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Target Overview
ATR, a serine/threonine protein kinase that is required for repair of stalled replication forks, is activated in response to double-strand breaks. It is a cell cycle checkpoint regulator.1
Inhibition of ATR activity interferes with DNA damage responses and can lead to irreparable DNA damage, apoptosis, and hypersensitivity of tumors to replication-associated DNA-damaging agents.
In addition, ATR inhibition modulates the tumor microenvironment to an "immune-effective state” enabling desensitization of tumors to immunotherapy.
Compound Overview
Ceralasertib is a potent and selective oral ATR inhibitor2 that is being clinically evaluated as a potential cancer treatment in advanced solid tumors. The lead indications are post-IO melanoma3 and post-IO NSCLC.4
Ceralasertib is being investigated in combination with IO agents, PARP inhibitors, and in combination with chemotherapy and other agents.
Mechanism of Action
References
1. Yazinski SA, Zou L. Annu Rev Genet. 2016;50:155-173. 2. Foote KM, Lau A, Nissink JW. Future Med Chem. 2015;7(7):873-891. 3. Kim R, Kwon M, An M, et al. Ann Oncol. 2022;33:193-203. 4. Hernandez M, Besse B, Awad M, et al. J Thorac Oncol. 2021;16:S350-S351.
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Abbreviations
AE
adverse event
ALK
anaplastic lymphoma kinase
ATR
ataxia telangiectasia and Rad3-related
BID
twice daily
CT
chemotherapy
CTCAE
Common Terminology Criteria for Adverse Events
DoR
duration of response
ECOG PS
Eastern Cooperative Oncology Group Performance Score
EGFR
epidermal growth factor receptor
HRQoL
health-related quality of life
IASLC
International Association For The Study Of Lung Cancer
IV
intravenous
NSCLC
non-small cell lung cancer
NTRK
neurotrophic tyrosine receptor kinase
ORR
overall or objective response rate
OS
overall survival
PD
progressive disease
PD-1
programmed cell death-1
PD-L1
programmed cell death-ligand 1
PFS
progression-free survival
PFS2
time to second progression or death
PtCh
platinum-based chemotherapy
R
randomization
RECIST
Response Evaluation Criteria in Solid Tumors
SCLC
small cell lung cancer
ssDNA
single-stranded DNA
TTD
time to deterioration
WHO
World Health Organization
Target Overview
ATR, a serine/threonine protein kinase that is required for repair of stalled replication forks, is activated in response to double-strand breaks. It is a cell cycle checkpoint regulator.1
Inhibition of ATR activity interferes with DNA damage responses and can lead to irreparable DNA damage, apoptosis, and hypersensitivity of tumors to replication-associated DNA-damaging agents.
In addition, ATR inhibition modulates the tumor microenvironment to an "immune-effective state” enabling desensitization of tumors to immunotherapy.
Compound Overview
Ceralasertib is a potent and selective oral ATR inhibitor2 that is being clinically evaluated as a potential cancer treatment in advanced solid tumors. The lead indications are post-IO melanoma3 and post-IO NSCLC.4
Ceralasertib is being investigated in combination with IO agents, PARP inhibitors, and in combination with chemotherapy and other agents.
Mechanism of Action
References
1. Yazinski SA, Zou L. Annu Rev Genet. 2016;50:155-173. 2. Foote KM, Lau A, Nissink JW. Future Med Chem. 2015;7(7):873-891. 3. Kim R, Kwon M, An M, et al. Ann Oncol. 2022;33:193-203. 4. Hernandez M, Besse B, Awad M, et al. J Thorac Oncol. 2021;16:S350-S351.
Clinical trial information
Select trial for more information
Arrange By
Selected Filter(s)
Abbreviations
AE
adverse event
ALK
anaplastic lymphoma kinase
ATR
ataxia telangiectasia and Rad3-related
BID
twice daily
CT
chemotherapy
CTCAE
Common Terminology Criteria for Adverse Events
DoR
duration of response
ECOG PS
Eastern Cooperative Oncology Group Performance Score
EGFR
epidermal growth factor receptor
HRQoL
health-related quality of life
IASLC
International Association For The Study Of Lung Cancer
IV
intravenous
NSCLC
non-small cell lung cancer
NTRK
neurotrophic tyrosine receptor kinase
ORR
overall or objective response rate
OS
overall survival
PD
progressive disease
PD-1
programmed cell death-1
PD-L1
programmed cell death-ligand 1
PFS
progression-free survival
PFS2
time to second progression or death
PtCh
platinum-based chemotherapy
R
randomization
RECIST
Response Evaluation Criteria in Solid Tumors
SCLC
small cell lung cancer
ssDNA
single-stranded DNA
TTD
time to deterioration
WHO
World Health Organization