov 29.
Res Sq

2025 Sep 11.
bioRxiv

2025 Sep 15.
University of Wisconsin

2025.
bioRxiv

2025 Aug 14.
bioRxiv

Prime assembly with linear DNA donors enables large genomic insertions. [Abstract]

2025 Jun 17:2025.06.16.659978. PMID: 40667017
bioRxiv

2025 April 10.
bioRxiv

Oncogene Silencing via ecDNA Micronucleation. [Abstract]

2025 Apr 18:2025.04.15.648906. PMID: 40321211
bioRxiv

2025 April 17.
bioRxiv

2025 March 15.
bioRxiv

2024 November 12.
bioRxiv

PAIRWISE: Deep Learning-based Prediction of Effective Personalized Drug Combinations in Cancer. [Abstract]

2024 Nov 6:2024.11.04.621884. PMID: 39574568
bioRxiv

2024 August 29.
bioRxiv

DNA-PKcs Inhibition Improves Sequential Gene Insertion of the Full-Length CFTR cDNA in Airway Stem Cells. [Abstract]

2024 Aug 12:2024.08.12.607571. PMID: 39185207
Res Sq

2024 Jun 25.
University of British Columbia

2024 Apr 30.
bioRxiv

2024 Feb 2.
bioRxiv

Single-Stranded DNA with Internal Base Modifications Mediates Highly Efficient Gene Insertion in Primary Cells. [Abstract]

2024 Feb 1:2024.02.01.578476. PMID: 38352420
bioRxiv

Non-homologous end joining shapes the genomic rearrangement landscape of chromothripsis from mitotic errors. [Abstract]

2023 Aug 11:2023.08.10.552800. PMID: 37609143
Res Sq

Haploinsufficiency of ZNF251 causes DNA-PKcs-dependent resistance to PARP inhibitors in BRCA1-mutated cancer cells. [Abstract]

2023 Apr 6:rs.3.rs-2688694. PMID: 37066268
bioRxiv

2023 Apr 14.

Solvent & Solubility

In Vitro:

DMSO : 5.83 mg/mL (15.33 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

2.6288 mL

13.1441 mL

26.2881 mL

5 mM

0.5258 mL

2.6288 mL

5.2576 mL

10 mM

0.2629 mL

1.3144 mL

2.6288 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, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

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

Mass Mass

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Molecular Weight Molecular Weight

Dilution Calculator

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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: 0.5% HPMC/0.1% Tween-80 in Saline water

Solubility: 10 mg/mL (26.29 mM); Suspended solution; Need ultrasonic

Protocols

All Cell Biology Signal Pathway Related Animals and Diseases

Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (279 KB)
SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
- Korean - KR (396 KB)
- Portuguese - PT (396 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]. Fok JHL, et al. AZD7648 is a potent and selective DNA-PK inhibitor that enhances radiation, chemotherapy and olaparib activity. Nat Commun. 2019 Nov 7;10(1):5065. [Content Brief]

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, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.6288 mL	13.1441 mL	26.2881 mL	65.7203 mL
	5 mM	0.5258 mL	2.6288 mL	5.2576 mL	13.1441 mL
	10 mM	0.2629 mL	1.3144 mL	2.6288 mL	6.5720 mL
	15 mM	0.1753 mL	0.8763 mL	1.7525 mL	4.3814 mL

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AZD-7648

Publications Citing Use of MedChemExpress (MCE) AZD-7648

All ATM/ATR Isoforms

All PI3K Isoforms