Art. -Nr.: HY-14731

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VE-821

55 Cited Publications

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Based on 55 publication(s) in Google Scholar

VE-821 is a potent ATP-competitive inhibitor of ATR with K_i/IC₅₀ of 13 nM/26 nM.

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Reinheit: 99.67%
CAS. Nr.: 1232410-49-9
Formel: C₁₈H₁₆N₄O₃S
Molecular Weight:368.41

Speicherung:

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

VE-821 Chemical Structure

CAS. Nr.: 1232410-49-9

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Use of MCE Products

Fluorescent Dye

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

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
Chemical Information
Publications (55)
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Protokoll
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

VE-821 is a potent ATP-competitive inhibitor of ATR with K_i/IC₅₀ of 13 nM/26 nM.

IC₅₀ & Target^[1]

ATR

13 nM (Ki)

ATM

16 μM (Ki)

DNA-PK

2.2 μM (Ki)

PI3Kγ

3.9 μM (Ki)

Alle ATM/ATR Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
K562	ED₅₀	448.883 μM Compound: 7; VE-821	Cytotoxicity against human K562 cells assessed as decrease in cell viability after 24 hrs by cell titer-glo luminescence assay Cytotoxicity against human K562 cells assessed as decrease in cell viability after 24 hrs by cell titer-glo luminescence assay	[PMID: 27177826]
K562	ED₅₀	71 μM Compound: 7; VE-821	Cytotoxicity against human K562 cells assessed as decrease in cell viability after 48 hrs by cell titer-glo luminescence assay Cytotoxicity against human K562 cells assessed as decrease in cell viability after 48 hrs by cell titer-glo luminescence assay	[PMID: 27177826]

In Vitro

VE-821 shows excellent selectivity for ATR with minimal cross-reactivity against the related PIKKs ATM, DNA-PK, mTOR and PI3Kγ (K_is of 16 μM, 2.2 μM, >1 μM and 3.9 μM, respectively) and against a large panel of unrelated protein kinases^[1]. VE-821 (compound 27) also inhibits ATM and DNA-PK wirh IC₅₀ of >8 μM, and 4.4 μM, respectively^[2]. VE-821 significantly enhances the sensitivity of PSN-1, MiaPaCa-2 and primary PancM pancreatic cancer cells to radiation and Gemcitabine under both normoxic and hypoxic conditions. ATR inhibition by VE-821 leads to inhibition of radiation-induced G₂/M arrest in cancer cells. In both PSN-1 and MiaPaCa-2 cells, 1 μM VE-821 inhibits phosphorylation of Chk1 (Ser 345) after treatment with Gemcitabine (100 nM), radiation (6 Gy) or both, at 2 h post-irradiation^[3].

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

Chemical Information

CAS. Nr. 1232410-49-9
Appearance Solid
Molecular Weight 368.41
Formel C₁₈H₁₆N₄O₃S
Color Light green to green
SMILES

O=C(NC1=CC=CC=C1)C2=NC(C3=CC=C(C=C3)S(=O)(C)=O)=CN=C2N
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

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

Publications (55)

All Cell Proliferation/Viability AssayWB

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Journal Impact Factor

Science

Different repair pathways support intact or truncated insertions by R2 retrotransposon protein. [Abstract]

2026 Feb 26;391(6788):eadz3121. PMID: 41231928
Cell

Extrachromosomal DNA replication and maintenance couple with DNA damage pathway in tumors. [Abstract]

2025 Jun 26;188(13):3405-3421.e27. PMID: 40300601
Mol Cancer

Deubiquitination of CDC6 by OTUD6A promotes tumour progression and chemoresistance. [Abstract]

2024 Apr 29;23(1):86. PMID: 38685067
Cell Res

Asymmetric division in a two-cell-like state rejuvenates embryonic stem cells. [Abstract]

2026 Mar;36(3):219-232. PMID: 41634384
Cancer Commun (Lond)

Radiotherapy-resistant prostate cancer cells escape immune checkpoint blockade through the senescence-related ataxia telangiectasia and Rad3-related protein. [Abstract]

2025 Mar;45(3):218-244. PMID: 39698847
Drug Resist Updat

ZBP1 antagonizes MRE11-mediated DNA end resection and confers synthetic lethality to PARP inhibition in ovarian cancer. [Abstract]

2026 Jan:84:101319. PMID: 41192279
Mol Cell

HSPA1A and DNAJB1 regulate NELF condensate dynamics to safeguard transcriptional recovery under heat stress. [Abstract]

2026 Feb 19;86(4):674-692.e10. PMID: 41653920
Mol Cell

Cytoplasmic PARP1 links the genome instability to the inhibition of antiviral immunity through PARylating cGAS. [Abstract]

2022 Jun 2;82(11):2032-2049.e7. PMID: 35460603
Nat Commun

Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. [Abstract]

2026 Feb 12;17(1):1214. PMID: 41680175
Nat Commun

ATR/Chk1 signaling induces autophagy through sumoylated RhoB-mediated lysosomal translocation of TSC2 after DNA damage. [Abstract]

2018 Oct 8;9(1):4139. PMID: 30297842
Hemasphere

Combined inhibition of CTPS1 and ATR is a metabolic vulnerability in p53-deficient myeloma cells. [Abstract]

2024 Oct 8;8(10):e70016. PMID: 39380841
Sci Transl Med

PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. [Abstract]

2018 Jul 18;10(450):eaaq1093. PMID: 30021885
Nat Chem Biol

Synergistic protection of nascent DNA at stalled forks by MSANTD4 and BRCA1/2-RAD51. [Abstract]

2025 Aug;21(8):1182-1193. PMID: 39809895
Nucleic Acids Res

BTG3-dependent VCP/p97 nuclear translocation is required for efficient repair of UV-induced DNA lesions. [Abstract]

2025 Jul 8;53(13):gkaf626. PMID: 40626560
Nucleic Acids Res

Phosphorylation of TRF2 promotes its interaction with TIN2 and regulates DNA damage response at telomeres. [Abstract]

2023 Feb 22;51(3):1154-1172. PMID: 36651296
Nucleic Acids Res

NRF2 preserves genomic integrity by facilitating ATR activation and G2 cell cycle arrest. [Abstract]

2020 Sep 18;48(16):9109-9123. PMID: 32729622
Cancer Lett

GPI inactivation mediates pentose phosphate pathway flux switch-on inducing temozolomide resistance in glioma stem cell. [Abstract]

2026 May 1:645:218384. PMID: 41763452
Cancer Lett

Inhibition of PRMT5 moderately suppresses prostate cancer growth in vivo but enhances its response to immunotherapy. [Abstract]

2024 Aug 30:217214. PMID: 39218291
Cell Death Dis

Senataxin prevents replicative stress induced by the Myc oncogene. [Abstract]

2025 Mar 19;16(1):187. PMID: 40108134
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
EMBO Mol Med

Thioparib inhibits homologous recombination repair, activates the type I IFN response, and overcomes olaparib resistance. [Abstract]

2023 Mar 8;15(3):e16235. PMID: 36652375
Cell Syst

Torin2 Exploits Replication and Checkpoint Vulnerabilities to Cause Death of PI3K-Activated Triple-Negative Breast Cancer Cells. [Abstract]

2020 Jan 22;10(1):66-81.e11. PMID: 31812693
Oncogene

BET bromodomain inhibitors synergize with ATR inhibitors to induce DNA damage, apoptosis, senescence-associated secretory pathway and ER stress in Myc-induced lymphoma cells. [Abstract]

2016 Sep 8;35(36):4689-97. PMID: 26804177

VE-821 purchased from MedChemExpress. Usage Cited in: Oncogene. 2016 Sep 8;35(36):4689-97. [Abstract]

Western blotting analysis of lysates from λ820 cells treated with vehicle (0.1% DMSO), 10 μM of the ATR inhibitor VE-821, 1 μM of ATR inhibitor AZ20, 1 μM PI3K/mTOR inhibitor NVP-BEZ235 or indicated concentrations of PI3K/mTOR inhibitor GSK1059615.
Cell Death Discov

Protein expression of nucleolar protein 12 in the retina and its implication in protection of retina from UV irradiation damage. [Abstract]

2024 Mar 11;10(1):130. PMID: 38467618
Cell Rep

Feedforward miR-181d degradation modulates population variance of methyl-guanine methyl transferase and temozolomide resistance. [Abstract]

2025 Nov 25;44(11):116516. PMID: 41217933
J Med Chem

YCH1899, a Highly Effective Phthalazin-1(2 H)-one Derivative That Overcomes Resistance to Prior PARP Inhibitors. [Abstract]

2023 Sep 14;66(17):12284-12303. PMID: 37605459
J Cell Biol

SLX4-XPF mediates DNA damage responses to replication stress induced by DNA-protein interactions. [Abstract]

2021 Jan 4;220(1):e202003148. PMID: 33347546
Cell Biol Toxicol

Exploring the ATR-CHK1 pathway in the response of doxorubicin-induced DNA damages in acute lymphoblastic leukemia cells. [Abstract]

2023 Jun;39(3):795-811. PMID: 34519926
Eur J Med Chem

New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs. [Abstract]

2017 Feb 15:127:691-702. PMID: 27823879

VE-821 purchased from MedChemExpress. Usage Cited in: Eur J Med Chem. 2017 Feb 15:127:691-702. [Abstract]

Relative cell viability (%) in MDCK CAIX^- and CAIX⁺ cells exposed to ATR inhibitors (VE-821 and VE-822) or the CAIXi conjugated derivatives in combination with radiation during normoxia (21% O₂) and anoxia (≤0.02% O₂). Normoxic cells are irradiated with 2 Gy and anoxic cells with 4 Gy to induce similar effects on cell viability. Cells were exposed to 500 nM VE-821 and 12, and to 50 nM VE-822 and 13.
Biochem Pharmacol

Inhibition of Pim-2 kinase by LT-171-861 promotes DNA damage and exhibits enhanced lethal effects with PARP inhibitor in multiple myeloma. [Abstract]

2021 Aug:190:114648. PMID: 34111425
Int J Mol Sci

ATR Contributes More Than ATM in Intra-S-Phase Checkpoint Activation after IR, and DNA-PKcs Facilitates Recovery: Evidence for Modular Integration of ATM/ATR/DNA-PKcs Functions. [Abstract]

2022 Jul 6;23(14):7506. PMID: 35886852
Mol Oncol

The one-carbon metabolic enzyme MTHFD2 promotes resection and homologous recombination after ionizing radiation. [Abstract]

2024 Sep;18(9):2179-2195. PMID: 38533616
J Mol Med (Berl)

Combination of PARP inhibitor and temozolomide to suppress chordoma progression. [Abstract]

2019 Aug;97(8):1183-1193. PMID: 31201471
Sci Rep

DNA-PKcs and ATM epistatically suppress DNA end resection and hyperactivation of ATR-dependent G2-checkpoint in S-phase irradiated cells. [Abstract]

2019 Oct 10;9(1):14597. PMID: 31601897
Sci Rep

Radiation-dose-dependent functional synergisms between ATM, ATR and DNA-PKcs in checkpoint control and resection in G2-phase. [Abstract]

2019 Jun 4;9(1):8255. PMID: 31164689
PLoS Genet

Strand break-induced replication fork collapse leads to C-circles, C-overhangs and telomeric recombination. [Abstract]

2019 Feb 4;15(2):e1007925. PMID: 30716077
Vet Res

Activation of the ATM-Chk2 DNA damage response pathway by Newcastle disease virus enhances viral replication. [Abstract]

2026 Jan 30;57(1):24. PMID: 41618459
Front Public Health

G2/M Checkpoint Abrogation With Selective Inhibitors Results in Increased Chromatid Breaks and Radiosensitization of 82-6 hTERT and RPE Human Cells. [Abstract]

2021 May 28:9:675095. PMID: 34123995
Life

Strong Shift to ATR-Dependent Regulation of the G2-Checkpoint after Exposure to High-LET Radiation. [Abstract]

2021 Jun 14;11(6):560. PMID: 34198619
Front Oncol

Targeting Ongoing DNA Damage in Multiple Myeloma: Effects of DNA Damage Response Inhibitors on Plasma Cell Survival. [Abstract]

2017 May 19:7:98. PMID: 28580318

VE-821 purchased from MedChemExpress. Usage Cited in: Front Oncol. 2017 May 19:7:98. [Abstract]

ATM inhibition by treatment with KU-55933 (10 µM) strongly reduces HR efficiency in JJN3-HR and U266-HR, although cells are still able to perform HR to some extent.
J Cancer Res Clin Oncol

Synergistic anticancer activity of combined ATR and ribonucleotide reductase inhibition in Ewing's sarcoma cells. [Abstract]

2023 Sep;149(11):8605-8617. PMID: 37097390
Radiat Res

Nucleoside Analogs Radiosensitize G0 Cells by Activating DNA End Resection and Alternative End-Joining. [Abstract]

2021 May 1;195(5):412-426. PMID: 33755161
DNA Repair

Proficiency in homologous recombination repair is prerequisite for activation of G2-checkpoint at low radiation doses. [Abstract]

2021 May:101:103076. PMID: 33640756
DNA Repair

DNA damage response (DDR) pathway engagement in cisplatin radiosensitization of non-small cell lung cancer. [Abstract]

2016 Apr:40:35-46. PMID: 26991853

VE-821 purchased from MedChemExpress. Usage Cited in: DNA Repair. 2016 Apr:40:35-46. [Abstract]

Impact of ATR inhibition on DNA damage response, γ-H2Ax foci formation and cytotoxicity: A representative immunoblot with vinculin used as a loading control(A) shows the impact of ATR inhibition (VE-821) on the early (0.5 h) and late (24 h) DDR to the indicated treatments in H460 cells. pATM fold change shown above the immunoblot (A).
Mol Cell Biol

UV Damage-Induced Phosphorylation of HBO1 Triggers CRL4DDB2-Mediated Degradation To Regulate Cell Proliferation. [Abstract]

2015 Nov 16;36(3):394-406. PMID: 26572825
DNA Repair

DNA-PK phosphorylation of RPA32 Ser4/Ser8 regulates replication stress checkpoint activation, fork restart, homologous recombination and mitotic catastrophe. [Abstract]

2014 Sep;21:131-9. PMID: 24819595
PLoS One

Differential modulation of haematopoietic and oxidative injury by PARP-1 and ATR kinase inhibition in a murine model of acute irradiation. [Abstract]

2026 Mar 6;21(3):e0344101. PMID: 41790832
bioRxiv

Loss of CFIm activates YAP/TAZ and connects mRNA cleavage and polyadenylation inhibition to BRCAness. [Abstract]

2025 Oct 21:2025.10.21.683728. PMID: 41278918
bioRxiv

2025 February 22.
bioRxiv

2024 Mar 29.
Research Square Print

2023 Feb.
Research Square Preprint

2022 Jul.
Research Square Preprint

2021 May.
Sahlgrenska Academy

University of Gothenburg. 2016 Mar.

VE-821 purchased from MedChemExpress. Usage Cited in: Sahlgrenska Academy. University of Gothenburg. 2016 Mar.

ATRi (VE821) reduces the phosphorylation of CHK1, but not of 4EBP1 or S6, validating our hypothesis.
Gerhard Mercator Universität Duisburg

2013 Jun.

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 50 mg/mL (135.72 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

H₂O : < 0.1 mg/mL (insoluble)

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

2.7144 mL

13.5718 mL

27.1437 mL

5 mM

0.5429 mL

2.7144 mL

5.4287 mL

10 mM

0.2714 mL

1.3572 mL

2.7144 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.

Molaritätsrechner

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

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

In Vivo:

The following protocol is derived from the literature and is for reference only. It is recommended to first try a small sample.

Protocol 1

VE-821 is prepared im vehicle (10% PEG300, 2.5% Tween-80, pH 4)^[4].

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Working solution concentration: 0.22 mg/mL

Protokoll

Kinase Assay^[2]

The ability of compounds (e.g., VE-821) to inhibit ATR, ATM or DNAPK kinase activity is tested using a radiometric-phosphate incorporation assay. A stock solution is prepared consisting of the appropriate buffer, kinase, and target peptide. To this is added the compound of interest, at varying concentrations in DMSO to a final DMSO concentration of 7%. Assays are initiated by addition of an appropriate [g-³³P]ATP solution and incubated at 25°C. Assays are stopped, after the desired time course, by addition of phosphoric acid and ATP to a final concentration of 100 mM and 0.66 μM, respectively. Peptides are captured on a phosphocellulose membrane, prepared, and washed six times with 200 μL of 100 mM phosphoric acid, prior to the addition of 100 μL of scintillation cocktail and scintillation counting on a 1450 Microbeta Liquid Scintillation Counter. Dose−response data are analyzed using GraphPad Prism software^[2].

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

Cell Assay^[3]

MiaPaCa-2, PSN-1 and Panc1 cells (5×10⁴) are plated in 96-well plates and after 4 h treated with increasing concentrations of VE-821 at 1 h before irradiation with a single dose of 4 Gy. Medium is replaced 72 h post-irradiation at which point viability is measured using the using the Alamar Blue assay. Cells are allowed to proliferate and cell viability is again analyzed at day 10 for the different treatment conditions. Cell viability and surviving fraction are normalized to the untreated (control) group^[3].

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

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (277 KB)
SDS (392 KB)
- English - EN (392 KB)
- Français - FR (392 KB)
- Deutsch - DE (392 KB)
- Norwegian - NO (392 KB)
- Español - ES (392 KB)
- Swedish - SV (392 KB)
- Italian - IT (392 KB)
- Korean - KR (392 KB)
- Portuguese - PT (392 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)

Verweise

[1]. Reaper PM, et al. Selective killing of ATM- or p53-deficient cancer cells through inhibition of ATR. Nat Chem Biol. 2011 Apr 13;7(7):428-30. [Content Brief]

[2]. Charrier JD, et al. Discovery of potent and selective inhibitors of ataxia telangiectasia mutated and Rad3 related (ATR) protein kinase as potential anticancer agents. J Med Chem. 2011 Apr 14;54(7):2320-30. [Content Brief]

[3]. Prevo R, et al. The novel ATR inhibitor VE-821 increases sensitivity of pancreatic cancer cells to radiation and chemotherapy. Cancer Biol Ther. 2012 Sep;13(11):1072-81. [Content Brief]

[4]. Muralidharan SV, et al. BET bromodomain inhibitors synergize with ATR inhibitors to induce DNA damage, apoptosis, senescence-associated secretory pathway and ER stress in Myc-induced lymphoma cells. Oncogene. 2016 Sep 8;35(36):4689-97. [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, 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	2.7144 mL	13.5718 mL	27.1437 mL	67.8592 mL
	5 mM	0.5429 mL	2.7144 mL	5.4287 mL	13.5718 mL
	10 mM	0.2714 mL	1.3572 mL	2.7144 mL	6.7859 mL
	15 mM	0.1810 mL	0.9048 mL	1.8096 mL	4.5239 mL
	20 mM	0.1357 mL	0.6786 mL	1.3572 mL	3.3930 mL
	25 mM	0.1086 mL	0.5429 mL	1.0857 mL	2.7144 mL
	30 mM	0.0905 mL	0.4524 mL	0.9048 mL	2.2620 mL
	40 mM	0.0679 mL	0.3393 mL	0.6786 mL	1.6965 mL
	50 mM	0.0543 mL	0.2714 mL	0.5429 mL	1.3572 mL
	60 mM	0.0452 mL	0.2262 mL	0.4524 mL	1.1310 mL
	80 mM	0.0339 mL	0.1696 mL	0.3393 mL	0.8482 mL
	100 mM	0.0271 mL	0.1357 mL	0.2714 mL	0.6786 mL

Keywords

VE-821

55 Cited Publications

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VE-821

Cell Cycle/DNA Damage Compound Library

Kinase Inhibitor Library

PI3K/Akt/mTOR Compound Library

Anti-Cancer Compound Library

Anti-Aging Compound Library

Oxygen Sensing Compound Library

Glycolysis Compound Library

Cytoskeleton Compound Library

Chemical Probe Library

Anti-Pancreatic Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Anti-Obesity Compound Library

Glucose Metabolism Compound Library

Targeted Diversity Library

Cancer Stem Cells Compound Library

Highly Selective Inhibitors Library

Serine/Threonine Kinase Inhibitor Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Bioactive Compound Library Max

Anti-Aging Compound Library Mini

MCE Bioactive Compound Library

Bioactive Compound Library

Protein Kinase Compound Library

High-Throughput Bioactive Compound Library

Posttranslational Modification Library

High-Efficiency Gene Editing Compound Library

Publications Citing Use of MedChemExpress (MCE) VE-821

Alle ATM/ATR Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Publications (55)

Lösungsmittel & Löslichkeit

Protokoll

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

VE-821

Cell Cycle/DNA Damage Compound Library

Kinase Inhibitor Library

PI3K/Akt/mTOR Compound Library

Anti-Cancer Compound Library

Anti-Aging Compound Library

Oxygen Sensing Compound Library

Glycolysis Compound Library

Cytoskeleton Compound Library

Chemical Probe Library

Anti-Pancreatic Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Anti-Obesity Compound Library

Glucose Metabolism Compound Library

Targeted Diversity Library

Cancer Stem Cells Compound Library

Highly Selective Inhibitors Library

Serine/Threonine Kinase Inhibitor Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Bioactive Compound Library Max

Anti-Aging Compound Library Mini

MCE Bioactive Compound Library

Bioactive Compound Library

Protein Kinase Compound Library

High-Throughput Bioactive Compound Library

Posttranslational Modification Library

High-Efficiency Gene Editing Compound Library

Publications Citing Use of MedChemExpress (MCE) VE-821

Alle ATM/ATR Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Publications (55)

Lösungsmittel & Löslichkeit

Protokoll

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

VE-821 Related Classifications

HY-14731 Related Classifications