Name | INF39 |
Synonyms | INF39 INF-39 INF 39 CS-2508 Ethyl 2-(2-chlorobenzyl)acrylate Benzenepropanoic acid, 2-chloro-α-methylene-, ethyl ester |
CAS | 866028-26-4 |
Molecular Formula | C12H13ClO2 |
Molar Mass | 224.68 |
Density | 1.131±0.06 g/cm3(Predicted) |
Boling Point | 309.3±30.0 °C(Predicted) |
Appearance | oil |
Color | colorless to light brown |
Storage Condition | -20°C |
In vitro study | INF39 inhibited NLRP3 ATPase activity in a concentration-dependent manner and prevented pyroptosis in THP-1 cells. In bone marrow derived macrophages (BMDMs), it can effectively inhibit the release of NLRP3 dependent IL-1β, and reduced caspase-1 activation and corresponding pyroptosis (by detection of extracellular LDH). |
In vivo study | In rats treated with 2,4-dinitrobenzensulfonic acid, oral administration of INF39 reduced systemic and colonic inflammatory responses. The macro injury Index of INF39 treated rats was significantly reduced. Oral administration of INF3 to DNBS-treated rats reduced colonic myeloperoxidase, IL-1β, and TNF levels. INF39 exerts an effective therapeutic effect on colitis in inflamed mice by reducing the levels of pro-inflammatory cytokines such as MP0, IL-1β, and TNF in colon blocking, this indicates that blocking the activation of NLRP3 may become a suitable drug target for the treatment of intestinal inflammation. After oral administration, INF39 is stable in the body and is absorbed by the intestinal epithelium, where it can exert its effect and produce non-toxic metabolites. |
Reference Show more | 1. [IF=6.543] Wang Yue et al."Polymethoxyflavones in Citrus Regulate Lipopolysaccharide-Induced Oscillating Decay of Circadian Rhythm Genes by Inhibiting Nlrp3 Expression."Oxid Med Cell Longev. 2021;2021:8419415 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 0 ml | 0 ml | 0 ml |
5 mM | 0 ml | 0 ml | 0 ml |
10 mM | 0 ml | 0 ml | 0 ml |
5 mM | 0 ml | 0 ml | 0 ml |
biological activity | INF39 is a non-toxic, irreversible inhibitor of NLRP3, activation of NLRP3 is prevented by irreversible direct interaction with NLRP3 and partial inhibition of LPS-driven pro-inflammatory gene expression. |
Target | Value |