1202764-53-1
中文名称
4-(1-(2-氨基-5-氯嘧啶-4-基)-2-(噻唑-2-基)-3-丁炔-2-醇
英文名称
4-(1-(2-amino-5-chloropyrimidin-4-yl)-2-(thiaol-2-yl)but-30-yn-2-ol
CAS
1202764-53-1
分子式
C19H16ClN5OS
分子量
397.88
MOL 文件
1202764-53-1.mol
更新日期
2024/05/08 20:34:29
1202764-53-1 结构式
基本信息
中文别名
B0224-(1-(2-氨基-5-氯嘧啶-4-基)-2-(噻唑-2-基)-3-丁炔-2-醇
英文别名
B0224-(1-(2-amino-5-chloropyrimidin-4-yl)-2-(thiaol-2-yl)but-30-yn-2-ol
2-Thiazolemethanol, α-[2-[1-(2-amino-5-chloro-4-pyrimidinyl)-2,3-dihydro-1H-indol-6-yl]ethynyl]-α-methyl-
物理化学性质
沸点644.4±65.0 °C(Predicted)
密度1.53±0.1 g/cm3(Predicted)
储存条件-20°C储存
溶解度DMSO: 250 mg/mL (628.33 mM)
酸度系数(pKa)10.71±0.29(Predicted)
形态Solid
颜色Light yellow to yellow
常见问题列表
生物活性
B022 是一种有效的选择性的 NF-κB 诱导激酶 (NIK) 抑制剂，Ki 为 4.2 nM。B022 可保护肝脏免受毒素引起的炎症，氧化应激和伤害。靶点
Ki: 4.2 nM (NF-κB-inducing kinase (NIK))
体外研究
B022 (0-5 μM; 12 hours; Hepa1 cells) treatment suppresses NIK-induced p52 formation in a dose-dependent manner.
B022 (0-5 μM; 12 hours; Hepa1 cells) treatment for 8 h completely blocks NIK-induced expression of TNF-a, IL-6, iNOS, CCL2, and CXCL5.
Western Blot Analysis
| Cell Line: | Hepa1 cells |
| Concentration: | 0 μM, 0.5 μM, 5 μM |
| Incubation Time: | 12 hours |
| Result: | Suppressed NIK-induced p52 formation in a dose-dependent manner. |
RT-PCR
| Cell Line: | Hepa1 cells |
| Concentration: | 0 μM, 0.5 μM, 5 μM |
| Incubation Time: | 12 hours |
| Result: | Dose-dependently blocked NIK-induced expression of chemokines, cytokines, and iNOS in these cells. Completely blocked NIK-induced expression of TNF-a, IL-6, iNOS, CCL2, and CXCL5. |
体内研究
B022 (30 mg/kg; intravenous injection; twice a day; for 10 days; STOP-NIK male mice) treatment inhibits NIK-triggered liver inflammation and injury in STOP-NIK mice infected with cre adenoviruses.
| Animal Model: | STOP-NIK male mice (8 weeks) infected with Ad-cre |
| Dosage: | 30 mg/kg |
| Administration: | Intravenous injection; twice a day; for 10 days |
| Result: | Completely prevents the lethal effect of abnormally high levels of hepatic NIK in mice. Inhibited the majority of the deteriorating effects of aberrant activation of hepatic NIK. |