IL-1F8 inhibitors are a class of chemical compounds designed to specifically target and inhibit IL-1F8, also known as interleukin-36 gamma (IL-36γ), which is a member of the IL-1 cytokine family. IL-1F8 is primarily involved in promoting immune responses, particularly in inflammatory and immune signaling pathways. It acts through the IL-36 receptor (IL-36R), triggering downstream pathways such as NF-κB and MAPK, which lead to the activation of immune cells, the production of pro-inflammatory cytokines, and the amplification of immune responses. By inhibiting IL-1F8, these compounds block its ability to bind to IL-36R, disrupting the signaling cascade that drives immune activation and inflammation.
In research settings, IL-1F8 inhibitors are essential for studying the precise role of IL-1F8 in immune regulation and inflammation. By inhibiting this cytokine, researchers can explore how IL-1F8 contributes to the activation and recruitment of immune cells, as well as its impact on cytokine networks. This enables the examination of how IL-1F8 signaling influences broader immune processes such as tissue repair, response to infections, and the regulation of immune cell behavior in various physiological conditions. Furthermore, IL-1F8 inhibitors help researchers investigate the complex interactions between members of the IL-1 family and how they coordinate to regulate immune responses. By modulating IL-1F8 activity, these inhibitors provide a valuable tool for understanding the contribution of IL-1F8 to immune homeostasis and the fine-tuning of inflammatory signaling pathways, helping to clarify its role in maintaining immune balance in the body.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Aspirin | 50-78-2 | sc-202471 sc-202471A | 5 g 50 g | $20.00 $41.00 | 4 | |
Aspirin may downregulate IL-1F8 by blocking the enzyme COX-1 and COX-2, leading to decreased synthesis of pro-inflammatory prostaglandins. | ||||||
Ibuprofen | 15687-27-1 | sc-200534 sc-200534A | 1 g 5 g | $52.00 $86.00 | 6 | |
Ibuprofen might decrease IL-1F8 expression by inhibiting the COX enzymes, which are pivotal in the biosynthesis of inflammatory prostaglandins. | ||||||
Dexamethasone | 50-02-2 | sc-29059 sc-29059B sc-29059A | 100 mg 1 g 5 g | $76.00 $82.00 $367.00 | 36 | |
Dexamethasone could suppress IL-1F8 through transrepression of NF-κB, diminishing the transcription of pro-inflammatory cytokines. | ||||||
Methotrexate | 59-05-2 | sc-3507 sc-3507A | 100 mg 500 mg | $92.00 $209.00 | 33 | |
Methotrexate may reduce IL-1F8 levels by hindering folate pathways in immune cells, leading to a general downregulation of cytokine production. | ||||||
Losmapimod | 585543-15-3 | sc-489299 sc-489299A | 10 mg 50 mg | $224.00 $809.00 | ||
Losmapimod could downregulate IL-1F8 production by specifically targeting p38 MAPK, a kinase involved in cytokine gene expression. | ||||||
BAY 11-7082 | 19542-67-7 | sc-200615B sc-200615 sc-200615A | 5 mg 10 mg 50 mg | $61.00 $83.00 $349.00 | 155 | |
Bay 11-7082 might inhibit IL-1F8 transcription by selectively blocking the phosphorylation of IκBα, thus preventing NF-κB activation. | ||||||
Wortmannin | 19545-26-7 | sc-3505 sc-3505A sc-3505B | 1 mg 5 mg 20 mg | $66.00 $219.00 $417.00 | 97 | |
Wortmannin may decrease IL-1F8 levels by blocking PI3K, thereby curtailing downstream AKT signaling and subsequent transcription of inflammatory genes. | ||||||
Trichostatin A | 58880-19-6 | sc-3511 sc-3511A sc-3511B sc-3511C sc-3511D | 1 mg 5 mg 10 mg 25 mg 50 mg | $149.00 $470.00 $620.00 $1199.00 $2090.00 | 33 | |
Trichostatin A could suppress IL-1F8 by inhibiting histone deacetylase (HDAC), which would lead to altered gene expression profiles including cytokines. | ||||||
Resatorvid | 243984-11-4 | sc-476758 | 5 mg | $360.00 | ||
Resatorvid is expected to decrease IL-1F8 by antagonizing TLR4, which ordinarily mediates the expression of inflammatory cytokines upon activation. | ||||||
CDDO Methyl Ester | 218600-53-4 | sc-504720 | 10 mg | $220.00 | ||
CDDO Methyl Ester could inhibit IL-1F8 expression by modifying the activity of Nrf2, leading to a reduced inflammatory response. | ||||||