2. Cell Cycle/DNA Damage PI3K/Akt/mTOR
  3. ATM/ATR
  4. ATM-IN-13

ATM-IN-13 (A36) is an orally active, selective ATM kinase inhibitor with a human IC50 of 0.3 nM. ATM-IN-13 blocks the ATM-mediated DNA double-strand break repair signaling pathway, reduces the phosphorylation levels of ATM and p53, and inhibits ATM-dependent DNA damage response. ATM-IN-13 can be used in the research of colorectal cancer.

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ATM-IN-13

ATM-IN-13 Chemical Structure

CAS No. : 3104731-13-4

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ATM-IN-13 Related Antibodies

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Description

ATM-IN-13 (A36) is an orally active, selective ATM kinase inhibitor with a human IC50 of 0.3 nM. ATM-IN-13 blocks the ATM-mediated DNA double-strand break repair signaling pathway, reduces the phosphorylation levels of ATM and p53, and inhibits ATM-dependent DNA damage response. ATM-IN-13 can be used in the research of colorectal cancer[1].

In Vitro

ATM-IN-13 (A36) potently inhibits purified ATM kinase with an IC50 of 0.3 nM[1].
ATM-IN-13 (A36) exhibits high kinase selectivity, with >3333-fold selectivity over ATR, mTOR, and PI3Kα, and 493-fold selectivity over DNA-PK relative to its ATM IC50 of 0.3 nM[1].
ATM-IN-13 (A36) inhibits proliferation of 2 Gy-irradiated HCT116 colorectal cancer cells with an IC50 of 1.7 nM[1].
ATM-IN-13 (A36) (20-40 nM; 6 days) potently enhances the cytotoxicity of irinotecan in HCT116 and SW620 colorectal cancer cells, with greater synergistic effects in SW620 cells[1].
ATM-IN-13 (A36) (10-20 nM) enhances the ability of irinotecan to suppress colony formation in colorectal cancer cells[1].
ATM-IN-13 (A36) (2 μM) inhibits the irinotecan-activated ATM signaling pathway in HCT116 colorectal cancer cells, reducing levels of γ-H2AX, phosphorylated ATM, and phosphorylated p53[1].
ATM-IN-13 (A36) (0.5-2 μM) concentration-dependently reduces irinotecan-induced γ-H2AX levels in HCT116 colorectal cancer cells, confirming inhibition of ATM-mediated DNA damage signaling[1].
ATM-IN-13 (A36) (0.008-1 μM; 48 h) alone does not alter cell cycle distribution in HCT116 or SW620 colorectal cancer cells, but enhances irinotecan-induced G2/M phase arrest in a concentration-dependent manner[1].
ATM-IN-13 (A36) (0.25-0.5 μM; 48 h) alone does not induce apoptosis in HCT116 colorectal cancer cells, but enhances irinotecan-induced apoptosis in a concentration-dependent manner[1].
ATM-IN-13 (A36) has good metabolic stability in human and rat liver microsomes and mouse/rat plasma, poor stability in mouse liver microsomes, and excellent aqueous solubility of 1258.1 μg/mL at 25°C (pH 7)[1].
ATM-IN-13 (A36) has low potential for drug-drug interactions, with IC50 > 30 μM for inhibition of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

ATM-IN-13 Related Antibodies

Cell Viability Assay[1]

Cell Line: HCT116 and SW620 colorectal cancer cells
Concentration: 20 nM, 40 nM (combination with irinotecan)
Incubation Time: 6 days
Result: Reduced the irinotecan IC50 by 10.2-fold and 12.2-fold in HCT116 cells when used at 20 nM and 40 nM in combination with irinotecan, respectively.
Reduced the irinotecan IC50 by 84.3-fold and 253-fold in SW620 cells when used at 20 nM and 40 nM in combination with irinotecan, respectively.

Cell Cycle Analysis[1]

Cell Line: HCT116 and SW620 colorectal cancer cells
Concentration: 1 μM (HCT116, monotherapy); 0.25 μM, 0.5 μM, 1 μM (HCT116, combination with 1 μM irinotecan); 0.2 μM (SW620, monotherapy); 0.008 μM, 0.04 μM, 0.2 μM (SW620, combination with 0.1 μM irinotecan)
Incubation Time: 48 h
Result: Had no effect on cell cycle distribution in HCT116 cells when used alone at 1 μM.
Increased the percentage of HCT116 cells in G2/M phase to 66.09%, 68.8%, and 78.01% when used at 0.25 μM, 0.5 μM, and 1 μM in combination with 1 μM irinotecan, respectively.
Had no effect on cell cycle distribution in SW620 cells when used alone at 0.2 μM.
Increased the percentage of SW620 cells in G2/M phase to 57.92%, 58.56%, and 60.26% when used at 0.008 μM, 0.04 μM, and 0.2 μM in combination with 0.1 μM irinotecan, respectively.
Parmacokinetics
Species Dose Route T1/2 Tmax Cmax AUC0-t Vz CL Bioavailability
Mice[1] 5 mg/kg i.v. 3.2 h 0.08 h 319.0 ng/mL 914.5 ng·h/mL 0.02 L/kg 0.01 L/h/kg /
Mice[1] 5 mg/kg p.o. 2.1 h 1.3 h 175.6 ng/mL 736.6 ng·h/mL 0.02 L/kg 0.01 L/h/kg 80.5 %
In Vivo

ATM-IN-13 (A36) (20-40 mg/kg; p.o.; daily; 12 days) in combination with liposomal irinotecan achieves 82.3% and 92.6% tumor growth inhibition, respectively, with a favorable safety profile in HCT116 colorectal cancer xenografts[1].
ATM-IN-13 (10-20 mg/kg; p.o.; daily; 16 days) in combination with liposomal irinotecan achieves 80.8% and 91.1% tumor growth inhibition, respectively, with a favorable safety profile in SW620 colorectal cancer xenografts[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Immunodeficient nude mice (implanted with HCT116 human colorectal cancer cells)[1]
Dosage: 20 mg/kg (combination TGI); 40 mg/kg (monotherapy TGI, combination TGI); 2 mg/kg (liposomal irinotecan)
Administration: p.o.; daily; 12 days
Result: Achieved a tumor growth inhibition (TGI) rate of 41.7% (monotherapy, 40 mg/kg).
Achieved TGI rates of 82.3% (20 mg/kg + liposomal irinotecan) and 92.6% (40 mg/kg + liposomal irinotecan).
Showed statistically significant enhanced efficacy in the 40 mg/kg combination group compared to single-agent groups.
Caused no treatment-related fatalities and only moderate body weight loss in the high-dose group.
Animal Model: Immunodeficient nude mice (implanted with SW620 human colorectal cancer cells)[1]
Dosage: 10 mg/kg (combination TGI); 20 mg/kg (monotherapy TGI, combination TGI); 2 mg/kg (liposomal irinotecan)
Administration: p.o.; daily; 16 days
Result: Achieved a tumor growth inhibition (TGI) rate of 28.4% (monotherapy, 20 mg/kg) without causing body weight loss.
Achieved TGI rates of 80.8% (10 mg/kg + liposomal irinotecan) and 91.1% (20 mg/kg + liposomal irinotecan).
Showed statistically significant enhanced efficacy in combination groups compared to liposomal irinotecan monotherapy.
Caused no treatment-related fatalities across all dosing regimens.
Molecular Weight

443.58

Formula

C27H33N5O
CAS No.
SMILES

CC1=NN(C2=C1C=NC3=CC=C(C=C23)C4=CC=C(N=C4)OCCCN5CCCCC5)C(C)C
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Please store the product under the recommended conditions in the Certificate of Analysis.
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Keywords:

ATM-IN-133104731-13-4ATM/ATRAtaxia telangiectasia mutatedATM and RAD3 relatedmTORcolorectal cancerATM kinaseHCT116 colorectal cancer cellsATRhuman liver microsomesDNA double-strand break repair signaling pathwayp53DNA-PKPI3KαInhibitorinhibitorinhibit

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