tnf-alpha-in-6

TNF-α-IN-6 is an orally efficacious, allosteric inhibitor of TNFα (K_D = 6.8 nM).

Manumycin A is an antibiotic with anticancer activity and is a mammalian thioredoxin reductase-1 (TrxR-1) inhibitor.Manumycin A inhibits the production of IL-1β, IL-6, and IL-8 in TNF alpha-stimulated THP-1 cells and peripheral blood mononuclear cells in a dose-dependent manner, inducing apoptosis.

Glucocorticoid receptor/NF-κB modulator-1 (Compound 20) is a derivative of ocotillol. It prevents degradation of glucocorticoid receptor (GR) mRNA and GR protein and inhibits the activation of the NF-κB signaling pathway. Additionally, it reduces levels of nitric oxide (NO), interleukin (IL-6), and tumor necrosis factor-alpha (TNF-α), and improves sepsis in mice.

Losmapimod hydrochloride (GW856553X) is an orally active, potent, and highly selective p38 alpha/beta MAPK inhibitor (IC50 = 0.8 nM). It greatly reduces the release of pro-inflammatory cytokines, including TNF-alpha and IL-6, by blocking inflammatory signaling cascades, showing remarkable efficacy in COPD and severe cardiovascular inflammation models.

CC-1088 is an analog of thalidomide with potential antineoplastic activity that belongs to the functional class of agents called selective cytokine inhibitory drugs (SelCIDs). SelCIDs inhibit phosphodiesterase-4 (PDE 4), an enzyme involved in tumor necrosis factor alpha (TNF alpha) production. CC-1088 inhibits production of the cytokines vascular endothelial growth factor (VEGF) (a pro-angiogenic factor) and interleukin-6 (IL-6).

Manelimab is a humanized monoclonal antibody fusion protein (immunocytokine) targeting the human interleukin-10 receptor alpha subunit (IL-10Ra). IL-10Ra is a critical component of the anti-inflammatory IL-10 signaling pathway. Manelimab specifically binds to and activates the IL-10Ra receptor, mimicking the biological functions of IL-10 and inducing the phosphorylation of the downstream JAK1/STAT3 signaling pathway. This activation significantly inhibits the release of pro-inflammatory cytokines (such as TNF-alpha, IL-1b, and IL-6) and enhances the polarization of immunosuppressive macrophages. This immunocytokine has potential applications in the research of autoimmune diseases, chronic inflammation, and as an immunotherapy to modulate the tumor microenvironment.

Mca-(endo-1a-Dap(Dnp))-TNF-Alpha (-5 to +6) amide (human) is a peptide used as a fluorescence resonance energy transfer (FRET) based substrate for proteolytic activity assays, with cleavage-induced changes in fluorescence intensity indicating enzymatic activity [1].

MAO-B-IN-30 is a selective and potent MAO-B inhibitor that crosses the blood-brain barrier with antiproliferative activity and inhibits both MAO-A and MAO-B.MAO-B-IN-30 reduces the levels of TNF-alpha, IL-6, and NF-kB in organisms, and can be used to study Parkinson's-type neurological disorders.

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.

Forsythoside B (Standard) is a reference standard for research and analysis in studies involving Forsythoside B. Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF-κB activation. Forsythoside B inhibits the inflammatory response and has antioxidant properties. Potent neuroprotective effects with a favorable therapeutic time-window, reduce of cerebral ischemia and reperfusion injury degree, attenuating blood-brain barrier (BBB) breakdown; Rescued cardiac function from I/R injury. Forsythoside B has antisepsis effect, is mediated by decreasing local and systemic levels of a wide spectrum of inflammatory mediators.