2. Signaling Pathways
  3. Immunology/Inflammation
  4. IFNAR

IFNAR

Interferon-α/β receptor; Interferon-alpha/beta receptor

IFNAR

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The interferon-α/β receptor (IFNAR) is composed of two subunits, IFNAR1 and IFNAR2, encoding transmembrane polypeptides. Type-I IFNs, interferon α (IFN-α) and interferon β (IFN-β), act through a shared receptor complex, IFNAR. Binding of type-I IFN to IFNAR1 will robustly activate Janus activated kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. Aberrant activation of the type-I IFN response results in a spectrum of disorders called interferonopathies.

Type-I IFN response occurs when IFN-α/β binds to their receptor complex, IFNAR. The ligand-receptor complex is phosphorylated, presumably by pre-associated Janus activated kinases (JAKs) namely tyrosine kinase 2 (TYK2) on IFNAR1 and JAK1 on IFNAR2. The phosphorylated receptors are docking sites for signal transducers and activators of transcription (STAT) factors that dimerise and translocate to the nucleus. STATs 1, 2, 3, 4, and 5 are activated by type-I IFNs in many cell types. Other kinases (e.g., mitogen-activated protein kinases) and transcription factors (e.g., nuclear factor-κB) can also be activated in response to type-I IFNs. Multiple pathways and IFN-regulated genes are activated by IFNs, many of which remain unknown.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-150749A
    ODN D-SL03 sodium
    		98.57%
    ODN D-SL03 sodium is a C class CpG oligonucleotides, and can induce stimulate PBMCs to produce high level of IFN-α. ODN D-SL03 sodium can activate human B cells, NK cells and mononuclear cells and up-regulate expression of CD80, CD86 and HLA-DR on the surface of subsets in human PBMCs. ODN D-SL03 sodium also can inhibit the growth of the tumor. ODN D-SL03 sequence: 5'-tcgcgaacgttcgccgcgttcgaacgcgg-3'.
    ODN D-SL03 sodium
  • HY-N4087
    Platycodin D2
    		99.84%
    Platycodin D2 is an orally active triterpenoid saponin found in Platycodon grandiflorum. Platycodin D2 induces mitophagy in cancer cells through NIX, thereby activating the P21/CyclinA2 pathway and promoting cell senescence. Platycodin D2 induces mitochondrial dysfunction, enhances autophagy, inhibits hepatocellular carcinoma cell proliferation, and exhibits anti-tumor activity against multiple cancer cell types. Platycodin D2 promotes mRNA expression of T-bet, GATA-3, Th1 cytokines IL-2 and IFN-γ, and Th2 cytokines IL-4 and IL-10, enhances splenocyte proliferation, and acts as a vaccine adjuvant with low rabbit red blood cell hemolytic activity. Platycodin D2 induces mitochondrial ROS production, incomplete autophagy, and ferroptosis to inhibit breast cancer cell proliferation. Platycodin D2 can be used for the research of cancer, inflammation and immunology.
    Platycodin D2
  • HY-161344
    Z36-MP5
    		99.41%
    Z36-MP5 is an Mi-2β-targeted inhibitor, with IC50 of 0.082 μM. Z36-MP5 can reduce Mi-2β ATPase activity and reactivates ISG transcription. Z36-MP5 can stimulate T-cell-mediated cytotoxicity.
    Z36-MP5
  • HY-107390A
    AX-024 hydrochloride
    		Inhibitor 99.23%
    AX-024 hydrochloride is an orally available, first-in-class inhibitor of the TCR-Nck interaction that selectively inhibits TCR-triggered T cell activation with an IC50 ~1 nM. AX-024 hydrochloride modulates cell signaling by targeting SH3 domains. AX-024 hydrochloride has low-acute toxicity and high potency and selectivity, and strongly inhibit the production of IL-6, TNF-α, IFN-γ, IL-10 and IL-17A.
    AX-024 hydrochloride
  • HY-P99390
    Tepoditamab
    		Inducer ≥99%
    Tepoditamab (MCLA-117) is a full-length human IgG1 bispecific monoclonal antibody that binds to CLEC12A of myeloid cells and CD3 of cytotoxic T cells. Among others, CLEC12A is a myeloid differentiation antigen. Tepoditamab kills AML leukaemia mother cells and AML leukaemia stem cells, induces T cell-mediated proliferative lysis of AML cells. Tepoditamab induces upto 30-fold T-cell expansion. Tepoditamab results in moderate to strong cytokine (IFNγ, IL-6, IL-8, IL-10, and TNFα) and IFNγ release in human whole blood and PBMC, respectively. Tepoditamab can be used in acute myeloid leukaemia (AML) research.
    Tepoditamab
  • HY-126066
    (-)-Syringaresinol
    		Inhibitor 99.93%
    (-)-Syringaresinol is an orally active isomer of syringaresinol (HY-N8307) found in Annona Montana. (-)-Syringaresinol exhibits antioxidant, anti-inflammatory, and anticancer activities. (-)-Syringaresinol can alleviate ulcerative colitis via the PI3K-Akt/MAPK/Wnt signaling pathway. (-)-Syringaresinol inhibits HL-60 cell proliferation by arresting the G1 phase and inducing apoptosis. (-)-Syringaresinol inhibits LPS (HY-D1056)-induced microglial activation by downregulating the NF-κB p65 signaling pathway and its interaction with ERβ, exerting anti-neuroinflammatory effects.
    (-)-Syringaresinol
  • HY-P990797
    Anti-Mouse IFN gamma Antibody (R4-6A2)
    		Inhibitor 99%
    Anti-Mouse IFN gamma Antibody (R4-6A2) is an anti-mouse IFN gamma IgG1 monoclonal antibody. Anti-Mouse IFN gamma Antibody (R4-6A2) can increase the total serum IgG level. Anti-Mouse IFN gamma Antibody (R4-6A2) can be used for researches on immunology and infection conditions such as nymphs infection. The recommend isotype control of Anti-Mouse IFN gamma Antibody (R4-6A2): Rat IgG1 kappa, Isotype Control (HY-P99979).
    Anti-Mouse IFN gamma Antibody (R4-6A2)
  • HY-P10710A
    BMP-4 (15-24) acetate
    		Inhibitor 99.30%
    BMP-4 (15-24) acetate is a cell-penetrating heparin-binding peptide with the sequence RKKNPNCRRH. BMP-4 (15-24) acetate exhibits anti-inflammatory and anti-chondrogenic activities. BMP-4 (15-24) acetate can be used in the research of arthritis.
    BMP-4 (15-24) acetate
  • HY-123805
    KIN1400
    		Activator 98.1%
    KIN1400 is a potent IRF3 activator. KIN1400 triggers IRF3-dependent innate immune antiviral genes (RIG-I, MDA5, IFIT1, and Mx1) and IFN-β expression. KIN1400 inhibits WNV and DV, two mosquito-borne members of the Flaviviridae and the genus Flavivirus. KIN1400 also inhibits HCV replication. KIN1400 induces innate antiviral immunity through a MAVS-IRF3 axis.
    KIN1400
  • HY-174802
    XL-3158
    		Inhibitor 99.55%
    XL-3158 is a selective and cross-species Cyclic GMP-AMP synthase (cGAS) inhibitor (IC50: 11.1 μM for human cGAS, 2.19 μM for mouse cGAS). XL-3158 simultaneously occupy allosteric and orthosteric sites, stabilizing the activation loop in a closed, inactive conformation and thereby attenuating the cGAS-DNA interactions. XL-3158 inhibits cGAS by targeting phase separation. XL-3158 efficiently penetrates cells by inhibiting aggregate formation, effectively reducing the local concentration of cGAS within cells. XL-3158 can be used for the study of cGAS-dependent inflammatory diseases.
    XL-3158
  • HY-P1745
    InsB (9-23)
    		98.98%
    InsB (9-23) (Insulin B chain (9-23)) is an HLA-DQ8-restricted insulin B-chain peptide composed of amino acid residues 9-23. InsB (9-23) serves as a major MHC II class-restricted antigen. InsB (9-23) supports the recognition and activation of T cells, stimulates the secretion of IFN-γ and cytokines, and induces cross-reactive immune responses. InsB (9-23)-specific CD4 T cells can initiate diabetes. InsB (9-23) can be used in research related to type 1 diabetes and autoimmune diabetes.
    InsB (9-23)
  • HY-176426
    Subquinocin
    		Activator 99.83%
    Subquinocin is a tumor suppressor CYLD inhibitor that inhibits USP family deubiquitinases (DUBs) activity of CYLD with an IC50 of 30 μM. Subquinocin enhances the activation of NF-κB and IFN pathways by inhibiting CYLD. Subquinocin promotes RIG-I-mediated activation of IRF3/IRF7 in the interferon pathway. Subquinocin can be used for the research of cancer and neurodegenerative diseases.
    Subquinocin
  • HY-P99292
    Fontolizumab
    		Inhibitor
    Fontolizumab (HuZAF) is a humanized monoclonal anti-IFN-gamma antibody. Fontolizumab is an immunosuppressive agent. Fontolizumab can be used in research of Crohn’s disease.
    Fontolizumab
  • HY-173425
    STING-IN-15
    		Inhibitor 99.04%
    STING-IN-15 is an orally active STING inhibitor, with an IC50 of 116 nM against h-STING and an IC50 of 96.3 nM against m-STING. STING-IN-15 inhibits the STING signaling pathway in cells, reduces the secretion of IFN-β and IP-10, downregulates the expression of ISG15, ISG56 and TNF-α, and suppresses the phosphorylation of TBK1/IRF3. STING-IN-15 alleviates systemic and renal inflammation induced by STING agonists in mice, reduces tissue damage and the expression of interferon pathway genes, and inhibits spontaneous tissue inflammation in mice. STING-IN-15 can be used for the research of acute kidney injury and autoimmune/inflammatory diseases.
    STING-IN-15
  • HY-159884
    MG-T-19
    		Activator 98.34%
    MG-T-19 is an effective TIM-3 inhibitor that can suppress the interaction of TIM-3 with PtdSer, CEACAM1, and Gal-9. MG-T-19 can increase the production of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in peripheral blood mononuclear cells (PBMCs) from healthy donors, and enhance the ability of PBMCs to inhibit the proliferation of Kasumi-1 cells (an acute myelogenous leukemia cell line).
    MG-T-19
  • HY-17663
    KMR-206
    		Activator 98.86%
    KMR-206 is a PARP7 inhibitor with an IC50 of 13.7 nM. KMR-206 relieves AHR-mediated transcriptional repression and enhances CYP1A1 expression in the presence of TCDD. KMR-206 induces the STING-dependent IFN-β signaling pathway and increases the levels of STAT1, pSTAT1 and nuclear PARP7 in cancer cells. KMR-206 reduces the viability of lung adenocarcinoma cells, enhances radiation-induced immunogenic signals, and induces the production of immunogenic signals in glioblastoma cancer stem cells. KMR-206 destabilizes FRA1 to increase IRF1 levels and promotes the IRF3-CBP/p300 interaction. KMR-206 can be used in studies related to lung adenocarcinoma and glioblastoma.
    KMR-206
  • HY-N0600
    Ginsenoside F3
    		Activator 99.84%
    Ginsenoside F3 is a saponin extracted from the leaves of Panax ginseng with immunoenhancing and antitumor immunostimulatory activities. Ginsenoside F3 upregulates RIPOR2 with a Kd value of 3.77 μM. Ginsenoside F3 enhances NF‑κB activation, upregulates T‑bet and downregulates GATA‑3, increases the production of IL‑2 and IFN‑γ, decreases the production of IL‑4 and IL‑10, reverses CD8⁺ T‑cell exhaustion, restores cytokine secretion, and enhances antitumor immunity in a mouse non‑small cell lung cancer model. Ginsenoside F3 can be used for the research of non-small cell lung cancer.
    Ginsenoside F3
  • HY-126242S
    Tyk2-IN-7
    		Inhibitor 99.58%
    Tyk2-IN-7 is an orally active TYK2 JH2 inhibitor, binds to TYK2 JH2 domain with IC50 and Ki.app of 0.00053 μM and 0.00007 μM, respectively. Tyk2-IN-7 provides a highly selective alternative to conventional TYK2 orthosteric inhibitors, inhibits TYK2/JAK1/JAK2 kinase domain. Tyk2-IN-7 can inhibit the IL-23 and IFN-α signaling pathways. Tyk2-IN-7 is commonly used in the study of inflammatory conditions such as colitis.
    Tyk2-IN-7
  • HY-153701S
    Envudeucitinibum
    		Inhibitor 99.56%
    Envudeucitinibum (Envudeucitinib) is a highly selective, allosteric and orally active TYK2 inhibitor binding to the JH2 domain of TYK2. Envudeucitinibum has no off-target effects on other kinases (JAK1-3). Envudeucitinibum reduces signaling and production of proinflammatory cytokines including IL-12, IL-23, IL-17, and type I interferons (IFNs). Envudeucitinibum can be used for the research of plaque psoriasis, systemic lupus erythematosus (SLE), and other immune-mediated diseases.
    Envudeucitinibum
  • HY-N6017
    Bakkenolide A
    		Inhibitor 99.99%
    Bakkenolide A is an anticancer agent. Bakkenolide A reduces the viability of leukemia cells, inhibits cell colony formation and invasion, and downregulates the expression of HDAC3 in cells. Bakkenolide A downregulates the expression of pro-inflammatory cytokines including TNF-α, interleukins such as IL-1β, TGF-β1 and IFN-γ, as well as the expression of PI3K, PDK and PKC in leukemia cells. Bakkenolide A downregulates activated Akt, GSK and Bad, while upregulates Cyto-c, cleaved Caspase3 and cleaved Caspase7, induces apoptosis (apoptosis) in leukemia cells and thereby inhibits inflammatory responses in leukemia cells. Bakkenolide A significantly slows the growth of subcutaneous leukemia tumors in nude mice. Bakkenolide A is applicable to leukemia-related research.
    Bakkenolide A
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