tnf-a , human

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

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.

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.

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

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.

DF-003 is a selective, orally active, ATP-competitive ALPK1 inhibitor capable of crossing the blood-brain barrier. It effectively inhibits human ALPK1 and ALPK1[T237M] with IC50 values of 1.5 nM and 16 nM, respectively. The compound exhibits selectivity over the nearest kinase by more than 860-fold. DF-003 suppresses the upregulation of TNF, CXCL10, or CXCL8 in HEK-293 cells. It has applications in the study of retinopathy, optic nerve edema, splenomegaly, anhidrosis, and headaches associated with ROSAH syndrome.

Benzo-17R-RvD2 is a benzo analog of RvD2 that enhances phagocytosis in human macrophages, limits neutrophil infiltration, lowers TNF-α levels, and increases the activity of IL-1 receptor antagonists during peritonitis. It promotes human leukocyte E. coli killing and reduces neutrophil aggregation area without affecting anti-Candida activity. Benzo-17R-RvD2 activates the human RvD2 receptor with an EC50 of approximately 1.5 nM. This compound is applicable in the research of inflammation-related diseases, including cardiovascular diseases, cancer, neuroinflammation, pain, and muscle regeneration.

Resolvin D5 n-3 DPA is a specific pro-resolving lipid mediator (SPM) derived from docosapentaenoic acid (DPA). It acts as an agonist for GPR101, GPR12, and GPR84 receptors, with EC50 values of 4.6 pM, 14 pM, and 1.5 pM, respectively. This compound exhibits potent pro-resolving and anti-inflammatory properties, reducing cell adhesion on TNF-α-activated human endothelial monolayers. It significantly enhances leukocyte-targeting activity by increasing the phagocytic capacity of neutrophils and macrophages to engulf bacteria. Resolvin D5 n-3 DPA is useful for studying intestinal inflammation.