SML0702
MRT67307 盐酸盐
≥98% (HPLC), IKKe and TBK-1 inhibitor, powder
别名:
N-[3-[[5-环丙基-2-[[3-（4-吗啉基甲基）苯基] 氨基]-4-嘧啶基] 氨基] 丙基]-环丁基甲酰胺 盐酸盐
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关于此项目
经验公式（希尔记法）:
C26H36N6O2 · xHCl
化学文摘社编号:
分子量:
464.60 (free base basis)
UNSPSC代码:
12352200
NACRES:
NA.77
产品名称
MRT67307 盐酸盐, ≥98% (HPLC)
质量水平
方案
≥98% (HPLC)
表单
powder
储存条件
desiccated
颜色
white to light brown
溶解性
H2O: 15 mg/mL, clear
储存温度
2-8°C
SMILES字符串
N5(CCOCC5)Cc1cc(ccc1)Nc2nc(c(cn2)C4CC4)NCCCNC(=O)C3CCC3
InChI
1S/C26H36N6O2/c33-25(21-5-2-6-21)28-11-3-10-27-24-23(20-8-9-20)17-29-26(31-24)30-22-7-1-4-19(16-22)18-32-12-14-34-15-13-32/h1,4,7,16-17,20-21H,2-3,5-6,8-15,18H2,(H,28,33)(H2,27,29,30,31)
InChI key
UKBGBACORPRCGG-UHFFFAOYSA-N
应用
MRT67307 盐酸盐已用于研究其对 LPS（脂多糖）诱导溶酶体管状结构的影响。
生化/生理作用
MRT67307 是 IKKe 和 TBK-1 的双重抑制剂。
MRT67307 是 IKKe 和 TBK-1 的双重抑制剂。IKKe 和 TBK-1 介导干扰素调节因子 3 (IRF3) 的磷酸化。
MRT67307 是氨基嘧啶衍生物，IC 50 值为 19。已知其可诱导 TLR（toll 样受体）介导的抗炎细胞因子生成。此外，MRT67307 还可预防促炎相关细胞因子的分泌。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
mTOR controls lysosome tubulation and antigen presentation in macrophages and dendritic cells.
Saric A, et al.
Molecular Biology of the Cell, 27(2), 321-333 (2016)
Daniel P.
The Inhibitor Index: A Desk Reference on Enzyme Inhibitors, Receptor Antagonists, Drugs, Toxins, Poisons, Biologics, and Therapeutic Leads (2017)
Zachary P Guinn et al.
Immunobiology, 224(4), 565-574 (2019-05-11)
IFN-γ produced during viral infections activates the IFN-γ receptor (IFNGR) complex for STAT1 transcriptional activity leading to expression of Interferon Regulatory Factors (IRF). Simultaneous activation of TBK/IKKε via TLR3 during viral infections activates the transcription factor IRF3. Together these transcription factors
Therapeutic potential of targeting TBK1 in autoimmune diseases and interferonopathies.
Hasan M and Nan Y
Pharmacological Research, 111, 336-342 (2016)
Noémie Pied et al.
PLoS pathogens, 18(7), e1010736-e1010736 (2022-07-21)
Intracellular pathogens cause membrane distortion and damage as they enter host cells. Cells perceive these membrane alterations as danger signals and respond by activating autophagy. This response has primarily been studied during bacterial invasion, and only rarely in viral infections.
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