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interferon

✓ Approved

Sidus · IFNAR2 · Recombinant Proteins

What is interferon?

interferon is a recombinant proteins developed by Sidus. It is approved for therapeutic indications via injectable (others).

Drug Profile

CompanySidus
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, Sidus

Mechanism of Action

Molecular Targets

interferon acts on 1 molecular target:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
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Therapeutic Indications

interferon is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsSalmonellosis✓ Approved

Related Research Articles

PubMedFrontiers in immunology2026-10-15

Hemin suppresses interferon responses in periodontal cell models through JAK2-STAT1 inhibition.

Huang Xiaoyu X, Gruber Reinhard R, Panahipour Layla L

Hemin, an oxidized heme species released during erythrocyte breakdown, is detectable in gingival crevicular fluid during periodontal inflammation, but its effects on local immune signaling remain unclear. We investigated whether hemin modifies cytokine-induced interferon responses in HSC-2 oral squamous cell carcinoma cells and primary human gingival fibroblasts. Cells were stimulated with interleukin-1β and tumor necrosis factor-α, or with interferon-γ, in the presence or absence of hemin. Transcriptomic changes were assessed by RNA sequencing and pathway analysis, and selected transcripts and proteins were validated by reverse-transcription quantitative PCR, enzyme-linked immunosorbent assay, immunoblotting, and immunofluorescence. Ligand-kinase interactions were examined by molecular docking and molecular dynamics simulations, and recombinant Janus kinase 2 activity was measured in a cell-free assay. Hemin preferentially suppressed an interferon-associated gene network, including CXCL10, CXCL11, MX1, OAS1, IFIT1, IFIT3, and ISG15, while nuclear factor κB-associated responses were comparatively preserved. Hemin also reduced signal transducer and activator of transcription 1 Tyr701 phosphorylation and nuclear accumulation induced by either the cytokine combination or interferon-γ. Computational analyses predicted stable hemin interactions within conserved ATP-binding pockets of Janus kinases, and the cell-free assay demonstrated inhibition of recombinant Janus kinase 2. Together, these findings show that hemin attenuates interferon-associated transcription in periodontal cell models, consistent with inhibition of the Janus kinase 2-signal transducer and activator of transcription 1 axis. This mechanism may enable blood-derived hemin to modify local mucosal immune signaling, although its relevance to periodontal tissues and antiviral defense requires confirmation in organotypic, infection, and in vivo models.

PMID 42876722
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PubMedFrontiers in immunology2026-10-15

Anti-interferon-γ autoantibodies: immunopathogenesis, diagnostic innovation, and emerging therapeutic strategies in an adult-onset immunodeficiency.

Tsai Chin-Shiang CS, Cheng Aristine A, Naz Farha F

Adult-onset immunodeficiency with anti-interferon-γ autoantibodies (AIGA) is a rare acquired immunodeficiency increasingly recognized in East and Southeast Asia, characterized by disseminated infections with nontuberculous mycobacteria and other intracellular pathogens. Recent studies have refined our understanding of its immunopathogenesis, including HLA-linked susceptibility, epitope-specific neutralization of IFN-γ, and molecular mimicry, while highlighting persistent gaps in diagnosis and treatment. This Perspective synthesizes emerging evidence into a clinically oriented framework spanning diagnosis, monitoring, and immunomodulatory therapy. We discuss functional confirmation of AIGA, repurposing of the QuantiFERON-TB platform as an accessible screening strategy, and quantitative titers and ¹8F-FDG PET as complementary biomarkers of disease activity and treatment response. We propose a clinical decision pathway in which refractory or progressive infection, rather than a fixed titer threshold, triggers immunomodulation, with rituximab and cyclophosphamide as the best-supported induction strategies, daratumumab reserved for refractory cases, and emerging AIGA-specific evidence supporting azathioprine for maintenance. Recognizing heterogeneous access to specialized testing and biologics across AIGA-endemic regions, we propose a resource-stratified approach integrating widely available markers with referral-based testing and resource-adapted treatment. We also highlight emerging antigen-specific strategies, including chimeric autoantibody receptor T cells engineered to eliminate autoantibody-producing B cells, as a future direction toward durable remission. Finally, we outline priorities for prospective validation and biomarker-guided therapy.

PMID 42876531
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PubMedFrontiers in immunology2026-10-15

Activation of cytosolic DNA sensing in NCM460 intestinal epithelial cells induces antiviral factors that restrict HIV infection in macrophages.

Majid Safah S, Khan Shazheb S, Wang Xu X, Khan Raheeb R et al.

The gastrointestinal tract is an important site of HIV persistence and contains susceptible target cells, including macrophages. Crosstalk between intestinal epithelial cells and macrophages may contribute to mucosal innate defense. NCM460 human intestinal epithelial cells were transfected with poly(dA). Expression and production of interferons, interferon-stimulated genes, and CC chemokines were assessed by quantitative RT-PCR, western blotting, and ELISA. Primary human macrophages were treated with conditioned supernatants from NCM460 cells, and HIV infection was assessed using cytopathic effects, luciferase activity, and HIV Gag RNA expression. Poly(dA) induced IFN-β, IFN-λ1, IFN-λ2/3, ISG15, viperin, OAS1, RANTES, and MIP-1α in NCM460 cells. Supernatants from poly(dA)-stimulated NCM460 cells induced GBP5, viperin, and MX2 in primary macrophages and significantly inhibited HIV infection. Activation of cytosolic DNA sensing in intestinal epithelial cells induces soluble antiviral factors that enhance innate antiviral responses in macrophages and may contribute to mucosal defense against HIV.

PMID 42876517
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PubMedFrontiers in immunology2026-10-15

Myeloid cell expression of the VDR and parathyroid hormone control the host response to influenza infection in mice.

Tang Mengzhu M, Froelich Nicole E NE, Hanna Nicholas J NJ, Weaver Veronika C VC et al.

Respiratory infections caused by seasonal influenza viruses remain a major global health burden. Vitamin D receptor (VDR) signaling regulates immune responses, but the role of the VDR and its interaction with parathyroid hormone (PTH) in host resistance to H1N1 influenza infection is not understood. Global VDR knockout (KO) mice, or myeloid (M) deletion of the VDR (M-VDR KO) and the respective wildtype (WT) littermates were infected with H1N1 influenza virus. Additional experiments treated WT mice with intermittent PTH or vehicle and then infected them with a H1N1 influenza A virus. Disease severity, mortality, viral burden and clearance, lung pathology, and inflammatory cytokine responses were evaluated. H1N1 influenza infection of WT mice resulted in non-lethal disease, whereas VDR KO mice had 21% mortality, delayed viral clearance, more severe symptoms and lung pathology. The increased severity of respiratory disease was accompanied by higher type I and II interferon responses in the lungs. M-VDR KO mice had increased disease severity and delayed viral clearance compared to WT littermates. PTH-treated WT mice had increased clinical scores, influenza M gene, and cytokine responses compared to vehicle treated WT mice. The work describes a novel paradigm in which the vitamin D-PTH axis governs host resistance to influenza virus disease by controlling the amount of inflammation and the amount of virus in the lung. In addition, the data suggest that VDR expression in myeloid cells is critical for controlling the early innate immune response to influenza viruses.

PMID 42876719
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PubMedJournal of immunology (Baltimore, Md. : 1950)2026-10-15

TNFα promotes brain-predominant EAE independent of IFNγ and IL-17A in HLA-DR3 transgenic mice.

Turner Ti-Ara J TJ, Peterson Stephanie R SR, Alt Lian E LE, Aguilar Meza Leeann S LS et al.

Multiple sclerosis (MS) is thought to be mediated by human leukocyte antigen (HLA) class II-restricted autoreactive CD4 T cells producing interleukin (IL)-17A and/or interferon γ (IFNγ), but the necessity of these cytokines for disease pathogenesis is unclear. Utilizing HLA-DR3 (DRβ1*0301) transgenic mice lacking IFNγ or IL-17A in experimental autoimmune encephalomyelitis (EAE), a model of MS, we found that neither cytokine is essential for disease induction, although both have distinct roles. The absence of IFNγ caused atypical, brain-predominant EAE characterized by high levels of IL-17A, while the absence of IL-17A resulted in classical EAE, targeting the spinal cord. To assess whether IL-17A drives atypical EAE in the absence of IFNγ, we generated HLA-DR3.IFNγ-/-.IL-17A-/- double knockout (DKO) mice. DKO mice developed atypical EAE with brain infiltration and inflammation of the brainstem and cerebellum, indicating that IL-17A is dispensable for brain-predominant disease in the absence of IFNγ. DKO mice exhibited significant CD4 T cell infiltration and increased expression of CD4 T cell-associated genes at peak disease. Prior to central nervous system infiltration, CD4 T cell accumulated in the spleen and inguinal lymph nodes of DKO mice, where they exhibited an altered cytokine milieu and upregulated genes involved in recruitment, activation, and migration to the brain. DKO mice exhibited elevated expression of tumor necrosis factor α (TNFα), granulocyte-macrophage colony-stimulating factor, and IL-17F; however, only TNFα inhibition ameliorated atypical disease. Together, our findings indicate TNFα promotes brain-predominant inflammatory pathology in the absence of IFNγ and IL-17A.

PMID 42876168
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PubMedJournal of experimental & clinical cancer research : CR2026-10-15

CXCL9-driven immune rewiring and tumor-intrinsic ATR signaling inhibition restore radiotherapy response in lung cancer.

Leon Sergio S, Otegui Nerea N, Redrado Miriam M, Marchena-Perea Eric Michel EM et al.

Non-small cell lung cancer (NSCLC) accounts for ~ 85% of lung cancers and is associated with poor outcomes in advanced stages. Radiotherapy (RT) is central to NSCLC treatment, yet locoregional relapse remains frequent. Increasing evidence indicates that, beyond tumor-intrinsic adaptations, the tumor microenvironment (TME) and immune contexture critically influence response to irradiation. However, most radioresistance models rely on human cell lines unsuitable for immunocompetent systems, limiting insight into immune-tumor interactions. We generated radioresistant (RR) isogenic variants of murine lung adenocarcinoma cell lines and investigated RT resistance using transcriptomics, 3D co-culture systems, and syngeneic mouse models. RR clones showed stable adaptations to DNA damage, including enhanced clonogenic survival, reduced immunogenic cell death, and constitutive activation of DNA damage response pathways, particularly ATR signaling. High ATR levels in NSCLC patients were significantly associated with immunosuppression. Transcriptomics revealed altered DNA repair and downregulation of type-I interferon and innate immune pathways. In vivo, RR tumors exhibited an immunosuppressive TME with increased T regulatory cells, M2-like macrophages, and myeloid-derived suppressor cells, alongside reduced cytotoxic T cell recruitment. In 3D co-cultures, immunosuppressive cells protected cancer cells from RT-induced cytotoxicity. Notably, RR tumors regained RT sensitivity in immunodeficient mice, highlighting the role of immune suppression in radioresistance. Therapeutically, activation of innate immunity using TLR3-TLR7/8 agonists (poly(I:C)+R848) restored antitumor responses and improved RT efficacy, partly via CXCL9/10-mediated immune recruitment. ATR inhibition with ceralasertib further sensitized RR tumors to RT. These findings identify cancer cell-intrinsic ATR signaling and immune suppression as key drivers of radioresistance and support combined therapeutic strategies to prevent locoregional relapse in NSCLC after radiotherapy.

PMID 42875793
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