For research use only.

Catalog No.S7693

34 publications

AZD6738(Ceralasertib) Chemical Structure

CAS No. 1352226-88-0

AZD6738 is an orally active, and selective ATR kinase inhibitor with IC50 of 1 nM. Phase 1/2.

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Selleck's AZD6738(Ceralasertib) has been cited by 34 publications

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Biological Activity

Description AZD6738 is an orally active, and selective ATR kinase inhibitor with IC50 of 1 nM. Phase 1/2.
ATR [1]
(Cell-free assay)
1 nM
In vitro

In four Kras mutant cell lines: H23, H460, A549, and H358, AZD6738 inhibits ATR kinase activity and impairs cell viability. In ATM-deficient H23 cells, AZD6738 strongly synergizes with cisplatin to induce rapid cell death. [1] In p53 or ATM defective cells, AZD6738 treatment results in replication fork stalls and accumulation of unrepaired DNA damage, resulting in cell death by mitotic catastrophe. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
LICR-LON-HN4 and LICR-LON-HN5 cells NUTmZmgxTnWwY4Tpc44h[XO|YYm= M3TMfVAvODNuIECuNUwhOC5|LDCxMEA{NCBzMDFOwG0> Ml;iRXpFPjd|ODDpcohq[mm2aX;uJI9nKEGWUjD0bJJwfWeqIHzvd5Mhd2ZiZH;3cpN1emWjbTDwbI9{eGixconsZZRqd25ib3[gR2hMOSCxbjDT[ZI{PDVw NUHSOppmOzByNUe4PVA>
K8484 cells NWDZeJpQTnWwY4Tpc44h[XO|YYm= MmL5NkDPxE1? MYq3JIhwfXK| MYXJckBMQDR6NDDj[YxteyxiQWrEOlc{QCCjdDCyJOK2VSClb33wcIV1\Wy7IIDy[ZZmdnSnZDDn[Y1kcXSjYnnu[U1qdmS3Y3XkJGNpczFicHjvd5Bpd3K7bHH0bY9vKG:wIGPldolv\SB|NEWsJJRp\SCmb4fud5Rz\WGvIFHUVkB1[XKpZYSu MUKyPVg6OTR6OB?=
SNU-601 cells MlTJR4VtdCCpcn;3eIghcW6qaXLpeIlwdiCjc4PhfS=> M{fYeFAuOSEQvH3vcE9N NUn5Z2Y5PSCmYYnz MoXJWIhmKFNiYX7kJJN2[i2JMTDwc5B2dGG2aX;ud{Bw\iCVTmWtOlAyKGOnbHzzJJdmemViZILhcYF1cWOjbHz5JIFv\CCmb4PlMYRmeGWwZHXueIx6KGmwY4LlZZNm\CCkeTDBXmQ3PzN6Lh?= M4HidlI5OTN6MEO0
breast cancer cell lines MWfD[YxtKGe{b4f0bEBqdmirYnn0bY9vKGG|c3H5 NUL0TnR[OC5zMkWsJFAvOjVuIECuOUBidmRiMT6wJO69VQ>? MXu1JIRigXN? M{HITWlEPTBidnHseYV{KHKjbnfl[EBnem:vIECuN{B1dyB-MTFOwI1wdC:O NH:1WpEzPzVyMUGxNy=>
LoVo cells NEHn[lRHfW6ldHnvckBie3OjeR?= MmnFNlQhcA>? NGrUU3NT\WS3Y4Tpc44hcW5iY3XscEBkd3WwdEugZUBxem:yb4L0bY9vKG:oIITo[UBk\WyuIIDvdJVt[XSrb36gZZJmKCirbjDh[IRqfGmxbjD0c{Bk\WyuIHP5Z4xmKGG{cnXzeEkhfW6mZYLnc4lv\yCjcH;weI9{cXNid3jlckBmgHCxc3XkJJRwKGS{dXegZZQh[2:wY3XueJJifGmxboOg[5Jm[XSncjD0bIFvKDQkgJpOwG0> M4rTcFI3OzFyM{Gy

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
pCHK1 / pCDC25c / pRPA32 / γH2AX / pHH3 / cleaved caspase-3 / RAD51; 

PubMed: 29605721     

MDA-231 or Hs578t cells were treated with 50 nM or 100 nM of AZD1775 with or without 500 nM of AZD6738 for 24 h. After treatment, western blot was performed using anti-γH2AX, anti-pCHK1 (S345), anti-CHK1, anti-pCDC25c (S216), anti-CDC25c, anti-pHH3, anti-RAD51 anti-pRPA32 (S4/S8), anti-cleaved-caspase 3, and anti-GAPDH antibodies. 

ATM pSer1981 / ATM / ATR / Chk1 pSer345 / Chk1 / Chk2 pThr68 / Chk2; 

PubMed: 26563132     

TP53/ATM wild-type (TP53/ATM-wt) primary CLL cells cocultured with and CLL cells, both CII-GFPsh and CII-ATMsh were treated with AZD6738 (1 μM) for 2 hours, or left untreated, prior to exposure to HU (1 mM) or IR (6 Gy) for a further 5 hours. AZD6738 treatment inhibited ATR signaling as indicated by a reduction in HU-induced Chk1 phosphorylation (lanes 3 vs 4 and 9 vs 10). In ATM-proficient CLL cells, this also led to ATM activation as evidenced by ATM phosphorylation and Chk2 phosphorylation (lane 3 vs 4). 

29605721 26563132
γH2AX / RAD51; 

PubMed: 29605721     

MDA-231 cells were treated with 50 nM or 100 nM of AZD1775 with or without 500 nM of AZD6738 for 24 h. Cells were probed with anti-γH2AX and anti-RAD51 antibodies. Scale bar: 5 μm. 


PubMed: 26563132     

Cells treated with AZD6738 (1 μM) for 48 hours were labeled with anti-53BP1 antibodies, and at least 200 cells were then analyzed in each sample using a ×60 lens. AZD6738 treatment led to an accumulation of 53BP1 foci in Mec1 and ATMi pretreated CII cells and an accumulation of 53BP1 bodies in CII cells without ATMi pretreatment.

29605721 26563132
Growth inhibition assay
Cell viability; 

PubMed: 26563132     

CII-GFPsh, CII-ATMsh (ATM-deficient), and Mec1 (p53-defective) cells were treated with AZD6738 for 4 days, and viability was measured using the CellTiter-Glo assay. Surviving fraction is expressed relative to untreated controls. AZD6738 induced significantly greater dose-dependent cytotoxicity with significantly lower AZD6738 EC50 in CII-ATMsh and Mec1 cells compared with CII-GFPsh cells.


PubMed: 28062704     

Cell line IC50 values assessed for growth inhibition in a 72-hour MTT assay

26563132 28062704
In vivo In nude mice bearing H460 and H23 tumors, AZD6738 (50 mg/kg, p.o.) results in tumor growth inhibition (TGI), and the the combination with cisplatin causes rapid regression of ATM-deficient H23 tumors. [1] In nude mice bearing LoVo xenografts, a combination of AZD6738 (50 mg/kg) + IR (2 Gy) avoids toxicity while still maintaining efficacy. [3]


Cell Research:[1]
- Collapse
  • Cell lines: H23, H460, A549, and H358 cells
  • Concentrations: ~30 μM
  • Incubation Time: 48 h
  • Method: Cells are treated in white walled, clear bottom 96-well plates with the indicated doses of AZD6738, cisplatin, gemcitabine, or combination for 48 h. ATP levels are assessed as surrogate measure of viability is assessed using the CellTiter-Glo Luminescent Cell Viability Assay and Safire2 plate reader. Raw data are corrected for background luminescence prior to further analysis. For AZD6738 treatment, log dose response curves are generated in GraphPad Prism 6 by nonlinear regression (log(inhibitor) vs. response with variable slope) of log-transformed (x = log(x)) data normalized to the mean of untreated controls. GI50 values, defined as the dose X at which Y = 50%, were extrapolated from dose response curves.
    (Only for Reference)
Animal Research: [1]
- Collapse
  • Animal Models: Female athymic nude mice bearing H23 or H460 xenografts
  • Dosages: 25 or 50 mg/kg
  • Administration: p.o.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 82 mg/mL (198.78 mM)
Ethanol 41 mg/mL warmed (99.39 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+40% propylene glycol+ddH2O
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 412.51


CAS No. 1352226-88-0
Storage powder
in solvent
Synonyms N/A
Smiles CC1COCCN1C2=NC(=NC(=C2)C3(CC3)S(=N)(=O)C)C4=C5C=CNC5=NC=C4

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04361825 Enrolling by invitation Drug: Durvalumab Small Cell Lung Cancer Samsung Medical Center|AstraZeneca June 17 2020 Phase 2
NCT04298008 Recruiting Drug: AZD6738|Drug: Durvalumab Bile Duct Cancer|Chemotherapy Effect Seoul National University Hospital June 25 2020 Phase 2
NCT04298021 Recruiting Drug: AZD6738|Drug: Durvalumab|Drug: Olaparib Bile Duct Cancer|Chemotherapy Effect Seoul National University Hospital June 25 2020 Phase 2
NCT03669601 Recruiting Drug: AZD6738|Drug: Gemcitabine Cancer CCTU- Cancer Theme|AstraZeneca|Cambridge University Hospitals NHS Foundation Trust October 15 2019 Phase 1
NCT03770429 Recruiting Drug: AZD6738 Leukemia|Myelodysplastic Syndrome Massachusetts General Hospital|AstraZeneca August 5 2019 Phase 1

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ATM/ATR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID