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Pathways Recommended: Neuronal Signaling JAK/STAT Signaling
Results for "

TIR signal

" in MedChemExpress (MCE) Product Catalog:

10

Inhibitors & Agonists

4

Peptides

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-112730
    PEO-IAA
    5+ Cited Publications

    2-(1H-Indol-3-yl)-4-oxo-4-phenyl-butyric acid

    Others Others
    PEO-IAA is an indole-3-acetic acid (IAA) antagonist. PEO-IAA is an auxin antagonist that binds to transport inhibitor response 1/auxin signaling F-box proteins (TIR1/AFBs).
    PEO-IAA
  • HY-P2565
    Pepinh-TRIF TFA
    4 Publications Verification

    Toll-like Receptor (TLR) Inflammation/Immunology
    Pepinh-TRIF (TFA) is a 30 aa peptide that blocks TIR-domain-containing adapter-inducing interferon-β (TRIF) signaling by interfering with TLR-TRIF interaction .
    Pepinh-TRIF TFA
  • HY-139397
    TJ-M2010-5
    Maximum Cited Publications
    21 Publications Verification

    MyD88 Cardiovascular Disease
    TJ-M2010-5 is a MyD88 inhibitor that binds to the TIR domain of MyD88 to interfere with its homodimerization, and the TLR/MyD88 signal pathway . TJ-M2010-5 can be used for the research of myocardial ischemia/reperfusion injury (MIRI) .
    TJ-M2010-5
  • HY-P10719

    MyD88 Infection Inflammation/Immunology
    Pepinh-MYD is a MyD88 inhibitor that contains a domain sequence from MyD88 TIR and a protein transduction sequence, enabling it to penetrate the cell membrane. Pepinh-MYD interferes with MyD88-mediated TLR signaling pathways, thereby inhibiting related immune responses. It holds potential for studying the role of MyD88 in viral infections .
    Pepinh-MYD
  • HY-P10719A

    MyD88 Infection Inflammation/Immunology
    Pepinh-MYD TFA is a MyD88 inhibitor that contains a domain sequence from MyD88 TIR and a protein transduction sequence, enabling it to penetrate the cell membrane. Pepinh-MYD TFA interferes with MyD88-mediated TLR signaling pathways, thereby inhibiting related immune responses. Pepinh-MYD TFA holds potential for studying the role of MyD88 in viral infections .
    Pepinh-MYD TFA
  • HY-19744
    T6167923
    10+ Cited Publications

    MyD88 Inflammation/Immunology
    T6167923 is a selective inhibitor of MyD88-dependent signaling pathways. T6167923 directly binds to Toll/IL1 receptor (TIR) domain of MyD88 and disrupts MyD88 homodimeric formation. T6167923 inhibits NF-κB driven Staphylococcus enterotoxin AP (SEAP) activity, and improves anti-inflammatory activity with IC50s of 2.7 μM, 2.9 μM, 2.66 μM and 2.66 μM for IFN-γ, IL-1β, IL-6 and TNF-α, respectively .
    T6167923
  • HY-113851

    Phytohormone Others
    BH-IAA is a potent auxin antagonist that specifically blocks TIR1-mediated auxin signaling .
    BH-IAA
  • HY-175022

    PROTACs IRAK Toll-like Receptor (TLR) Interleukin Related Inflammation/Immunology
    PROTAC IRAK4 degrader-13 (Degrader 1) is a selective IRAK4 PROTAC degrader with DC50s of 0.86 and 1.1 nM for monocytes and lymphocytes in PBMCs, respectively. PROTAC IRAK4 degrader-13 significantly induces TIR signal activation, and inhibits the expression of circulating proinflammatory cytokines in Imiquimod (HY-B0180) induced psoriasis mice model. PROTAC IRAK4 degrader-13 can be used for TLR- and IL-1R-driven driven neutrophilic inflammation diseases like hidradenitis suppurativa (HS) and atopic dermatitis (AD) research . Pink: IRAK4 ligand; Blue: E3 ligase ligand; Black: linker
    PROTAC IRAK4 degrader-13
  • HY-176423

    Bacterial Infection Inflammation/Immunology
    His-ADPR is a Toll/interleukin-1 receptor (TIR) domain protein that produces an immune signaling molecule. His-ADPR is generated in response to phage infection and activates the cognate Thoeris effector by binding a Macro domain located at the C terminus of the effector protein .
    His-ADPR
  • HY-P10718

    Toll-like Receptor (TLR) Inflammation/Immunology
    IMG-2005 is a TLR signaling pathway inhibitor. IMG-2005 mimics the Toll/interleukin-1 receptor (TIR) domain of MyD88, thereby preventing its homodimerization, which causes damage to tracheal epithelial cells and triggers pulmonary immune diseases .
    IMG-2005

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