Cyclo(L-Phe-L-Pro), isolated from Pseudomonas fluorescens and Pseudomonas alcaligenes cell-free culture supernatants is an antifungal cyclic dipeptide[1]. Cyclo(L-Phe-L-Pro) inhibits IFN-β production by interfering with retinoic-acid-inducible gene-I (RIG-I) activation[2]. Cyclo(L-Phe-L-Pro) exhibits free-radical scavenging activity with the IC50 of 24 µM in the DPPH assay[3].
Mipeginterferon alfa-2b is an interferon alpha-2b (IFNA2b) analogue, with an average number of 5 substituted among 11 amino groups (one N-terminal and 10 lysine N6). Mipeginterferon alfa-2b has the relative molecular mass of 40 kDa[1].
Interferon receptor agonist is an interferon (IFN) receptor agonist.
IFN-γ Antagonist 1 (AYCRDGKIGPPKLDIRKEEKQI) is an antagonist of interferon γ (IFN γ). IFN-γ Antagonist 1 inhibits IFN-γ induced HLR/DR antigen expression in Colon 205 cells with an IC50 value of approximately 35 μM. IFN-γ Antagonist 1 has potential applications in immune regulation[1].
ODN D-SL03 is a C class CpG oligonucleotides, can induce stimulate PBMCs to produce high level of IFN-α. ODN D-SL03 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 also can inhibit the growth of the tumor. ODN D-SL03 sequence: 5'-tcgcgaacgttcgccgcgttcgaacgcgg-3'[1].
GSK2245035 is a highly potent and selective intranasal Toll-Like receptor 7 (TLR7) agonist with preferential Type-1 interferon (IFN)-stimulating properties. GSK2245035 has pEC50s of 9.3 and 6.5 for IFNα and TFNα. GSK2245035 effectively suppresses allergen-induced Th2 cytokine production in human peripheral blood cell cultures. GSK2245035 is used for the treatment of asthma[1].
IFN alpha-IFNAR-IN-1 is a nonpeptidic, low-molecular-weight inhibitor of the interaction between IFN-α and IFNAR; inhibit MVA-induced IFN-α responses by BM-pDCs (IC50=2-8 uM).IC50 value:Target: IFN alpha-IFNAR interaction inhibitorIFN alpha-IFNAR-IN-1 specifically inhibits MVA-induced IFN-α responses by BM-pDCs. IFN alpha-IFNAR-IN-1 inhibited the IFN-α responses that were elicited after treatment with CpG2216, stimulation with poly(I:C), and infection with VSV-M2, whereas the total IL-12 production was notably less affected under those conditions. IFN alpha-IFNAR-IN-1 exerts immunosuppressive activity by the direct interaction with IFN-α [1].
SM-276001 is a potent selective TLR7 agonist that can induce antitumor immune responses. SM-276001 is an orally active interferon (IFN) inducer[1][2].
AX-024 hydrochloride is an cytokine release inhibitor which can strongly inhibit the production of interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), interferon-γ (IFN-γ), IL-10 and IL-17A.
AX-024 is an cytokine release inhibitor which can strongly inhibit the production of interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), interferon-γ (IFN-γ), IL-10 and IL-17A.
2',3'-cGAMP (2'-3'-cyclic GMP-AMP) is a molecule in endogenous cGAMP mammalian cells which contains two distinct phosphodiester linkages, one between 2′-OH of GMP and 5′-phosphate of AMP, and the other between 3′-OH of AMP and 5′-phosphate of GMP. 2',3'-cGAMP is produced in mammalian cells in response to DNA in the cytoplasm and binds to STING with a high affinity and is a potent inducer of interferon-β (IFNβ)[1].
Delmitide (RDP58) acetate is an orally active d-isomer decapeptide with potent anti-inflammatory activity. Delmitide acetate inhibits production of TNF-α, IFN-γ, and interleukin (IL)-12, and up-regulates heme oxygenase 1 activity. Delmitide acetate can be used for the research of ulcerative colitis[1][2].
ODN 1585 is a potent inducer of IFN and TNFα production. ODN 1585 is a potent stimulator of NK (natural killer) function. ODN 1585 increases CD8+ T-cell function, including the CD8+ T cell-mediated production of IFN-γ. ODN 1585 induces regression of established melanomas in mice. ODN 1585 can confer complete protection against malaria in mice. ODN 1585 can be used for acute myelogenous leukemia (AML) and malaria research. ODN 1585 can be used as a vaccine adjuvant[1][2][3].
ODN 2216 is a TLR9 (toll-like receptor 9) ligand or agonist. ODN 2216 induces high amounts of IFN-α and IFN-β. ODN 2216 induces IFN-α by pDC (plasmacytoid DC) and IL-12 (p40) production by DC (dendritic cells). ODN 2216 stimulates IFN-γ production in peripheral blood mononuclear cells (PBMC), which is indirect and mediated by IFN-α/β. ODN 2216 can activate NK cells and promote IFN-γ production of TCR-triggered CD4+ T cells[1][2][3][4].
A potent RIG-I-like receptor (RLR) agonist that triggers IRF3-dependent innate immune antiviral genes and IFN-β expression; shows antiviral activity against a broad range of RNA viruses, including dengue virus, and hepatitis C virus, as well as viruses of the families Filoviridae (Ebola virus), Orthomyxoviridae (influenza A virus), Arenaviridae (Lassa virus), and Paramyxoviridae (respiratory syncytial virus, Nipah virus).
IFN-α Receptor Recognition Peptide 1 is a peptide of IFN-α associated with receptor interactions[1].
TYK2-IN-12 (compound 30) is an orally active, potent and selective TYK2 (tyrosine kinase 2) inhibitor, with a Ki of 0.51 nM. TYK2-IN-12 inhibits IL-12 induced IFNγ, with IC50 values of 2.7 and 7.0 μM in human and mouse whole blood, respectively. TYK2-IN-12 can be used for psoriasis research[1].
Emapalumab (NI-0501) is a humanized monoclonal IgG1 antibody that noncompetitively inhibits IFN-γ. Emapalumab binds with high affinity (Kd= 1.4 pM) to both free IFN-γ as well as IFN-γ bound to its receptor. Emapalumab can be used in research of hemophagocytic lymphohistiocytosis (HLH)[1].
RIG012 is a potent RIG-I inhibitor with an IC50 of 0.71 μM using the NADH-coupled ATPase assay. RIG012 inhibits IFN-β and ISG hRsad2 expression[1].
EM 163 is a TIR-TIR interaction inhibitor, which is a TIR (Toll/interleukin-1 receptor) structural domain mimic of the MyD88 protein. EM 163 targets the TIR structural domain in the IL-1 receptor and blocks the interaction with MyD88. EM 163 inhibits the production of inflammatory cytokines in vivo caused by staphylococcal enterotoxin B (SEB). EM 163 protects mice from SEB shock-induced death. In rat hippocampal neurons in vitro, EM 163 blocked the activation of p38 and the inhibitory effect of IL-1β on chemically induced long-term potentiation (LTP)-triggered protein synthesis.
Bifarcept is a recombinant antibody of interferon receptor type I (IFN-RI). Bifarcept can bind IFN-β and prolong its serum half-life[1].
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[1].
Cridanimod is a small-molecule immunomodulator and interferon inducer[1]. Cridanimod is a potent progesterone receptor (PR) activator mediated through induction of IFNα and IFNβ expression[2].
RO8191 (RO4948191), an imidazonaphthyridine compound, is an orally active and potent interferon (IFN) receptor agonist. RO8191 activates IFN-stimulated genes (ISGs) expression and JAK/STAT phosphorylation. RO8191 shows antiviral activity against both HCV and EMCV with an IC50 of 200 nM for HCV replicon[1].
(R,R)-VVD-118313 is the isomer of VVD-118313 (HY-151385). VVD-118313 is a selective JAK1 inhibitor and blocks JAK1-dependent trans-phosphorylation and cytokine signaling. VVD-118313 can be used for research of cancer[1].
Peginterferon lambda-1a (BMS-914143) is a monoclonal antibody targeting IFNLR1 and consists of IFNL1 conjugated to pegol[1].
Faralimomab (64G12) is an immunomodulator, and a murine anti-IFNA1 IgG1 mAb[1].
Monalizumab is a first-in-class immune checkpoint inhibitor targeting Natural Killer Group 2A (NKG2A). Monalizumab, a humanized anti-NKG2A blocking mAb, increases IFN-γ production, thereby promoting NK cell effector functions. Monalizumab can be used for the research of head and neck squamous cell carcinoma (HNSCC)[1][2].
Cirsilineol, a natural flavone compound, selectively inhibits IFN-γ/STAT1/T-bet signaling in intestinal CD4+ T cells. Cirsilineol has potent immunosuppressive and anti-tumor properties. Cirsilineol significantly ameliorates trinitro-benzene sulfonic acid (TNBS)-induced T-cell-mediated experimental colitis in mice[1].