SML1415
VE-821
≥98% (HPLC), ATP-competitive ATR inhibitor, powder
동의어(들):
3-Amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide, 3-Amino-6-[4-(methylsulfonyl)phenyl]-N-phenyl-2-pyrazinecarboxamide, VE821
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크기 선택
보기 변경
제품정보 (DICE 배송 시 비용 별도)
실험식(Hill 표기법):
C18H16N4O3S
CAS 번호:
Molecular Weight:
368.41
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
제품 이름
VE-821, ≥98% (HPLC)
Quality Level
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: ≥10 mg/mL, clear
storage temp.
−20°C
SMILES string
CS(C(C=C1)=CC=C1C2=NC(C(NC3=CC=CC=C3)=O)=C(N)N=C2)(=O)=O
InChI
1S/C18H16N4O3S/c1-26(24,25)14-9-7-12(8-10-14)15-11-20-17(19)16(22-15)18(23)21-13-5-3-2-4-6-13/h2-11H,1H3,(H2,19,20)(H,21,23)
InChI key
DUIHHZKTCSNTGM-UHFFFAOYSA-N
Application
VE-821 has been used as an inhibitor of ATM- and Rad3-related (ATR) protein in human cancer cells.
Biochem/physiol Actions
VE-821 is a ATP-competitive inhibitor of ATR.
VE-821 is a potent ATP-competitive inhibitor of the DNA damage response (DDR) kinase Ataxia telangiectasia-mutated (ATM) and ATM- and Rad3-related (ATR) with a Ki of 13 nM. VE-821 has minimal cross-reactivity against the related PIKKs ATM, DNA-dependent protein kinase (DNA-PK), mTOR and PI3-kinase-γ (Ki of 16 μM, 2.2 μM, >1 μM and 3.9 μM, respectively) and against a large panel of unrelated protein kinases. VE-821 used alone caused death in a large fraction of cancer cell populations and also showed strong synergy with genotoxic agents. VE-821 increased sensitivity of cells to radiation and also sensitized cancer cells to a variety of chemotherapeutic agents.
Other Notes
VE-821 has been expertly reviewed and recommended by the Chemical Probes Portal. For more information, please visit the VE-821 probe summary on the Chemical Probes Portal website.
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Tingting Li et al.
Aging, 12(14), 14791-14807 (2020-07-21)
Protection of telomere 1 (POT1), the telomeric single-stranded DNA (ssDNA)-binding protein in the shelterin complex, has been implicated in the DNA damage response, tumorigenesis and aging. Telomere dysfunction induced by telomere deprotection could accelerate cellular senescence in primary human cells.
Human cancer cells utilize mitotic DNA synthesis to resist replication stress at telomeres regardless of their telomere maintenance mechanism
Ozgun Ozer, et al.
Oncotarget null
Aldo S Bader et al.
Nature communications, 14(1), 8419-8419 (2023-12-19)
DNA double-strand breaks (DSBs) are the most mutagenic form of DNA damage, and play a significant role in cancer biology, neurodegeneration and aging. However, studying DSB-induced mutagenesis is limited by our current approaches. Here, we describe iMUT-seq, a technique that