登录 查看组织和合同定价。
选择尺寸
关于此项目
经验公式(希尔记法):
C20H14ClN3O2 · xH2O
化学文摘社编号:
分子量:
363.80 (anhydrous basis)
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
产品名称
Chk2 抑制剂 II 水合物, ≥98% (HPLC)
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)
SMILES string
O=C(C1=CC=C2C(N=C(C3=CC=C(OC4=CC=C(Cl)C=C4)C=C3)N2)=C1)N
InChI key
UXGJAOIJSROTTN-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
solid
color
off-white to tan
solubility
DMSO: ≥2 mg/mL (warmed)
originator
Johnson & Johnson
storage temp.
2-8°C
Quality Level
Gene Information
human ... CHEK2(11200)
相关类别
Biochem/physiol Actions
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.
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).
Features and Benefits
This compound was developed by Johnson & Johnson. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Elena Oropeza et al.
Science advances, 9(26), eadf2860-eadf2860 (2023-06-30)
Cell cycle dysregulation is prerequisite for cancer formation. However, it is unknown whether the mode of dysregulation affects disease characteristics. Here, we conduct comprehensive analyses of cell cycle checkpoint dysregulation using patient data and experimental investigations. We find that ATM
Lauren E Williamson et al.
Journal of virology, 93(8) (2019-02-08)
The human B cell response to natural filovirus infections early after recovery is poorly understood. Previous serologic studies suggest that some Ebola virus survivors exhibit delayed antibody responses with low magnitude and quality. Here, we sought to study the population
Wenyu Zhang et al.
Cell death and differentiation, 27(2), 482-496 (2019-06-19)
Both the stress-response protein, SIRT1, and the cell cycle checkpoint kinase, CHK2, play critical roles in aging and cancer via the modulation of cellular homeostasis and the maintenance of genomic integrity. However, the underlying mechanism linking the two pathways remains
Yi Luan et al.
Science advances, 8(51), eade1846-eade1846 (2022-12-22)
Cyclophosphamide and doxorubicin lead to premature ovarian insufficiency as an off-target effect. However, their oocyte death pathway has been debated. Here, we clarified the precise mechanism of ovarian depletion induced by cyclophosphamide and doxorubicin. Dormant oocytes instead of activated oocytes
Ran Guo et al.
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
我们的科学家团队拥有各种研究领域经验,包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持