Berzosertib (VE-822)

For research use only.

Catalog No.S7102 Synonyms: VX970, M6620

63 publications

Berzosertib (VE-822) Chemical Structure

CAS No. 1232416-25-9

Berzosertib (VE-822, VX970, M6620) is an ATR inhibitor with IC50 of 19 nM in HT29 cells.

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Selleck's Berzosertib (VE-822) has been cited by 63 publications

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Biological Activity

Description Berzosertib (VE-822, VX970, M6620) is an ATR inhibitor with IC50 of 19 nM in HT29 cells.
Features The first ATR-targeted drug candidate with high selectivity for ATR.
ATR [1]
(HT29 cells)
19 nM
In vitro

VE-822 (80 nM) attenuates ATR signaling pathway and reduces survival in tumor cells in response to XRT and gemcitabine. VE-822 (80 nM) attenuates ATR signaling in normal cells without enhancing radiation and gemcitabine killing in normal cells. VE-822 (80 nM) increases XRT-induced residual γH2AX and 53BP1 foci compared with XRT in MiaPaCa-2 and PSN-1 cells. VE-822 (80 nM) pre-treatment decreases Rad51 foci after XRT in MiaPaCa-2 and PSN-1 cells. VE-822 (80 nM) alone increases the G1-phase-fraction in MiaPaCa-2 and PSN-1 cells. VE-822 (80 nM) abrogates XRT enriched G2/M-phase-fraction in MiaPaCa-2 and PSN-1 cells. VE-822 has little effect alone, while VE-822 (80 nM) combined with XRT and/or gemcitabine enhances early and late apoptosis in PSN-1 cells that is strongest in the triple combination. [1] VE-822 increases tumor response to DNA damaging agents associated with blockade of pChk1 Ser345. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HCK1T-HPV16 NUn4[Zk2TnWwY4Tpc44hSXO|YYm= M{GyRVAvPSCwTR?= NEnnUIMzPCCqwrC= M3TjN4VvcGGwY3XzJGUyNWSncHXu[IVvfCC{ZYDsbYNifGmxbjDv[kB1cGViSGDWNVYh\2Wwb33l MoTmQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjV5MUexNFgoRjJ3N{G3NVA5RC:jPh?=
HCK1T-HPV16 NHfnRWJHfW6ldHnvckBCe3OjeR?= NH\BOYwxNjVibl2= NFnJ[IkzPCCqwrC= NGLqcZlqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjDFNS=> M{[3W|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ3N{G3NVA5Lz5{NUexO|ExQDxxYU6=
MDCK NX;semYyS3m2b4TvfIlkcXS7IHHzd4F6 M{nVfFUxKG6P NVfXVno1PzJiaB?= MXLDfZRwfG:6aXPpeJkh[WejaX7zeEBOTEONIHPlcIx{KGW6cILld5NqdmdiY3HyZo9vcWNiYX7ofYRz[XOnIEmgZZN{\XO|ZXSgZZMhemWmdXP0bY9vKGmwIHPlcIwhfmmjYnnsbZR6KGG2IEWwJI5OKHC{ZYTy[YF1\WRiZn;yJFczKGi{czDmc4xtd3enZDDifUA4OiCqcoOgbY5kfWKjdHnvckB2dmSncjDuc5Jud3irYzDjc45lcXSrb36gZpkhSWyjbXHyJIJtfWViYYPzZZk> MoTVQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjd6MkO4O|koRjJ5OEKzPFc6RC:jPh?=

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
p-STAT3 / STAT3 / AKT / p-AKT; 

PubMed: 29890208     

VE-822 treatment inhibited STAT3-AKT pathway activation in both KYSE70 and KYSE450.

p21 / caspase-3 / PARP / γ-H2AX; 

PubMed: 29890208     

Expression of several markers which reflects the cell proliferation or cell apoptosis or cell cycle progression or DNA damage was examined using western blotting. Caspase-3 and cleaved-PARP expression remarkably increased in cells exposure to combination of VE-822 and cisplatin. In the ATMdeficient cell, VE-822 combination with cisplatin more dramatic changes in the expression of p-AKT, p21, and γ-H2AX than control cells.

PARP / RPA32 / γH2AX / H4 / MEK; 

PubMed: 31014753     

(A and B) THP-1 (Panel A) and MOLM-13 (Panel B) cells were treated with VE-822 and AZD1775, alone or in combination for 24 h. Chromatin-bound RPA32 and γH2AX were analyzed by western blotting and probed with the indicated antibodies.

WEE1 / p-CDC25c / p-CDK1 / CDK1 / p-CDK2 / CDK2 / RRM1 / RRM2; 

PubMed: 31014753     

THP-1 and MOLM-13 cells were treated with VE-822, AZD1775, or VE + AZD for 24 h. Whole cell lysates were subjected to western blotting and probed with the indicated antibodies. The fold changes for the densitometry measurements, normalized to GAPDH and compared to the untreated control, are shown below the corresponding blot.

29890208 31014753
Growth inhibition assay
Cell viability; 

PubMed: 31014753     

AML cells were cultured in 96-well plates with 0, 0.125, 0.25, 0.5, 1, and 2 µM VE-822 for 72 h and cells were incubated with MTT.

PD-L1 / Hsp90B1; 

PubMed: 30094103     

HeLa-GFP-PD-L1 cells were treated with cisplatin (10 μM) for 24 hours with or without VE-822 (0.1 μM) pretreatment, and PD-L1 localization was analyzed by immunofluorescence.

γH2AX / p53; 

PubMed: 29890208     

Combination treatment enhanced the DNA damage effect presented by examining fluorescence intensity of γ-H2A.X and p53 in ESCC cells. Cells treated with cisplatin, VE-822, or combination of two drugs for 24 h were fixed and co-labeled with anti -γH2AX and anti-p53 antibodies. The γ-H2A.X and p53 foci were analyzed by immunofluorescence microscopy. Combination treatment resulted in accumulation of DNA damage presented by stronger and more fluorescence staining of γ-H2AX and p53.

30094103 29890208
In vivo VE-822 (60 mg/kg) inhibits phospho-Ser-345-Chk1 in mice bearing PSN-1 tumors after DNA-damaging agents. VE-822 (60 mg/kg) combined with XTR doubles the time for tumors to grow to 600 mm3 of XRT alone in mice bearing both PSN-1 and MiaPaCa-2 tumors. VE-822 (60 mg/kg) added to the combination of gemcitabine and XRT substantially prolongs the tumor growth delay compared with the Gem+XRT1 group n mice bearing both PSN-1 tumors. VE-822 (60 mg/kg) combined with XRT1 increases uptake in tumors by 44% compared with XRT1, suggesting that addition of VE-822 increased γH2AX phosphorylation and persistence of DNA damage caused by XRT. [1]


Animal Research:[1]
- Collapse
  • Animal Models: mice bearing PSN-1 or MiaPaCa-2 tumors
  • Dosages: 60 mg/kg
  • Administration: Oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 36 mg/mL (77.66 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+45% PEG 300+H2O
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 463.55


CAS No. 1232416-25-9
Storage powder
in solvent
Synonyms VX970, M6620
Smiles CC(C)S(=O)(=O)C1=CC=C(C=C1)C2=CN=C(C(=N2)C3=CC(=NO3)C4=CC=C(C=C4)CNC)N

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Frequently Asked Questions

  • Question 1:

    I want to have information to prepare VE-822 for mouse gavage. Thank you for your answer

  • Answer:

    VE-822 can be dissolved in 1% CMC Na at 30mg/ml as a suspension for oral gavage.

ATM/ATR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID