3-Hydroxykynurenamine, also known as 3-Hydroxy-L-kynurenamine or 3-HKA, is a biogenic amine produced via an alternative pathway of tryptophan metabolism. In vitro, 3-HKA has an anti-inflammatory profile by inhibiting the IFN-γ mediated STAT1 NF-κΒ pathway in both mouse and humandendriticcells (DCs) with a consequent decrease in the release of pro-inflammatory chemokines and cytokines, most notably TNF, IL-6, and IL12p70. 3-HKA has protective effects in an experimental mouse model of psoriasis by decreasing skin thickness, erythema, scaling and fissuring, reducing TNF, IL-1β, IFN-γ, and IL-17 production, and inhibiting generation of effector CD8+ T cells. Similarly, in a mouse model of nephrotoxic nephritis, besides reducing inflammatory cytokines, 3-HKA improves proteinuria and serum urea nitrogen, overall ameliorating immune-mediated glomerulonephritis and renal dysfunction.This compound is unstable in powder form and other related salt forms are recommended.
1-Arachidonoyl lysophosphatidic acid is a phospholipid containing arachidonic acid at the sn-1 position. It has been found in rat brain as 37% of the arachidonic acid-containing lysophosphatidic acid (LPA) species and is a precursor to 1-arachidonoyl glycerol . 1-Arachidonoyl lysophosphatidic acid binds to the LPA2 EDG4 receptor with an EC50 value of approximately 10 nM. It prevents TNF-α and IL-6 secretion in wild-type but not Lpa2- - dendriticcells stimulated by LPS. It also decreases differentiation of HT-29 human colon carcinoma cells to goblet cells in the presence of sodium butyrate.
BLX3887 is an inhibitor of 15-lipoxygenase type 1 (15-LO-1; IC50 = 32 nM in a cell-free enzyme assay).1 It is selective for 15-LO-1 over 15-LO-2, which it does not inhibit, 5-LO (IC50 = 472 nM), and 12-LO (IC50 = 3,310 nM). BLX3887 inhibits the production of 15-LO metabolites selectively in eosinophils over neutrophils when used at a concentration of 10 μM. It also inhibits endocytosis in, and the migration of, isolated human peripheral blood mononuclear cell-derived dendriticcells in vitro. |1. Archambault, A.-S., Turcotte, C., Martin, C., et al. Comparison of eight 15-lipoxygenase (LO) inhibitors on the biosynthesis of 15-LO metabolites by human neutrophils and eosinophils. PLoS One 13(8), e0202424 (2018).
PSMα3 is a peptide compound that can be utilized to induce tolerance in dendriticcells (DCs) for DC vaccination strategies. It effectively penetrates and modulates human monocyte-derived DCs by modifying the maturation process induced by TLR2 or TLR4. Additionally, PSMα3 inhibits the production of both pro- and anti-inflammatory cytokines and decreases antigen uptake. Notably, PSMα3 is a significant virulence factor released by the most pathogenic strains of methicillin-resistant Staphylococcus aureus (MRSA).
M04 acts as a stimulator of interferon genes (STING) agonist, effectively inducing IFN reporter gene expression in HEK293T cells equipped with wild-type human STING. Its activity is specific, not affecting HEK293T cells with the R71H-G230A-R293Q (HAQ) human STING variant or mouse RAW 264.7 cells, showcasing allelic- and species-dependent effects at a concentration of 75 µM. This compound also stimulates the production of TNF-α, IL-10, IL-1β, and IL-12p70 in human peripheral blood mononuclear cells (PBMCs). At 50 µM, M04 enhances human monocyte-derived dendriticcells' expression of HLA-DR (MHC class II receptor) and co-stimulatory molecules CD40, CD80, and CD86, improving T cell cross-priming in an ex vivo assay.
T-Cadinol (Cedrelanol) 是一种从 C. sylvestris 中分离得到的倍半萜化合物,具有抗克氏锥虫活性和潜在的抗癌活性,抑制锥鞭毛体和无鞭毛体,诱导人单核细胞的树突状细胞并驱动 Th1 极化。T-Cadinol 是一种钙拮抗剂,以浓度依赖性方式松弛 60 mM K + 诱导的收缩。