1202764-53-1
中文名稱
4-(1-(2-氨基-5-氯嘧啶-4-基)-2-(噻唑-2-基)-3-丁炔-2-醇
英文名稱
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
2024/11/09 16:37:05
1202764-53-1 結(jié)構(gòu)式
基本信息
中文別名
B0224-(1-(2-氨基-5-氯嘧啶-4-基)-2-(噻唑-2-基)-3-丁炔-2-醇
英文別名
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-
物理化學(xué)性質(zhì)
沸點(diǎn)644.4±65.0 °C(Predicted)
密度1.53±0.1 g/cm3(Predicted)
儲存條件-20°C儲存
溶解度DMSO: 250 mg/mL (628.33 mM)
酸度系數(shù)(pKa)10.71±0.29(Predicted)
形態(tài)Solid
顏色Light yellow to yellow
常見問題列表
生物活性
B022 是一種有效的選擇性的 NF-κB 誘導(dǎo)激酶 (NIK) 抑制劑，Ki 為 4.2 nM。B022 可保護(hù)肝臟免受毒素引起的炎癥，氧化應(yīng)激和傷害。靶點(diǎn)
Ki: 4.2 nM (NF-κB-inducing kinase (NIK))
體外研究
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. |
體內(nèi)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. |