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Merck
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Key Documents

SML0702

Sigma-Aldrich

MRT67307 盐酸盐

≥98% (HPLC)

同義詞:

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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About This Item

經驗公式（希爾表示法）:
C26H36N6O2 · xHCl
CAS號碼:
1190378-57-4
分子量：:
464.60 (free base basis)
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

100

化驗

≥98% (HPLC)

形狀

powder

儲存條件

desiccated

顏色

white to light brown

溶解度

H2O: 15 mg/mL, clear

儲存溫度

2-8°C

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 密鑰

UKBGBACORPRCGG-UHFFFAOYSA-N

應用

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。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。

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

分析證明 (COA)

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存取文件庫

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)
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)
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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