| Field | Specification |
|---|---|
| Target | |
| Alternative names | AZD6738 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C20H24N6O2S |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Ceralasertib, also known as AZD6738, is an orally active and bioavailable inhibitor of ATR kinase, with an IC50 of 1 nM. It is supplied as an off-white to light brown solid (C20H24N6O2S, MW 412.51) at 99.43% purity.
Physical & Chemical Properties
| CAS Number | 1352226-88-0 |
|---|---|
| Molecular Formula | C20H24N6O2S |
| Molecular Weight | 412.51 g/mol |
| Purity | 99.43% |
| Appearance | Solid |
| Color | Off-white to light brown |
| SMILES | O=[S@@](C1(CC1)C2=NC(C3=C4C(NC=C4)=NC=C3)=NC(N5CCOC[C@H]5C)=C2)(C)=N |
| Target | ATR, PI3Kδ, DYRK |
| Signaling Pathway | Cell Cycle/DNA Damage; PI3K/Akt/mTOR |
| Solubility | In Vitro: DMSO: 70 mg/mL (169.69 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 1 year; -20°C, 6 months. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
ATR 1 nM (IC50) |
PI3Kδ 6.8 μM (IC50) |
DYRK 10.8 μM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 70 mg/mL (169.69 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 1 year) or -20°C (up to 6 months); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 5 mg/mL (12.12 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (50.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.08 mg/mL (5.04 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (20.8 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.08 mg/mL (5.04 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (20.8 mg/mL) to 900 μL corn oil. |
Direct preparation of the working solution
These formulations are prepared directly, without a DMSO stock; use them promptly after preparation.
Protocol 4
| Composition | 50% PEG300 + 50% saline |
|---|---|
| Result | 10 mg/mL (24.24 mM); clear solution; requires sonication |
Data provided by the manufacturer.
In Vitro
Ceralasertib (AZD6738) potently inhibits isolated ATR kinase (IC50 of 0.001 μM) and ATR kinase-dependent CHK1 phosphorylation in cells (0.074 μM). In non-small cell lung cancer (NSCLC) cell lines, Ceralasertib (AZD6738) induces cell death and senescence. Ceralasertib (AZD6738) reduces the viability of four Kras mutant cell lines (H23, H460, A549, and H358), H460 and H23 cells show the lowest GI50 and greatest maximal inhibition (1.05 μM, 88.0% and 2.38 μM, 86.2%, respectively). In NSCLC cell lines with intact ATM kinase signaling, Ceralasertib (AZD6738) potentiates the cytotoxicity of CDDP and NSC 613327, and it synergizes potently with CDDP in ATM-deficient NSCLC cells[1]. In human breast cancer cell lines, Ceralasertib (AZD6738) shows IC50 values of less than 1 μM in an MTT assay. Ceralasertib (AZD6738) induces cell cycle arrest and apoptosis, and downregulates DNA damage response molecules and cell proliferative signaling molecules[2].
In Vivo
In mice, 14 consecutive days of daily administration of Ceralasertib (AZD6738) and ATR kinase inhibition is tolerated, and the therapeutic efficacy of CDDP in xenograft models is enhanced. Remarkably, ATM-deficient lung cancer xenografts are resolved by CDDP combined with Ceralasertib (AZD6738)[1].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Cell Assay[1]
Dissolve Ceralasertib (AZD6738) in DMSO at 30 mM and dilute in DMSO to the desired working concentrations. Keep the final DMSO concentration in media for all conditions and controls at 0.1% for dose response experiments with Ceralasertib (AZD6738), 0.05% for viability experiments with Ceralasertib (AZD6738) + chemotherapy, and 0.025% for every experiment that uses 0.3 μM and 1.0 μM doses of Ceralasertib (AZD6738)[1].
Animal Administration[1]
Mice[1]: Dissolve Ceralasertib (AZD6738) in DMSO at 25 mg/mL or 50 mg/mL and dilute 1:5 in propylene glycol. Administer Ceralasertib (AZD6738) at 25 mg/kg (H23) or 50 mg/kg (H460) by oral gavage for 14 consecutive days. Use a dosing volume of 10 mL/kg[1].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Different repair pathways support intact or truncated insertions by R2 retrotransposon protein. Science 2026 Feb 26;391(6788):eadz3121. PMID: 41231928
Radiotherapy-resistant prostate cancer cells escape immune checkpoint blockade through the senescence-related ataxia telangiectasia and Rad3-related protein. Cancer Commun (Lond) 2025 Mar;45(3):218-244. PMID: 39698847
Targeting de novo pyrimidine synthesis confers vulnerability to copper-mediated ATR inactivation in PARP inhibitor-resistant ovarian cancer. Nat Commun 2026 Feb 25;17(1):3142. PMID: 41735312
PAF1c links S-phase progression to immune evasion and MYC function in pancreatic carcinoma. Nat Commun 2024 Feb 16;15(1):1446. PMID: 38365788
TP53-dependent toxicity of CRISPR/Cas9 cuts is differential across genomic loci and can confound genetic screening. Nat Commun 2022 Aug 4;13(1):4520. PMID: 35927263
Treacle controls the nucleolar response to rDNA breaks via TOPBP1 recruitment and ATR activation. Nat Commun 2020 Jan 8;11(1):123.
Rapid phosphorylation of glucose-6-phosphate dehydrogenase by casein kinase 2 sustains redox homeostasis under ionizing radiation. Redox Biol 2023 Sep:65:102810. PMID: 37478541
SLFN11-mediated ribosome biogenesis impairment induces TP53-independent apoptosis. Mol Cell 2025 Mar 6;85(5):894-912.e10. PMID: 39909041
The MYCN oncoprotein is an RNA-binding accessory factor of the nuclear exosome targeting complex. Mol Cell 2024 Jun 6;84(11):2070-2086.e20. PMID: 38703770
Human REV1 interacts with DHX36 to promote replication and tolerance of G-quadruplex DNA. Nucleic Acids Res 2026 Jun 8;54(11):gkag562. PMID: 42258547
