C3742
Chk2 Inhibitor II hydrate
≥98% (HPLC)
Sinónimos:
2-(4-(4-Chlorophenoxy)phenyl)-1H-benzimidazole-5-carboxamide hydrate
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About This Item
Fórmula empírica (notación de Hill):
C20H14ClN3O2 · xH2O
Número de CAS:
Peso molecular:
363.80 (anhydrous basis)
Número MDL:
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
NACRES:
NA.77
Productos recomendados
Nivel de calidad
Ensayo
≥98% (HPLC)
Formulario
solid
color
off-white to tan
solubilidad
DMSO: ≥2 mg/mL (warmed)
emisor
Johnson & Johnson
temp. de almacenamiento
2-8°C
cadena SMILES
O=C(C1=CC=C2C(N=C(C3=CC=C(OC4=CC=C(Cl)C=C4)C=C3)N2)=C1)N
InChI
1S/C20H14ClN3O2/c21-14-4-8-16(9-5-14)26-15-6-1-12(2-7-15)20-23-17-10-3-13(19(22)25)11-18(17)24-20/h1-11H,(H2,22,25)(H,23,24)
Clave InChI
UXGJAOIJSROTTN-UHFFFAOYSA-N
Información sobre el gen
human ... CHEK2(11200)
Acciones bioquímicas o fisiológicas
Chk2 Inhibitor II is a checkpoint kinase 2 inhibitor, which controls the p53 response to DNA breaks induced by radiation, leading to apoptosis. Protection of T-cells from apoptosis implies use as an adjuvant for radiation therapy in cancer. IC50 = 15 nM; Ki = 37 nM. Chk2 Inhibitor II shows 1000-fold greater selectivity for the Chk2 serine/threonine kinase than for the Cdk1/B and CK1 kinases (for which IC50 = 12 μM and 17 μM, respectively). Chk2 Inhibitor II weakly inhibits a panel of 31 other kinases (<25% inhibition at a concentration of 10 μM and prevents apoptosis of human CD4+ and CD8+ T-cells subjected to ionizing radiation (EC50 = 3 μM and 7.6 μM, respectively).
Características y beneficios
This compound was developed by Johnson & Johnson. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
Código de clase de almacenamiento
11 - Combustible Solids
Clase de riesgo para el agua (WGK)
WGK 3
Punto de inflamabilidad (°F)
Not applicable
Punto de inflamabilidad (°C)
Not applicable
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Antioxidants (Basel, Switzerland), 11(6) (2022-06-25)
Reactive oxygen species (ROS) act as a signaling intermediate to promote cellular adaptation to maintain homeostasis by regulating autophagy during pathophysiological stress. However, the mechanism by which ROS promotes autophagy is still largely unknown. Here, we show that the ATM/CHK2/ULK1
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