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Results for "

ATM/ATR

" in MedChemExpress (MCE) Product Catalog:

By Targets:	ATM/ATR (9) Apoptosis (1) Autophagy (1) Bacterial (1) CMV (1) DNA/RNA Synthesis (1) Histone Methyltransferase (1) HSV (1) mTOR (2) Nucleoside Antimetabolite/Analog (1) PROTACs (1)
By Research Areas:	Cancer (11) Infection (1)

Inhibitors & Agonists

Screening Libraries

Targets Recommended: ATM/ATR

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-15520

CGK733

5 Publications Verification

ATM/ATR Cancer

CGK733 is a potent ATM/ATR inhibitor, used for the research of cancer.

CGK733 5 Publications Verification	ATM/ATR	Cancer
CGK733 is a potent *ATM/ATR* inhibitor, used for the research of cancer.

HY-13902

Berzosertib 10+ Cited Publications VE-822; VX-970	ATM/ATR	Cancer
Berzosertib (VE-822) is an *ATR* inhibitor with a K_i value of less than 0.2 nM. It also inhibits *ATM* with a K_i of 34 nM.

HY-12016

KU-55933 Maximum Cited Publications 32 Publications Verification	ATM/ATR Autophagy	Cancer
KU-55933 is a potent *ATM* inhibitor with an IC₅₀ and K_i of 12.9 and 2.2 nM, respectively, and is highly selective for ATM as compared to DNA-PK, PI3K/PI4K, ATR and mTOR.

HY-151915

ATR-IN-20	ATM/ATR mTOR	Cancer
ATR-IN-20 is a potent *ATR* (ATM/ATR) inhibitor with an IC₅₀ of 3 nM. ATR-IN-20 possess an inhibitory effect on mTOR (IC₅₀ of 18 nM) while displaying good selectivity against PI3Kα (100 nM), ATM (100 nM), and DNA-PK (662 nM). ATR-IN-20 exhibits excellent pharmacokinetic profile (F = 30%), and has anticancer effects .

HY-157767

Abd110	PROTACs ATM/ATR	Cancer
Abd110 (compound 42i) is a Lenalidomide-based *PROTAC ATR* kinase** degrader. Abd110 selectively decreases ATR and phospho-ATR without affecting related kinases ATM and DNA-PKcs .

HY-112198

AZ31	ATM/ATR	Cancer
AZ31 is a a potent, highly selective, and orally active *ATM* inhibitor with an IC₅₀ of <1.2 nM for ATM enzyme, and an IC₅₀ of 46 nM for ATM in cell. AZ31 shows excellent selectivity over ATR (>500-fold) and excellent PIKK-family selectivity and pan-kinase selectivity. AZ31 is a potent radiosensitizer in vitro, it can be used for the research of cancer .

HY-157941

ART0380	ATM/ATR	Cancer
ART0380 is a potent and selective *ATR* kinase inhibitor. ART0380 has selective antitumor activity that can be used for the research of Ataxia-Telangiectasia Mutated (ATM) aberrant cancers .

HY-144217

SKLB-197	ATM/ATR	Cancer
SKLB-197 showed an IC₅₀ value of 0.013 μM against ATR but very weak or no activity against other 402 protein kinases. It displayed potent antitumor activity against ATM-deficent tumors both in vitro and in vivo.

HY-139609

Camonsertib RP-3500; ATR inhibitor 4	ATM/ATR mTOR	Cancer
Camonsertib (RP-3500) is an orally active, selective *ATR* kinase inhibitor (ATRi) with an IC₅₀ of 1.00 nM in biochemical assays. Camonsertib shows 30-fold selectivity for ATR over mTOR (IC₅₀=120 nM) and >2,000-fold selectivity over ATM, DNA-PK, and PI3Kα kinases. Camonsertib has potent antitumor activity .

HY-B0097

Floxuridine 3 Publications Verification 5-Fluorouracil 2'-deoxyriboside	Nucleoside Antimetabolite/Analog DNA/RNA Synthesis Bacterial CMV HSV Apoptosis	Infection Cancer
Floxuridine (5-Fluorouracil 2'-deoxyriboside) is a pyrimidine analog and known as an oncology antimetabolite. Floxuridine inhibits Poly(ADP-Ribose) polymerase and induces DNA damage by activating the ATM and ATR checkpoint signaling pathways in vitro. Floxuridine is a extreamly potent inhibitor for S. aureus infection and induces cell apoptosis . Floxuridine has antiviral effects against HSV and CMV .

HY-16705

BRD4770 2 Publications Verification	Histone Methyltransferase	Cancer
BRD4770 is a histone methyltransferase G9a inhibitor. BRD4770 reduces di- and trimethylation of lysine 9 on histone H3 (H3K9) with an EC₅₀ of 5 µM, and has less or little effect toward H3K27me3, H3K36me3, H3K4me3, and H3K79me3. BRD4770 can activate the ataxia telangiectasia mutated (ATM) pathway and induce cell senescence .

Cat. No.	Product Name

HY-L173

Anti-Ovarian Cancer Compound Library	1883 Compounds compounds
Ovarian cancer is the most common cause of death in female genital malignancies, with the highest mortality rate in female genital malignancies. It is characterized by difficulty in detection in the early stage of the disease, high recurrence rate and poor prognosis. In fact, ovarian cancer includes many pathologic types. It is usually divided into epithelial ovarian cancer, malignant germ cell tumors and sex cord stromal tumors, of which epithelial ovarian cancer is the most dominant form. Clinical treatment of ovarian cancer prioritizes surgery combined with paclitaxel chemotherapy. However, due to the spread and drug resistance of tumor cells, the recurrence of ovarian cancer is high. In this case, combined with traditional methods, the development of new therapeutic agents can help to improve the treatment effect of ovarian cancer. MCE designs a unique collection of 1883 compounds with definite or potential anti-ovarian cancer activity, which mainly targeting the main targets of ovarian cancer such as PARP, ATM/ATR, VEGFR and HIF/HIF Prolyl-Hydroxylase, etc. It is an essential tool for development and research of anti-ovarian compounds.

Anti-Ovarian Cancer Compound Library

1883 Compounds compounds

Ovarian cancer is the most common cause of death in female genital malignancies, with the highest mortality rate in female genital malignancies. It is characterized by difficulty in detection in the early stage of the disease, high recurrence rate and poor prognosis. In fact, ovarian cancer includes many pathologic types. It is usually divided into epithelial ovarian cancer, malignant germ cell tumors and sex cord stromal tumors, of which epithelial ovarian cancer is the most dominant form. Clinical treatment of ovarian cancer prioritizes surgery combined with paclitaxel chemotherapy. However, due to the spread and drug resistance of tumor cells, the recurrence of ovarian cancer is high. In this case, combined with traditional methods, the development of new therapeutic agents can help to improve the treatment effect of ovarian cancer.

MCE designs a unique collection of 1883 compounds with definite or potential anti-ovarian cancer activity, which mainly targeting the main targets of ovarian cancer such as PARP, ATM/ATR, VEGFR and HIF/HIF Prolyl-Hydroxylase, etc. It is an essential tool for development and research of anti-ovarian compounds.

HY-L004

Cell Cycle/DNA Damage Compound Library	2001 compounds
DNA is prone to numerous forms of damage that can injure cells and impair fitness. Cells have developed an array of mechanisms to repair these injuries. Proliferating cells are especially vulnerable to DNA damage due to the added demands of cellular growth and division. Cell cycle checkpoints represent integral components of DNA repair that coordinate cooperation between the machinery of the cell cycle and several biochemical pathways that respond to damage and restore DNA structure. By delaying progression through the cell cycle, checkpoints provide more time for repair before the critical phases of DNA replication, when the genome is replicated, and of mitosis, when the genome is segregated. Loss or attenuation of checkpoint function may increase spontaneous and induced gene mutations and chromosomal aberrations by reducing the efficiency of DNA repair. MCE owns a unique collection of 2001 cell cycle/DNA damage-related compounds which can be used in the research of the same.

Cell Cycle/DNA Damage Compound Library

2001 compounds

DNA is prone to numerous forms of damage that can injure cells and impair fitness. Cells have developed an array of mechanisms to repair these injuries. Proliferating cells are especially vulnerable to DNA damage due to the added demands of cellular growth and division. Cell cycle checkpoints represent integral components of DNA repair that coordinate cooperation between the machinery of the cell cycle and several biochemical pathways that respond to damage and restore DNA structure. By delaying progression through the cell cycle, checkpoints provide more time for repair before the critical phases of DNA replication, when the genome is replicated, and of mitosis, when the genome is segregated. Loss or attenuation of checkpoint function may increase spontaneous and induced gene mutations and chromosomal aberrations by reducing the efficiency of DNA repair.

MCE owns a unique collection of 2001 cell cycle/DNA damage-related compounds which can be used in the research of the same.

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