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Berzosertib


CAS No. : 1232416-25-9

(Synonyms: VE-822; VX-970; M6620)

1232416-25-9
Price and Availability of CAS No. : 1232416-25-9
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10mg $114 In-stock
25mg $190 In-stock
50mg $288 In-stock
100mg $460 In-stock
200mg $670 In-stock
500mg $1340 In-stock
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Cat. No. : HY-13902
M.Wt: 463.55
Formula: C24H25N5O3S
Purity: >98 %
Solubility: DMSO : 16.67 mg/mL (ultrasonic;warming;heat to 60°C)
Introduction of 1232416-25-9 :

Berzosertib (VE-822) is an orally active, CNS-penetrant, and selective ATR kinase inhibitor. Berzosertib blocks ATR kinase activity, abrogates G2/M cell cycle checkpoint, impairs DNA damage repair. Berzosertib induces apoptosis, inhibnits conlony migration, inhibits cell proliferation, and activates cGAS-STING axes in cancer cells. Berzosertib can be used for the research of cancers, such as head and neck squamous cell carcinoma, and colorectal cancer[1][2][3][4][5][6]. IC50 & Target:Ki: <0.2 nM (ATR), 34 nM (ATM)[1]
IC50: 19 nM (ATR, in PSN-1 and MiaPaCa-2 cells), 2.6 μM (ATM, in PSN-1 and MiaPaCa-2 cells)[1] In Vitro:Berzosertib (0.031-1 µM; 72 h) reduces cell viability in Cal-27 and FaDu HNSCC cell lines with IC50 values of 0.285 µM and 0.252 µM, respectively[1].
Berzosertib (0.125-0.5 µM; 24-48 h) inhibits migration in Cal-27 and in FaDu HNSCC cells[1].
Berzosertib (0.25-0.5 µM; 48 h) induces apoptosis in Cal-27 and FaDu cells[1].
Berzosertib (48-72 h) inhibits proliferation of A549, NCI-H226, and NCI-H520 cells with IC50 values in the 1-4 μM range[2].
Berzosertib (40-80 nM; 1 h) enhances radiosensitivity of A549, NCI-H226, and NCI-H520 NSCLC cell lines[2].
Berzosertib (40 nM; 1 h) inhibits radiation-induced ATR (Thr1989) phosphorylation in A549, NCI-H226, and NCI-H520 NSCLC cell lines without affecting ATM (Ser1981) activation[2].
Berzosertib (40 nM; 1 h) abrogates the radiation-induced G2/M cell cycle checkpoint in A549 NSCLC cells, shifting cells into G1 phase[2].
Berzosertib (40-80 nM; 1 h) enhances radiation-induced apoptosis in A549 NSCLC cells when combined with 10 Gy, but not 2 Gy, irradiation[2].
Berzosertib (40 nM; 1 h) inhibits DNA double-strand break repair in A549 cells[2].
Berzosertib (1 µM; 2 h) impairs irradiation-induced G2/M checkpoint initiation and maintenance in HCT116 and CT26 cells, promoting mitotic entry after DNA damage[4].
Berzosertib (1 µM; 2 h) combined with 5 Gy irradiation increases micronuclei formation and cytosolic dsDNA levels in HCT116 and CT26 colorectal cancer cell lines[4].
Berzosertib (1 µM; 2 h) combined with 5 Gy irradiation robustly activates the canonical cGAS-STING-pTBK1/pIRF3 pathway, and upregulates expression of interferon-stimulated genes CXCL10, CCL5, and IFNB in HCT116, SW480, CT26, and MC38 cells[4].
Berzosertib (1 µM; 2 h) combined with 5 Gy irradiation inhibits the recruitment of SHP1 to the TRAF6/STING complex in HCT116 cells, enhancing TRAF6-STING interaction[4]. In Vivo:Berzosertib (60 mg/kg; p.o.; daily; 10 days; 1 h before 2 Gy local tumor irradiation) acts synergistically with daily 2 Gy local radiation to delay subcutaneous NSCLC brain metastasis PDX tumor growth in mice[2].
Berzosertib (60 mg/kg; p.o.; daily; 5 days; 1 h before 2.5 Gy whole brain irradiation) combined with daily 2.5 Gy whole brain irradiation significantly improves median overall survival and reduces intracranial tumor growth in mouse NSCLC brain metastasis xenograft model[2].
Berzosertib (60 mg/kg; i.g.; 2 h before Gy IR, then daily for 3 days) produces antitumor efficacy in mouse MC38 and CT26 models, when combined with 5 Gy irradiation and anti-PD-L1[4].

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