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Results for "

TRAF6

" in MedChemExpress (MCE) Product Catalog:

27

Inhibitors & Agonists

2

Biochemical Assay Reagents

5

Peptides

8

Natural
Products

4

Recombinant Proteins

3

Antibodies

4

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B1829A
    Dexamethasone phosphate disodium
    10+ Cited Publications

    Dexamethasone 21-phosphate disodium

    		 Glucocorticoid Receptor TGF-β Receptor Interleukin Related Neurological Disease Inflammation/Immunology
    Dexamethasone phosphate (Dexamethasone 21-phosphate) disodium is a prodrug form of the glucocorticoid Dexamethasone (HY-14648). Dexamethasone phosphate disodium is produced by introducing a phosphate ester group at the 21-position of the Dexamethasone molecule, forming a salt with sodium ions, thereby significantly improving water solubility. Dexamethasone phosphate disodium inhibits LPS (HY-D1056)-induced degradation of IRAK-1 and IRAK-4, and blocks LPS-induced activation of TRAF6, p-TAK1 and p-JNK. Dexamethasone phosphate disodium inhibits the secretion of RANTES, TGF-β1 and NO, promotes the production of MIP-1α and IL-10, and blocks microglial migration. Dexamethasone phosphate disodium is almost completely converted to Dexamethasone in rat blood, and supports transdermal delivery via iontophoresis. Dexamethasone phosphate disodium can be used in research related to steroid-dependent ulcerative colitis, chemotherapy-induced vomiting, allergic asthma and acute colitis (inflammatory bowel disease) [6].
    Dexamethasone phosphate disodium
  • HY-120934
    C25-140
    Maximum Cited Publications
    26 Publications Verification

    		 TNF Receptor E1/E2/E3 Enzyme Inflammation/Immunology
    C25-140, a first-in-class, orally active, and fairly selective TRAF6-Ubc13 inhibitor, directly binds to TRAF6, and blocks the interaction of TRAF6 with Ubc13. C25-140 lowers TRAF6 activity, reduces NF-κB activation, and combats autoimmunity .
    C25-140
  • HY-N0481
    Roburic acid
    1 Publications Verification

    		 COX TNF Receptor NO Synthase Interleukin Related NF-κB Apoptosis p38 MAPK JNK ERK Keap1-Nrf2 RANKL/RANK Neurological Disease Inflammation/Immunology Cancer
    Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki of 7.066 μM against human TNF, an IC50 of 9 μM against human COX-2, and an IC50 of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases .
    Roburic acid
  • HY-N0026
    2'-Acetylacteoside
    1 Publications Verification

    2'-AA

    		 Monoamine Oxidase RANKL/RANK TNF Receptor NF-κB IKK Cardiovascular Disease Neurological Disease Metabolic Disease
    2'-Acetylacteoside (2'-AA) is a natural compound with oral activity and blood-brain barrier permeability. 2'-Acetylacteosideexhibits MAO‑B inhibitory activity (IC50 = 17.71 μM, Ki = 13.81 μM). 2'-Acetylacteoside downregulates the expression of RANK, TRAF6, NF‑κB, NFATc1 and IKKβ, disrupts the RANKL/RANK interaction, blocks downstream signaling pathways, and increases the level of phosphorylated Akt. 2'-Acetylacteoside possesses potent anti-osteoclastogenic, anti-bone resorptive, pro-neurogenic, neuroprotective and antioxidant activities. 2'-Acetylacteoside can be used in the research of osteoporosis, ischemic stroke and Parkinson's disease .
    2'-Acetylacteoside
  • HY-110247
    TRAF-STOP inhibitor 6877002
    4 Publications Verification

    		 TNF Receptor NF-κB Cardiovascular Disease Inflammation/Immunology
    TRAF-STOP inhibitor 6877002 is a selective CD40-TRAF6 interaction inhibitor. TRAF-STOP inhibitor 6877002 exerts anti-atherosclerotic activity by blocking the CD40-TRAF6 signaling pathway, inhibiting classical monocyte activation, leukocyte recruitment, and macrophage activation and migration. TRAF-STOP inhibitor 6877002 reduces the phosphorylation levels of signaling intermediates in the canonical NF-κB pathway .
    TRAF-STOP inhibitor 6877002
  • HY-N1431
    Tabersonine
    3 Publications Verification

    		 NOD-like Receptor (NLR) Apoptosis Cytochrome P450 NF-κB PI3K Akt CDK Caspase Interleukin Related p38 MAPK Inflammation/Immunology Cancer
    Tabersonine is a selective, orally active NLRP3 inhibitor. Tabersonine directly binds to the NACHT domain of NLRP3, inhibiting its ATPase activity and oligomerization, thereby blocking ASC spot formation and caspase-1 activation, and reducing the release of pro-inflammatory cytokines such as IL-1β. Tabersonine also inhibits K63-linked ubiquitination of TRAF6, blocking NF-κB, PI3K/Akt, and p38 MAPK signaling pathways. Tabersonine can inhibit inflammatory responses, induce apoptosis of liver cancer cells through mitochondrial pathways and death receptor pathways, reduce mitochondrial membrane potential, promote cytochrome c release, and activate caspase proteins. Tabersonine is mainly used in the study of NLRP3-driven inflammatory diseases (such as acute lung injury, sepsis, peritonitis) and tumors such as liver cancer .
    Tabersonine
  • HY-W013636C
    2-Ketoglutaric acid potassium
    5+ Cited Publications

    Alpha-Ketoglutaric acid potassium

    		 Tyrosinase Endogenous Metabolite TNF Receptor Neurological Disease Metabolic Disease
    2-Ketoglutaric acid (Alpha-Ketoglutaric acid) (potassium) is an intermediate in the production of ATP or GTP in the Krebs cycle. 2-Ketoglutaric acid potassium is a reversible and orally active inhibitor of tyrosinase with an IC50 value of 15 mM. 2-Ketoglutaric acid potassium also acts as the major carbon skeleton for nitrogen-assimilatory reactions. 2-Ketoglutaric acid potassium significantly suppresses abnormal intestinal permeability, delocalization of tight junction proteins from the intestinal cells, expression of TNFα in vitro and in vivo. 2-Ketoglutaric acid potassium directly binds to TAK1, and inhibits the TRAF6-TAK1 interaction. 2-Ketoglutaric acid potassium also alleviates inflammatory bowel disease (IBD) symptoms and gut microbiota dysbiosis, evident by the improvements in the intestine length .
    2-Ketoglutaric acid potassium
  • HY-P3708
    TRAF6 control peptide

    		E1/E2/E3 Enzyme p62 Others
    TRAF6 control peptide is a control peptide for TRAF6 .
    TRAF6 control peptide
  • HY-P3709
    TRAF6 peptide

    		p62 E1/E2/E3 Enzyme Neurological Disease
    TRAF6 peptide is a specific TRAF6-p62 inhibitor. TRAF6 peptide potently abrogates NGF-dependent TrkA ubiquitination. TRAF6 peptide has good research potential in neurological diseases such as alzheimer's disease (AD), parkinson's, ALS, head trauma, epilepsy and stroke .
    TRAF6 peptide
  • HY-NP134
    Flagellin from S. typhimurium

    		Toll-like Receptor (TLR) MyD88 NF-κB Interleukin Related IFNAR Inflammation/Immunology Cancer
    Flagellin from S. typhimurium is a potent TLR5 agonist. Flagellin from S. typhimurium activates immune cells and inhibits the activity of melanoma cells. Flagellin from S. typhimurium activates the NF-κB pathway dependent on the TLR5/MyD88/TRAF6 signaling axis in cells. Flagellin from S. typhimurium induces a proinflammatory response in the primary chicken hepatocyte-nonparenchymal cell co-culture system by promoting IL-8 production, inhibiting IL-10 production, and increasing the IFN-γ/IL-10 ratio. Flagellin from S. typhimurium can be used for research on melanoma and inflammatory diseases .
    Flagellin from S. typhimurium
  • HY-142026
    Vitisin A

    (+)-Vitisin A

    		 Caspase ERK NF-κB Influenza Virus PAK LDLR PPAR PCSK9 Androgen Receptor Keap1-Nrf2 Monoamine Oxidase Cholinesterase (ChE) IKK Wnt β-catenin Reactive Oxygen Species (ROS) Apoptosis Cuproptosis Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC50 values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases .
    Vitisin A
  • HY-P3709A
    TRAF6 peptide TFA

    		p62 E1/E2/E3 Enzyme Neurological Disease
    TRAF6 peptide TFA is a specific TRAF6-p62 inhibitor. TRAF6 peptide TFA potently abrogates NGF-dependent TrkA ubiquitination. TRAF6 peptide TFA has good research potential in neurological diseases such as alzheimer's disease (AD), parkinson's, ALS, head trauma, epilepsy and stroke .
    TRAF6 peptide TFA
  • HY-125025
    SMI 6860766

    		TNF Receptor Metabolic Disease Inflammation/Immunology
    SMI 6860766, a small molecule inhibitor of CD40-TRAF6 interaction, improves glucose tolerance, reduces immune cell accumulation in adipose tissue, and reduces AT inflammation .
    SMI 6860766
  • HY-N0320
    Salvianolic acid D

    		Bcl-2 Family Caspase Toll-like Receptor (TLR) MyD88 NF-κB Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Salvianolic acid D is a depside. Salvianolic acid D can be isolated from Salvia miltiorrhiza (Danshen). Salvianolic acid D promotes the expression of Bcl-2, and inhibits the expressions of Bax, Cleaved caspase-3 and -9. Salvianolic acid D reduces the expression levels of TLR4, MyD88 and TRAF6 proteins both in vitro and in vivo, and significantly inhibits the nuclear translocation of NF-κB. Salvianolic acid D inhibits the cytoplasmic translocation of HMGB1. Salvianolic acid D suppresses inflammatory responses and alleviates cerebral ischemia-reperfusion injury. Salvianolic acid D serves as a potential antiplatelet active component .
    Salvianolic acid D
  • HY-B1829
    Dexamethasone phosphate
    10+ Cited Publications

    Dexamethasone 21-phosphate

    		 Glucocorticoid Receptor TGF-β Receptor Interleukin Related Neurological Disease Inflammation/Immunology
    Dexamethasone phosphate (Dexamethasone 21-phosphate) is a prodrug form of the glucocorticoid Dexamethasone (HY-14648). Dexamethasone phosphate is prepared by introducing a phosphate ester group to the hydroxyl group at position 21 of the Dexamethasone molecule. Dexamethasone phosphate inhibits LPS (HY-D1056)-induced degradation of IRAK-1 and IRAK-4, and blocks LPS-induced activation of TRAF6, p-TAK1 and p-JNK. Dexamethasone phosphate inhibits the secretion of RANTES, TGF-β1 and NO, promotes the production of MIP-1α and IL-10, and blocks microglial migration. Dexamethasone phosphate is almost completely converted to Dexamethasone in rat blood, and supports transdermal delivery via iontophoresis. Dexamethasone phosphate can be used in research related to steroid-dependent ulcerative colitis, chemotherapy-induced vomiting, allergic asthma and acute colitis (inflammatory bowel disease) [6].
    Dexamethasone phosphate
  • HY-155801
    CRX 527

    		Toll-like Receptor (TLR) NF-κB TNF Receptor MyD88 Apoptosis DNA/RNA Synthesis Cardiovascular Disease Infection Neurological Disease Inflammation/Immunology Cancer
    CRX 527 is a TLR4 agonist. CRX 527 activates the MyD88-dependent, TRIF-dependent, and TRAF6/NF-κB signaling pathways downstream of TLR4, mimics lipid A, and regulates antigen processing and presentation by dendritic cells. CRX 527 stimulates innate immune responses and enhances vaccine efficacy. CRX 527 maintains the structural integrity of hematopoietic tissues, spleen and intestine, alleviates radiation-induced damage, preserves intestinal homeostasis, and inhibits apoptosis, inflammatory responses, oxidative stress and DNA damage. CRX 527 can be used in the research of acute radiation syndrome, melanoma, HPV-related tumors and intracerebral hemorrhage .
    CRX 527
  • HY-RS14975
    TRAF6 Human Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others

    TRAF6 Human Pre-designed siRNA Set A contains three designed siRNAs for TRAF6 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.

    TRAF6 Human Pre-designed siRNA Set A
    TRAF6 Human Pre-designed siRNA Set A
  • HY-N1431A
    Tabersonine hydrochloride
    3 Publications Verification

    		 NOD-like Receptor (NLR) Apoptosis Cytochrome P450 NF-κB PI3K Akt CDK Caspase Interleukin Related p38 MAPK Neurological Disease Inflammation/Immunology
    Tabersonine hydrochloride is a selective, orally active NLRP3 inhibitor. Tabersonine hydrochloride directly binds to the NACHT domain of NLRP3, inhibiting its ATPase activity and oligomerization, thereby blocking ASC spot formation and caspase-1 activation, and reducing the release of pro-inflammatory cytokines such as IL-1β. Tabersonine hydrochloride also inhibits K63-linked ubiquitination of TRAF6, blocking NF-κB, PI3K/Akt, and p38 MAPK signaling pathways. Tabersonine hydrochloride can inhibit inflammatory responses, induce apoptosis of liver cancer cells through mitochondrial pathways and death receptor pathways, reduce mitochondrial membrane potential, promote cytochrome c release, and activate caspase proteins. Tabersonine hydrochloride is mainly used in the study of NLRP3-driven inflammatory diseases (such as acute lung injury, sepsis, peritonitis) and tumors such as liver cancer .
    Tabersonine hydrochloride
  • HY-P11001
    RANK-derived TRAF6 inhibitor

    		TNF Receptor Cancer
    RANK-derived TRAF6 inhibitor is a TRAF6 inhibitor peptide that blocks the interaction of TRAF6 and LMP1 with an IC50 of 177 nM. RANK-derived TRAF6 inhibitor causes a severe reduction in cell viability in the LMP1-dependent lymphoblastoid cell lines (LCLs) .
    RANK-derived TRAF6 inhibitor
  • HY-RS23098
    Traf6 Rat Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others

    Traf6 Rat Pre-designed siRNA Set A contains three designed siRNAs for Traf6 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.

    Traf6 Rat Pre-designed siRNA Set A
    Traf6 Rat Pre-designed siRNA Set A
  • HY-RS16663
    Traf6 Mouse Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others

    Traf6 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Traf6 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.

    Traf6 Mouse Pre-designed siRNA Set A
    Traf6 Mouse Pre-designed siRNA Set A
  • HY-164670
    D228

    		p38 MAPK MyD88 Inflammation/Immunology
    D228 is an orally active antiinflammatory agent. D228 reduces ConA induced T lymphocyte cell proliferation (IC50: 42.85 μM) and LPS induced B lymphocyte cell proliferation (IC50: 3.15 μM). D228 is effective against inflammatory bowel disease (IBD). D228 alleviates the DSS (HY-116282C)-induced inflammation response in the IBD model by downregulating the MyD88/TRAF6/p38 signaling .
    D228
  • HY-P11002
    PTD

    Antennapedia leader peptide

    		 TNF Receptor Cancer
    PTD (Antennapedia leader peptide) is a negative control of TRAF6 inhibitor peptide DRQIKIWFQNRRMKWKK-RKIPTEDEY .
    PTD
  • HY-176220
    GPX4-AUTAC

    		AUTACs Autophagy Glutathione Peroxidase Ferroptosis Cancer
    GPX4-AUTAC is a GPX4-targeting autophagy-mediated degrader (AUTAC). GPX4-AUTAC consists of an inhibitor ML162-yne (HY-153748), a degradation tag FBnG (HY-W073762) and a glycol linker (HY-W021401). GPX4-AUTAC promotes the ubiquitination of GPX4 by E3 ligase TRAF6, and enhances the binding with GPX4 and p62, leading to the selective autophagy-dependent degradation of GPX4. GPX4-AUTAC significantly induces ferroptosis and shows a potent anti-cancer activity in breast cancer cells, breast cancer-derived organoids (PDOs) and MDA-MB-231 tumor xenograft mice model, with potent synergistic effects when combined with Sulfasalazine (SAS) (HY-14655) or chemotherapy drugs (Paclitaxel (HY-B0015) or Cisplatin (HY-17394)) .
    GPX4-AUTAC
  • HY-N0026R
    2'-Acetylacteoside (Standard)

    2'-AA (Standard)

    		 Reference Standards Monoamine Oxidase RANKL/RANK TNF Receptor NF-κB IKK Cardiovascular Disease Neurological Disease Metabolic Disease
    2'-Acetylacteoside (Standard) is the analytical standard of 2'-Acetylacteoside (2'-AA) (HY-N0026). This product is intended for research and analytical applications. 2'-Acetylacteoside is a natural compound with oral activity and blood-brain barrier permeability. 2'-Acetylacteosideexhibits MAO‑B inhibitory activity (IC50 = 17.71 μM, Ki = 13.81 μM). 2'-Acetylacteoside downregulates the expression of RANK, TRAF6, NF‑κB, NFATc1 and IKKβ, disrupts the RANKL/RANK interaction, blocks downstream signaling pathways, and increases the level of phosphorylated Akt. 2'-Acetylacteoside possesses potent anti-osteoclastogenic, anti-bone resorptive, pro-neurogenic, neuroprotective and antioxidant activities. 2'-Acetylacteoside can be used in the research of osteoporosis, ischemic stroke and Parkinson's disease .
    2'-Acetylacteoside (Standard)
  • HY-N0481R
    Roburic acid (Standard)

    		Reference Standards COX TNF Receptor NO Synthase Interleukin Related NF-κB Apoptosis p38 MAPK JNK ERK Keap1-Nrf2 RANKL/RANK Inflammation/Immunology
    Roburic acid (Standard) is the analytical standard of Roburic acid. This product is intended for research and analytical applications. Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki of 7.066 μM against human TNF, an IC50 of 9 μM against human COX-2, and an IC50 of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases.
    Roburic acid (Standard)
  • HY-174520
    Human TLR8 mRNA

    		mRNA Inflammation/Immunology
    Human TLR8 mRNA encodes the human toll like receptor 8 (TLR8) protein, a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLR8 acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response.
    Human TLR8 mRNA

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