tnf-α

TNF-α-IN-9 is an NDM-1 inhibitor-3 analog and is a TNF-α inhibitor.TNF-α-IN-9 shows low inhibitory activity.

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

R-7050 (TNF-α Antagonist III) is a tumor necrosis factor receptor (TNFR) antagonist that exhibits heightened selectivity for TNFα.

TNF-α antagonist is an exocyclic peptide that mimics the critical TNF-α recognition loop on TNF receptor I complex and, thus, prevents ligand interaction with the receptor. By blocking the TNF receptor ligand contact site, this peptide interferes with both activating receptor activator of NF-κB (RANK) and TNF-α's recruitment and activation of osteoclasts. TNF-α antagonist has been used to block bone resorption in the study of systemic bone loss in rheumatoid arthritis and inflammatory bone destruction.

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

Human TNF alpha (46-65) peptide.

TNF-α-IN-12, a TNF-α inhibitor with an IC50 of 0.1 μM, can reduce TNF-α blood levels [1].

TNF-α-IN-14, a potent TNFα inhibitor, exhibits a selective inhibition profile with an IC50 of 1.1 µM and demonstrates antiinflammatory properties (WO2001072735A2; compound 12) [1].

TNF-α-IN-8 (compound I-42) is an isoindole-imide inhibitor of tumor necrosis factor-alpha (TNF-α), used in research on cancer, heart disease, osteoporosis, and autoimmune disorders. It also acts as a click chemistry reagent, with an Azide group suitable for CuAAc or SPAAC reactions with Alkyne, DBCO, or BCN groups.

TNF-α-IN-11 (Compound 10) is a TNF-α inhibitor with a dissociation constant (K D) of 12.06 μM. It impedes TNF-α-induced caspase activation and the NF-κB signaling pathway by binding to TNF-α, suppressing the phosphorylation of IκBα and the nuclear migration of NF-κB p65. This compound is utilized in the study of TNF-α-mediated autoimmune diseases [1].

TNF-α-IN-2 is a highly potent and orally bioavailable inhibitor of tumor necrosis factor alpha (TNFα), exhibiting an IC50 of 25 nM in the HTRF assay. It induces conformational changes in the TNFα trimer upon binding, disrupting signaling when the trimer interacts with TNFR1. TNF-α-IN-2 holds promise as a valuable tool for investigating the pathogenesis of rheumatoid arthritis [1].

TNF-α-IN-1 is a TNF-α inhibitor.

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

TNF-α-IN-16, a potent TNFα inhibitor, exhibits an IC50 of less than 0.6 μM and possesses anti-inflammatory properties (WO2001072735A2; example 18) [1].

TNF-α-IN-18 (Compound 61) is an inhibitor of TNF-α, operating with an IC50 of 1.8 μM by blocking the migration of NF-kB from the cytoplasm to the nucleus, thus suppressing the TNF signaling pathway. It exhibits minimal cytotoxicity in mouse fibroblast LM cells with a CC50 greater than 50 μM. TNF-α-IN-18 has been shown to alleviate sepsis induced by TNF or Lipopolysaccharide in mouse models and provides protection against rheumatoid arthritis in mice.

TNF-α (46-65), human (TFA) is a peptide of human TNF-α.

TNF-α-IN-10 (compound 8a) is an inhibitor of IL-6 and TNF-α, exhibiting anti-inflammatory activity [1].

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

TNF-α-IN-15, a TNF-α inhibitor, effectively reduces TNF-α blood levels [1].

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

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

TNF-α (31-45), human (TFA), is a peptide of tumor necrosis factor-α (TNF alpha), an inflammatory cytokine that induces necrosis or apoptosis.

TNF-α-IN-13, a potent inhibitor of TNFα, exhibits an IC 50 of less than 0.6 μM and possesses antiinflammatory properties (WO2001072735A2; example 6) [1].

Necrostatin-1 (Nec-1) is a specific RIP1 inhibitor and necrotic apoptosis inhibitor, which inhibits TNF-α-induced necrotic apoptosis and also inhibits IDO.

MSA-2 is an orally available non-nucleotide STING agonist. The non-covalent dimer of MSA-2 binds to STING with nanomolar affinity. It shows anti-tumor activity in syngeneic mouse tumor models, synergizes with anti-PD-1, stimulates tumor secretion of interferon-β, induces tumor regression, and has long-lasting anti-tumor immunity. [3]

Resiniferatoxin ((+)-Resiniferatoxin) is a highly potent synthetic TRPV1 agonist that inhibits the production of Th1 cytokines and has anti-inflammatory activity, reducing serum levels of IL-12, INF-γ, IL-1β, TNF-α, NO, and PGE.

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.

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

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.

LTβR-IN-1 is a potent and selective lymphin β receptor (LTβR) inhibitor with a selective inhibitory effect on the nuclear translocation of p52 of TNF12A, without affecting the nuclear translocation of p65 mediated by the TNF-α receptor. It inhibits p52 nuclear translocation stimulated by TWEAK or Anti-LTβR with an IC50 of 10 μM and regulates the NF-kB signaling pathway in a ligand-independent manner.

Vialinin A (Terrestrin A), a p-terphenyl compound, exhibits antioxidant properties and acts as a potent inhibitor of TNF-α, USP4, USP5, and sentrin/SUMO-specific protease 1 (SENP1). Its efficacy in autoimmune diseases and cancer research is noteworthy, highlighting its potential therapeutic applications.

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.

Muscone (3-Methylcyclopentadecanone) is an organic compound that is the primary contributor to the odor of musk.

Apremilast (CC-10004) (CC-10004) is a potent and orally active PDE4 (IC50=74 nM) with anti-inflammation activities.

Citronellol ((±)-β-Citronellol) is used in insect repellents and perfumes and as a mite attractant.

Taurochenodeoxycholic Acid (12-Deoxycholyltaurine) is one of the main bioactive substances of animals' bile acid.

Cepharanthine (NSC-623442) is a natural alkaloid that inhibits TNF-α-mediated NFκB stimulation, plasma membrane lipid peroxidation, and platelet aggregation, as well as cytokine production. Cepharanthine exhibits anti-inflammatory, antioxidant, and antitumor activities.

4-Hydroxychalcone (P-Cinnamoylphenol) attenuates hyperaldosteronism, inflammation, and renal injury in cryptochrome-null mice.

Pyrrolidinedithiocarbamate ammonium (1-Pyrrolidinedithiocarboxylic acid ammonium salt), a selective NF-κB inhibitor, inhibits translation of nitric oxide synthase mRNA to prevent induction.

5,6-Benzoflavone (β-Naphthoflavone) is an exogenous ligand for the aryl hydrocarbon receptor, which disrupts zinc homeostasis in human hepatocellular carcinoma HepG2 cells. 5,6-Benzoflavone (β-Naphthoflavone) possesses anti-inflammatory and antioxidant activities, inhibits LPS-induced inflammation through the AKT Nrf-2 HO-1-NF-kappaB signaling axis, inhibits TNF-α-induced ICAM-1 and VCAM-1 expression, which can be used to study neurodegenerative diseases.

ABzOH is a benzoic acid derivative, similar in structure to non-steroidal anti-inflammatory drugs such as aspirin, with anti-inflammatory, anti-tumor and anti-proliferative effects. ABzOH can not only inhibit the expression of tumor necrosis factor-α (TNF-a), interleukin-1β (IL-1β), interleukin-6 (IL-6) and other pro-inflammatory cytokines, but also inhibit breast cancer, lung cancer and pancreatic cancer.

1. 2,5-Dihydroxyacetophenone (Quinacetophenone) possess anti-anxiety, and neuroprotective qualities. 2. 2,5-Dihydroxyacetophenone (Quinacetophenone) reatment can induce a sustained activation of JNK, ERK1 2, and p38 MAPKs, it also can potentiate the pro-apoptotic and anti-proliferative effects of bortezomib in U266 cells. 3. 2,5-Dihydroxyacetophenone (Quinacetophenone) has anti-inflammatory activity in activated macrophages, raising the possibility that this compound has a therapeutic potential for inflammatory conditions. 4. 2,5-Dihydroxyacetophenone (Quinacetophenone) is an uncompetitive inhibitor of murine tyrosinase (K(I) 0.28mm), it strongly inhibits both melanogenesis and cellular tyrosinase activity in vitro in 3-isobutyl-1-methylxanthin-stimulated B16 mouse melanoma cells or in vivo in zebrafish and mouse models.

Pomalidomide (CC-4047) is an anti-angiogenic and immunomodulatory agent. Pomalidomide is a ligand for the ubiquitin E3 ligase cereblon (CRBN) and is commonly used in the synthesis of PROTAC products.

1. Linalool (Linalol), a natural compound of the essential oils, has been shown to have antinociceptive, antimicrobial, and anti-inflammatory properties. 2. Linalool was protected against LPS GalN-induced liver injury through induction of antioxidant defense via Nrf2 activating and reduction inflammatory response via NF-κB inhibition. 3. Linalool biosynthesis and accumulation might be involved in plant defense against bacterial and fungal pathogens and be associated with field resistance to citrus canker. 4. Linalool significantly increased the expression of antioxidant enzymes regulated by Nrf-2 and diminished lung tissue levels of several pro-inflammatory cytokines, including tumor necrosis factor α (TNF-α) and interleukin (IL)-6.

Lenalidomide (CC-5013) is an immunomodulator with oral activity. Lenalidomide is a ligand for the ubiquitin E3 ligase cereblon (CRBN), which selectively ubiquitinates and degrades two lymphoid transcription factors, IKZF1 and IKZF3, via the CRBN-CRL4 ubiquitin ligase, and is commonly used in the synthesis of PROTAC products.

Fumaric acid (2-Butenedioic acid) attenuates the eotaxin-1 expression in TNF-α-stimulated fibroblasts by suppressing p38 MAPK-dependent NF-κB signaling. Fumaric acid has recently been identified as an oncometabolite or an endogenous, cancer-causing metabolite. High levels of this organic acid can be found in tumors or biofluids surrounding tumors. Its oncogenic action appears due to its ability to inhibit prolyl hydroxylase-containing enzymes.

Magnolol (5,5'-Diallyl-2,2'-biphenyldiol) is a dual agonist of RXRα( EC50=10.4 μM) and PPARγ(EC50=17.7 μM). It blocks TNF-α-induced NF-KB activation.

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].