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Tumor necrosis factor alpha (TNF-α) inhibitors reduce the production or signaling of a central inflammatory cytokine. In 1975 an endotoxin-induced serum factor that causes necrosis of tumors was described and named tumor necrosis factor. Cloning of human TNF in 1984 revealed a precursor related to lymphotoxin. Through its two receptors, TNF-α activates nuclear factor kappa B (NF-κB) and cell death pathways. Etanercept is a soluble receptor fusion protein that binds the cytokine, and C 87 is a small-molecule TNF-α inhibitor. In 1991 thalidomide was shown to inhibit TNF-α production by stimulated human monocytes, and its analogs lenalidomide and pomalidomide are also listed. Pathway compounds include the NF-κB inhibitor QNZ and necrostatin-1, an inhibitor of receptor-interacting protein kinase 1 (RIPK1).
TNF-α-IN-13 is a potent inhibitor of tumor necrosis factor-alpha (TNFα) with an IC50 of less than 0.6 μM. This compound exhibits significant anti-inflammatory properties, making it valuable for research into inflammatory diseases and therapeutic interventions targeting TNFα-mediated pathways. Its application in biochemical assays and cellular models allows for the investigation of TNFα's role in various inflammatory conditions.
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TNF-α-IN-14 is a potent and selective inhibitor of tumor necrosis factor alpha (TNFα), demonstrating an IC50 value of 1.1 µM. This compound possesses significant anti-inflammatory properties and is relevant for research applications focused on inflammatory diseases and cytokine signaling pathways. Its ability to modulate TNFα activity positions TNF-α-IN-14 as a valuable tool in the study of therapeutic strategies targeting inflammatory processes.
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TNF-α-IN-16 is a potent inhibitor of tumor necrosis factor alpha (TNFα) with an IC50 of less than 0.6 μM. This compound exhibits significant anti-inflammatory properties, making it a valuable tool for research into inflammatory diseases. It can be utilized in studies exploring the modulation of TNFα signaling pathways and the development of therapeutic strategies for conditions driven by TNFα-mediated inflammation.
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GW-3333 is a potent inhibitor of TNF-alpha-converting enzyme (TACE) and matrix metalloproteinases (MMPs). By inhibiting TACE, GW-3333 effectively reduces the production of tumor necrosis factor-alpha (TNF-alpha), which plays a critical role in inflammatory processes. This compound is primarily utilized in research applications related to arthritis and other inflammatory diseases.
Opinercept is a recombinant fusion protein that functions as an inhibitor of tumor necrosis factor-alpha (TNF-alpha) by linking TNFRSF1B to a human IgG1 Fc domain. This compound exhibits significant anti-inflammatory activity and is primarily utilized in the research of rheumatoid arthritis (RA). Its ability to modulate TNF-alpha signaling makes Opinercept a valuable tool for studies focused on autoimmune disorders and therapies targeting inflammatory pathways.
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TNF-α-IN-26 is a selective inhibitor of tumor necrosis factor-alpha (TNF-α), exhibiting an IC50 of 0.10 μM against CSBP ligands. This compound effectively inhibits LPS-stimulated TNF production in mouse models, making it a valuable tool for studying the mechanisms of inflammation. TNF-α-IN-26 is particularly relevant for research focused on inflammatory diseases and related therapeutic interventions.
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ISIS 104838 is an antisense oligonucleotide that specifically inhibits the production of tumor necrosis factor-alpha (TNF-alpha), a cytokine implicated in the pathogenesis of rheumatoid arthritis. By targeting TNF-alpha, ISIS 104838 effectively reduces inflammation and alleviates symptoms associated with joint pain and swelling. This reagent is valuable for research into therapeutic strategies for inflammatory conditions and autoimmune diseases.
(R)-Benpyrine is the isomeric form of Benpyrine, serving as a critical experimental control in research. This compound acts as a highly specific, orally active inhibitor of TNF-α, demonstrating a KD value of 82.1 μM. It exhibits strong binding to TNF-α, effectively blocking its interaction with TNFR1, as indicated by an IC50 value of 0.109 μM. (R)-Benpyrine is suitable for investigations into TNF-α-mediated inflammatory and autoimmune diseases.
Cleomiscosin A is a coumarino-lignoid that functions as a TNF-alpha inhibitor. It effectively reduces TNF-alpha secretion in mouse peritoneal macrophages, making it a valuable reagent for research focused on inflammation and immune responses. This compound has potential applications in studying the modulation of cytokine activity and the development of anti-inflammatory therapies.
Synonyms: GBL-5g
UTL-5g is a potent TNF-α inhibitor that exhibits significant anti-inflammatory properties. It demonstrates chemoprotective effects and protects liver tissues from radiation-induced damage. UTL-5g effectively reduces hepatotoxicity, nephrotoxicity, and myelotoxicity associated with Cisplatin treatment through the inhibition of TNF-α, making it a valuable reagent for research in toxicology and inflammation pathways.
TNF/IFN-γ-IN-1 is a dual inhibitor targeting tumor necrosis factor (TNF) and interferon-gamma (IFN-γ). This compound is primarily utilized in research focused on inflammatory pathways and neurodegenerative diseases, such as Alzheimer's disease. Its ability to modulate these cytokines makes it a valuable tool for studying their role in disease mechanisms and therapeutic interventions.
A-802715 is a selective TNF receptor inhibitor with potential applications in inflammatory disease research. As a methylxanthine derivative, this compound demonstrates significant biological activity by modulating TNF receptor signaling pathways. Its bioactive properties make it a valuable tool for studying the mechanisms of TNF-related diseases and evaluating therapeutic strategies.
LY 303511 hydrochloride is a structural analogue of LY294002 and acts as a TNF receptor activator. It enhances the sensitivity of SHEP-1 neuroblastoma cells to TRAIL, making it a valuable tool for investigating apoptosis mechanisms in cancer research. Additionally, LY 303511 reversibly blocks potassium currents in MIN6 insulinoma cells with an IC50 value of 64.6 ± 9.1 μM, facilitating studies in insulin secretion and pancreatic function.
Synonyms: Cycloicaritin
β-Anhydroicaritin is a TNF receptor inhibitor derived from Boswellia carterii. This compound exhibits significant biological activities, including anti-osteoporosis effects, estrogen regulation, and antitumor properties. It has been shown to improve periodontal tissue degradation and inhibit the synthesis and secretion of pro-inflammatory cytokines such as TNF-α and MMP-3 in diabetic rat models. Additionally, β-Anhydroicaritin decreases the production of inflammatory mediators like NO, IL-10, MCP-1, and IL-6 in peritonitis mice, while also reducing intracellular calcium levels and iNOS protein expression.
IW927 is a photochemically enhanced inhibitor that targets the TNF-α-TNFR1 interaction, effectively blocking the binding of TNF-α to TNFR1 with an IC50 of 50 nM. It exhibits weak reversible binding affinity (Kd = 40-100 μM) and covalently modifies TNFR1 through a photochemical reaction, without affecting TNFR2 or CD40. IW927 also inhibits TNF-α induced IκB phosphorylation with an IC50 of 600 nM, making it a valuable tool for studying TNF-α signaling pathways and the development of light-independent inhibitors.
EJMC-1 is a moderately potent inhibitor of tumor necrosis factor-alpha (TNF-α) with an IC50 value of 42 μM. By inhibiting TNF-α, this compound demonstrates potential in research applications related to inflammation and autoimmune disorders. EJMC-1 can be utilized to study the effects of TNF-α modulation in various biological systems, contributing to the understanding of its role in inflammatory responses.
TNF-α-IN-18 is a selective inhibitor of tumor necrosis factor-alpha (TNF-α) with an IC50 of 1.8 μM. It disrupts the TNF signaling pathway by preventing NF-kB translocation from the cytoplasm to the nucleus, thereby modulating inflammatory responses. This compound demonstrates mild cytotoxicity in mouse fibroblast LM cells, with a CC50 greater than 50 μM. In preclinical mouse models, TNF-α-IN-18 effectively mitigates sepsis induced by TNF or lipopolysaccharide, and provides protective effects against rheumatoid arthritis.
TNF-α-IN-8 is a selective TNF-α inhibitor that targets tumor necrosis factor-alpha, a key cytokine involved in inflammation and immunological responses. This isoindole-imide compound demonstrates significant potential in the study of various pathologies, including cancer, heart disease, osteoporosis, and inflammatory, allergic, and autoimmune disorders. Additionally, TNF-α-IN-8 serves as a click chemistry reagent, with an azide functionality that enables it to participate in copper-catalyzed azide-alkyne cycloaddition (CuAAc) and strain-promoted alkyne-azide cycloaddition (SPAAC) reactions, allowing for versatile applications in bioconjugation and biomolecular research.
JNJ525 is a selective TNFα inhibitor that shows IC50 values of 1.2 μM and 1.1 μM against TNFR1 and TNFR2, respectively. It effectively disrupts the protein-protein interaction between TNFα and its receptors by forming ordered aggregates and inducing structural transitions of the TNFα protein. JNJ525's inhibitory activity may be compromised in the presence of 0.1% Triton X-100, highlighting its specificity for TNFα interactions. This compound is valuable for studies involving inflammation and autoimmune disorders.
TNF-α-IN-2 is an effective oral inhibitor of tumor necrosis factor alpha (TNFα), demonstrating an IC50 of 25 nM in HTRF assays. By binding to TNFα, TNF-α-IN-2 disrupts the trimeric structure, resulting in altered signaling through TNFR1. This reagent is valuable for research applications related to inflammatory conditions, particularly rheumatoid arthritis.
UCB-6876 is a selective inhibitor of TNFα, specifically binding to the asymmetric crystalline form of the TNF-α trimer with a KD of 22 μM. This compound exhibits key biological activity in modulating inflammatory responses and is relevant for research applications focused on autoimmune diseases such as rheumatoid arthritis and Crohn's disease. UCB-6876 offers valuable insights into TNFα-mediated pathways, facilitating the exploration of therapeutic strategies in chronic inflammatory conditions.
TNF-α-IN-6 is an allosteric inhibitor of the tumor necrosis factor-alpha (TNFα) receptor, demonstrating a dissociation constant (KD) of 6.8 nM. This compound exhibits significant anti-inflammatory properties, making it a valuable tool in research applications focused on inflammatory diseases and cytokine signaling pathways. Its oral bioavailability allows for convenient use in various experimental settings.
UCB-5307 is a potent inhibitor of tumor necrosis factor (TNF) signaling, exhibiting a dissociation constant (KD) of 9 nM for human TNFα. This compound effectively disrupts the preformed human TNF/human TNF receptor 1 (hTNF/hTNFR1) complex, making it a valuable tool for investigating the role of TNF in various inflammatory and autoimmune conditions. UCB-5307 has significant potential for research applications aimed at understanding TNF-mediated pathways and developing therapeutic strategies targeting TNF signaling.
Synonyms: SAR-441566; TNFα activity modulator 3
Balinatunfib is an orally active inhibitor of TNF receptor 1 (TNFR1) signaling. It functions by binding to the central pocket of the soluble TNFα trimer, stabilizing an asymmetric conformation that prevents TNFα from associating with TNFR1, while sparing TNFR2. This inhibition results in a reduction of inflammatory pathways, making Balinatunfib useful for investigating mechanisms of autoimmune diseases and exploring potential therapeutic interventions.
Benpyrine is a selective TNF-α inhibitor that effectively disrupts the interaction between TNF-α and its receptor TNFR1, demonstrating an IC50 value of 0.109 µM. With a KD value of 82.1 μM, this orally active compound is suitable for exploring the mechanisms involved in TNF-α mediated inflammatory and autoimmune diseases. Benpyrine is a valuable tool for research applications focused on chronic inflammation and therapeutic modulation of immune responses.
