tnf α-induced protein 6

NF-κB/MAPK-IN-2 (compound 14) is a potent inhibitor of NF-κB and MAPK pathways. It effectively reduces the protein expression levels of p-p65, p-IκB, p-p38, p-JNK, and p-ERK. This compound decreases the release of TNF-α and IL-6 induced by LPS and inhibits the nuclear translocation of p65 and c-Fos. NF-κB/MAPK-IN-2 shows potential for research in sepsis.

Keap1-Nrf2-IN-27 is an inhibitor of the Keap1-Nrf2 protein-protein interaction (PPI) with a KD2 value of 0.119 μM. It suppresses the expression of pro-inflammatory cytokines TNF-α and IL-6 in an LPS-induced RAW264.7 cell model.

Paeoniflorin-6′-O-benzene sulfonate (CP-25) acts as an inhibitor of G protein-coupled receptor kinase 2 (GRK2), preventing its translocation to the cell membrane and inhibiting the JAK1/STAT3 signaling pathway. It suppresses HaCaT cell proliferation induced by IL-17A/CXCL2. In mouse models, CP-25 reduces the levels of inflammatory cytokines and chemokines such as IL-17A, IL-17F, IFN-γ, TNF-α, IL-22, IL-23, CXCL2, CXCL3, and CXCL9, thereby alleviating psoriasis induced by Imiquimod.

Givinostat (ITF-2357) is an HDAC inhibitor with IC50 values of 198 nM for HDAC1 and 157 nM for HDAC3.

Ansatrienin B is an ansamycin antibiotic and antifungal agent first isolated from S. collinus and S. rishiriensis., In fetal rat long bones, it is an inhibitor of parathyroid hormone-induced calcium release (IC50 = 21 nM), which is a measure of bone resorption, and pp60c-src kinase (IC50 = 50 nM). It is an inhibitor of translation at the protein synthesis stage by specific inhibition of L-leucine incorporation (IC50 = 58 nM in A549 cells). It also inhibits TNF-α-induced expression of intercellular adhesion molecule-1 (ICAM-1; IC50 = 300 nM). Early in vitro studies showed that ansatrienin B potentiates the chemotherapeutic action of 5-fluorouracil , cisplatin , bleomycin , mitomycin C , and 6-mercaptopurine. Ansatrienin B is a hydroquinone form of ansatrienin A .

F1, an anti-inflammatory peptide, incorporates the HIV-1 Tat protein transduction domain linked with a 15-amino acid sequence from residues 46-60 of the inhibitor of NF-κB kinase-interacting peptide (IKIP). It effectively blocks LPS-induced phosphorylation of IκB kinase α (IKKα) and IKKβ, along with the nuclear translocation of NF-κB (p65) in mouse peritoneal macrophages at 5 µM concentration. F1, administered at 5 mg/kg in vivo, significantly reduces IL-6, TNF-α, and IL-1β serum levels and enhances survival in a mouse sepsis model induced by LPS.

GHK-Cu acetate, a complex of the tripeptide Gly-His-Lys and a copper(II) ion, exhibits wound healing and anti-inflammatory properties. It enhances fibroblast proliferation, collagen production, and the release of pro-matrix metalloproteinase-2 (MMP-2) and glycosaminoglycans (GAGs), while also increasing decorin expression in rat wound tissue. Furthermore, at a concentration of 10 µM, it reduces levels of reactive oxygen species (ROS), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) in LPS-stimulated RAW 264.7 cells. Additionally, GHK-Cu at 10 µg/g mitigates LPS-induced reductions in lung superoxide dismutase (SOD) activity and glutathione (GSH) levels, decreases the accumulation of cells and total protein in bronchoalveolar lavage fluid (BALF), and thus, attenuates acute lung injury in mice.

Euphohelioscopin A, an activator of protein kinase C (PKC), it inhibits proliferation and induces differentiation of the myeloid leukemia cell lines THP-1 and HL-60. Euphohelioscopin A has anti-inflammary activity, it exhibits moderate inhibitory activity