tnf-a , human

TNF-α (31-45), human, is a peptide of tumor necrosis factor-α.

TNF-α (10-36), human (TFA) is a peptide of human TNF-α.

TNF-α (10-36), human, is a potent pro-inflammatory cytokine involved in the acute phase stress response.

Human TNF alpha (46-65) peptide.

Adalimumab (anti-TNF-alpha) is the first fully human recombinant IgG1 monoclonal antibody that specifically targets human TNF-alpha.

Infliximab is a monoclonal antibody, a human-mouse chimeric monoclonal antibody that inhibits TNF-α and prevents TNF-α from interacting with TNFR1 and TNFR2. Infliximab can be used to treat Crohn's disease and rheumatoid arthritis.

TNF-α (31-45), human acetate is a peptide of tumor necrosis factor-α.

Cot inhibitor-1 is a selective inhibitor of Cot protein kinase (also known as Tpl2 or MAP3K8) (IC50 at 28 nM). Cot inhibitor-1 inhibited TNF-alpha production in human whole blood with IC50 of 5.7 nM. Cot is involved in a variety of cellular signaling pathways, particularly those involved in inflammation and immune responses. Cot inactivate-1 inhibits Cot activity and may have potential therapeutic effects on rheumatoid arthritis, inflammatory bowel disease and some types of cancer.

Cot inhibitor-2 is a cot (Tpl2/MAP3K8) inhibitor (IC50: 1.6 nM) with potency, selectivity and oral activity. cot inhibitor-2 inhibits LPS-stimulated TNF-α production in human whole blood with an IC50 of 0.3 μM.

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 human dendritic cells (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.

Ataquimast inhibits IL-5 secretion along with that of TNF-a, IL-4 and GM-CSF from human cells.

J-113863 is also a potent antagonist of the human CCR3 (IC50 of 0.58 nM) , but a weak antagonist of the mouse CCR3 (IC50 of 460 nM). J-113863 is inactive against CCR2, CCR4 and CCR5, as well as the LTB4 or TNF-α receptors. Anti-inflammatory effect. J-113863 is a potent and selective CCR1 (CD18) antagonist with IC50 values of 0.9 nM and 5.8 nM for human and mouse CCR1 receptors, respectively.

Tpl2 Kinase Inhibitor 1 is a potent, reversible, and highly selective ATP-competitive inhibitor of Tpl2 (MAP3K8/COT) serine/threonine kinase, with an IC₅₀ of 50 nM for Tpl2 kinase inhibition. In vitro, Tpl2 Kinase Inhibitor 1 inhibits LPS-induced TNF-α release from human primary monocytes (IC₅₀ = 0.7 μM). Tpl2 Kinase Inhibitor 1 can be used in research on inflammatory responses and certain cancers.

MN-25 (compound 4a) is an orally active indole pyridinone that functions as a novel cannabinoid ligand. It exhibits binding affinities (Ki) of 245 nM for CB1 and 11 nM for CB2 receptors. As a CB2 agonist, MN-25 inhibits TNF-R release from human peripheral blood mononuclear cells in vitro, with an IC50 of 33 μM. However, in an acute inflammation model in mice, MN-25 did not demonstrate efficacy at oral doses up to 50 mg/kg.

hMAO-B-IN-11 (Compound 12) is a selective and reversible inhibitor of human monoamine oxidase B (hMAO-B) with an IC50 value of 0.11 µM. It operates by competitively binding to the active site of hMAO-B, thereby preventing the oxidative deamination of monoamines and reducing hydrogen peroxide production. Additionally, hMAO-B-IN-11 inhibits pro-inflammatory mediators (NO, TNF-α, IL-1β) in activated microglia. This compound holds potential for research in neurodegenerative diseases such as Parkinson's and Alzheimer's.

SMU-14a is a TLR3 inhibitor with an IC50 of 0.18 µM. It suppresses IL-6 secretion in mouse peritoneal macrophages and downregulates TNF-α in human peripheral blood mononuclear cells. The compound exerts anti-inflammatory effects by reducing the phosphorylation of p65, ERK, and TBK1 via the NF-κB, MAPK, and IRF3 signaling pathways, and by lowering serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). SMU-14a is applicable in acute hepatitis research.

12-Nitrolinoleate is a linoleic acid derivative that acts as an agonist of peroxisome proliferator-activated receptor γ (PPARγ). Formed via exposure to acidified nitrite, it is present in human red blood cells and plasma. This compound stimulates PPARγ-dependent gene expression, demonstrated in a reporter assay with MCF-7 cells expressing human PPARγ, with an EC50 of 0.045 µM. At 2.5 µM, 12-Nitrolinoleate reduces the secretion of IL-6, TNF-α, and chemokine (C-C motif) ligand 2 (CCL2) in THP-1 and RAW 264.7 macrophages, and it suppresses LPS-induced NF-κB transcriptional activity in RAW 264.7 macrophages. Additionally, it inhibits TNF-α-induced increases in vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs) and enhances heme oxygenase-1 (HO-1) levels in primary human aortic endothelial cells at concentrations of 1, 5, or 10 µM.

TLR7 agonist22 (Compound 11a) is a selective TLR7 agonist with an IC50 value of 25.86 μM. It inhibits the secretion of cell HBsAg and effectively activates TLR7, inducing the release of TLR7-regulated cytokines IL-12, TNF-α, and IFN-α in human PBMC cells. TLR7 agonist22 shows promise for developing novel immunomodulatory drugs in HBV research.

TLR7 agonist21 (Compound 27B) is a selective activator of Toll-like receptor 7 (TLR7), with an EC50 of 17.53 nM for human TLR7 and 41.7 nM for mouse TLR7. It induces the secretion of pro-inflammatory cytokines, including IL-6, TNF-α, IFN-α1, and IL-4. Acting as a vaccine adjuvant, TLR7 agonist21 enhances IgG and IgA levels, offering protection for mice against influenza virus infection.

RJG-2036 is a potent covalent inhibitor of human prostaglandin reductase 2 (PTGR2) with an IC50 of 100 nM. It effectively inhibits NADPH-dependent reduction reactions, significantly reducing the secretion of inflammatory factors such as TNF-α and the release of various pro-inflammatory eicosanoids in LPS-stimulated THP-1 macrophages. RJG-2036 shows promise for research in inflammatory diseases.

1-Arachidonoyl-2-hydroxy-sn-glycero-3-PA is a phospholipid that contains arachidonic acid at the sn-1 position, serving as a precursor to 1-Monoarachidin. It binds with the LPA2/EDG4 receptor and can inhibit the secretion of TNF-α and IL-6 induced by LPS in wild-type dendritic cells but does not affect Lpa2-/- dendritic cells. Additionally, it reduces the differentiation of HT-29 human colon cancer cells into goblet cells in the presence of sodium butyrate.

CD28-IN-1 (Compound 19MS-5) is a CD28 inhibitor with a dissociation constant (KD) of 12.48 μM. It demonstrates excellent binding affinity to CD28, effectively hindering the CD28-B7 interaction. CD28-IN-1 suppresses CD28-driven immune activation and reduces cytokine production (IFN-γ, IL-2, and TNF-α) in primary human T cells co-cultured with tumor spheroids and human epithelial tissues. This compound is suitable for use in tumor immunology research.

STINGagonist-45 is a selective STING agonist (EC50= 0.28 μM) that activates the innate immune response through the cGAS-STING pathway, increasing key markers such as p-TBK1 and IRF3. This compound exhibits potent STING activation in human peripheral blood mononuclear cells (PBMC), inducing type I interferons like IFN-β and downstream cytokines such as TNF-α and IL-6. In mouse models, STINGagonist-45 enhances anti-tumor immunity, inhibits tumor growth, and increases CD8+ T cell infiltration. It is applicable for research on STING-associated diseases.

BChE-IN-44 is a potent and highly selective butyrylcholinesterase (BChE) inhibitor that can penetrate the blood-brain barrier, demonstrated by [equineBChEIC50= 18.00 pM, humanBChEIC50= 1.50 nM]. BChE-IN-44 offers neuroprotective effects against Aβ1-42-induced damage models and halts the self-aggregation of Aβ1-42. It reduces levels of inflammatory factors (NO, IL-6, and TNF-α) in BV2 cells induced by lipopolysaccharides. Additionally, BChE-IN-44 significantly ameliorates cognitive impairment caused by scopolamine. It also regulates BChE and acetylcholine levels in the hippocampus of mice. BChE-IN-44 is applicable for Alzheimer's disease (AD) research.