Ceralasertib (AZD6738)

For research use only.

Catalog No.S7693

47 publications

Ceralasertib (AZD6738) Chemical Structure

CAS No. 1352226-88-0

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

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Selleck's Ceralasertib (AZD6738) has been cited by 47 publications

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Biological Activity

Description Ceralasertib (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 MmTvSpVv[3Srb36gZZN{[Xl? M3fLRlAvODNuIECuNUwhOC5|LDCxMEA{NCBzMDFOwG0> MnHzRXpFPjd|ODDpcohq[mm2aX;uJI9nKEGWUjD0bJJwfWeqIHzvd5Mhd2ZiZH;3cpN1emWjbTDwbI9{eGixconsZZRqd25ib3[gR2hMOSCxbjDT[ZI{PDVw Mly4QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOzByNUe4PVAoRjNyMEW3PFkxRC:jPh?=
K8484 cells MnruSpVv[3Srb36gZZN{[Xl? M3jOSFIh|ryP NG[0ZnI4KGixdYLz M3zPUmlvKEt6NEi0JINmdGy|LDDBXmQ3PzN6IHH0JFIhyrWPIHPvcZBt\XSnbImgdJJmfmWwdHXkJIdmdWOrdHHibY5mNWmwZIXj[YQhS2itMTDwbI9{eGixconsZZRqd25ib36gV4VzcW6nIEO0OUwhfGinIHTve45{fHKnYX2gRXRTKHSjcnfleE4> MoDuQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl6OUG0PFgoRjJ7OEmxOFg5RC:jPh?=
SNU-601 cells NGPxdoFE\WyuIHfyc5d1cCCrbnjpZol1cW:wIHHzd4F6 Mly3NE0yKM7:bX;sM2w> NIL2UFM2KGSjeYO= NF:0TmZVcGViUzDhcoQhe3WkLVexJJBweHWuYYTpc45{KG:oIGPOWU03ODFiY3XscJMhf2W{ZTDkdoFu[XSrY3HscJkh[W6mIHTvd4Uu\GWyZX7k[Y51dHliaX7jdoVie2WmIHL5JGFbTDZ5M{iu MVi8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQDF|OECzOEc,OjhzM{iwN|Q9N2F-
breast cancer cell lines M3yyVWNmdGxiZ4Lve5RpKGmwaHnibZRqd25iYYPzZZk> NHqxe5YxNjF{NTygNE4zPSxiMD61JIFv\CBzLkCg{txO MWO1JIRigXN? NXyxcWZIUUN3MDD2ZYx2\XNicnHu[4VlKG[{b32gNE4{KHSxIE6xJO69dW:uL1y= MVq8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPzVyMUGxN{c,Ojd3MEGxNVM9N2F-
LoVo cells NFTOO3FHfW6ldHnvckBie3OjeR?= M2XC[VI1KGh? NHq4N5RT\WS3Y4Tpc44hcW5iY3XscEBkd3WwdEugZUBxem:yb4L0bY9vKG:oIITo[UBk\WyuIIDvdJVt[XSrb36gZZJmKCirbjDh[IRqfGmxbjD0c{Bk\WyuIHP5Z4xmKGG{cnXzeEkhfW6mZYLnc4lv\yCjcH;weI9{cXNid3jlckBmgHCxc3XkJJRwKGS{dXegZZQh[2:wY3XueJJifGmxboOg[5Jm[XSncjD0bIFvKDQkgJpOwG0> NWT5[odbRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[zNVA{OTJpPkK2N|ExOzF{PD;hQi=>
HT29 cells MofrSpVv[3Srb36gZZN{[Xl? NHjyVW03OCCvaX7z NXXQUHNsUUN3MDC9JFAvODd2IN88US=> MUW8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8{ODN2Nke3Nkc,OzB|NE[3O|I9N2F-
LoVo cells NYnSXngxS3m2b4TvfIlkcXS7IHHzd4F6 MorQO|IhcHK| Ml3kS2k2OCB;IECuOFQh|ryP NUnOc2F[RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxM{CzOFY4PzJpPkOwN|Q3Pzd{PD;hQi=>
LoVo cells M{T2emZ2dmO2aX;uJIF{e2G7 Mmf1NlUhdWdxa3e= Mnn4PEBpenN? M4nWXGNxKD1iMD63OEDPxE1? NX3OWIJvRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxM{CzOFY4PzJpPkOwN|Q3Pzd{PD;hQi=>
LoVo cells M3q1[2Z2dmO2aX;uJIF{e2G7 MkDaOVAhdWdxa3e= NVn6XHc2QCCqcoO= M37HNWNxKD1iMj6yJO69VQ>? NXvibZVHRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxM{CzOFY4PzJpPkOwN|Q3Pzd{PD;hQi=>
HT-29 cells NUDyXotSS3m2b4TvfIlkcXS7IHHzd4F6 NFz0dYI4OiCqcoO= MmnJS2k2OCB;IEKuOkDPxE1? M4rh[VxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyM{S2O|czLz5|MEO0Olc4OjxxYU6=
LoVo cells NILwWJJHfW6ldHnvckBie3OjeR?= M3frZ|c2KG2pL3vn MXK4JIhzew>? M3vnemNxKD1iMj62JO69VQ>? MmHjQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOzB|NE[3O|IoRjNyM{S2O|czRC:jPh?=
MDA-MB-468 cells MWrGeY5kfGmxbjDhd5NigQ>? NUjFWXhjUUN3MDC9JFUvPyEQvF2= NWnEV|h3RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxM{CzOFY4PzJpPkOwN|Q3Pzd{PD;hQi=>

... 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)
Water Insoluble
Ethanol '41 mg/mL warmed
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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID