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interferon

✓ Approved

HK inno.N · IFNAR2 · Recombinant Proteins

What is interferon?

interferon is a recombinant proteins developed by HK inno.N. It is approved for therapeutic indications via injectable (others) or topical.

Drug Profile

CompanyHK inno.N
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others), Topical
StatusApproved
Sources: ClinicalTrials.gov, HK inno.N

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 6 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Kaposi's sarcoma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Plasma cell myeloma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Renal cancer✓ Approved

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Related Research Articles

PubMedAsian Pacific journal of allergy and immunology2026-09-20

Type 2-interferon imbalance in allergic barrier disease: An asthma-centered, cross-disease perspective.

Rao Shenghong S, Li Shumei S, Shen Haoyue H, Jin Tengchuan T

Allergic diseases are typically regarded as type 2 inflammatory disorders driven by interleukin-4, interleukin-5, and interleukin-13, which mediate immunoglobulin E class switching, eosinophilic inflammation, mucus hypersecretion, pruritus, tissue remodeling, and epithelial barrier dysfunction. However, type 2 cytokine activity alone does not fully account for variations in exacerbation risk, susceptibility to infections, comorbidities, or responses to biologic therapy. This narrative review proposes an asthma-centered type 2-interferon imbalance framework and discusses its cautious, disease-specific extension to atopic dermatitis, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis, and food allergy. The model emphasizes that, particularly in asthma, allergic barrier inflammation arises and persists in injured tissues where excessive type 2 inflammation may coexist with impaired interferon-mediated host defense. Evidence is strongest in asthma, where deficiencies in type I and type III interferon responses are linked to rhinovirus susceptibility, delayed viral clearance, and recurrent exacerbations. In other allergic diseases, interferon dysfunction appears more variable, reflecting differences in tissue context, disease stage, and environmental exposure. In asthma, and potentially in selected allergic barrier diseases, persistent inflammation may result from a cycle of epithelial injury, alarmin release, cytokine amplification, impaired antiviral defense, ongoing exposure, and incomplete tissue repair. These mechanisms provide a rationale for tiered intervention, including blockade of upstream epithelial alarmins, inhibition of downstream type 2 effector pathways, and selected investigational approaches aimed at restoring mucosal host defense.

PMID 42763805
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PubMedMolecular cancer2026-09-20

Immune-pressure redistribution in resistance to PD-1/PD-L1 blockade: mechanisms, biomarkers, and therapeutic design.

Wang Xiaodong X, Liu Jiayi J, Hairulajiang Alifujiang A, Wang Junjie J et al.

PD-1/PD-L1 blockade can produce durable tumor control, yet primary, adaptive, and acquired resistance remain common. Existing accounts often catalogue resistance by cellular compartment, obscuring the coordinated nature of tumor adaptation. Here, we introduce immune-pressure redistribution as a treatment-oriented framework that complements cancer immunoediting by asking where therapeutic immune pressure is diverted after checkpoint release. Resistance is organized into three coupled routes: transfer into tumor-intrinsic escape through antigen-presentation loss, interferon-response defects, oncogenic rewiring, and lineage plasticity; weakening through defective priming, terminal T-cell differentiation, compensatory checkpoints, metabolic constraint, and chronic cytokine signaling; and unloading into stromal, vascular, myeloid, regulatory, microbial, and systemic host compartments. We integrate clinically validated mechanisms with emerging evidence, including the temporal duality of interferon-JAK signaling, the role of tumor-draining lymph nodes in sustaining progenitor-exhausted T cells, and the limited translation of TIGIT, IDO1, TGF-β, and CSF-1R targeting. We further propose a biomarker-guided strategy that combines tumor visibility, immune-cell state, spatial architecture, systemic inflammation, and early treatment dynamics to identify the dominant resistance topology. This framework supports topology-matched combinations and adaptive sequencing rather than uniform escalation, with the aim of restoring productive immune pressure while limiting compensatory escape and toxicity.

PMID 42763389
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PubMedBritish journal of cancer2026-09-20

Inflammatory biomarkers and risk of postmenopausal oestrogen receptor-positive breast cancer: a case-cohort analysis.

Albers Frances Em FE, Swain Christopher Tv CT, Dashti S Ghazaleh SG, Rinaldi Sabina S et al.

The role of systemic inflammation in postmenopausal breast carcinogenesis remains unclear. Using a case-cohort study within the Melbourne Collaborative Cohort Study, we estimated the effects of circulating inflammatory biomarkers on the risk of postmenopausal oestrogen receptor (ER)-positive breast cancer. We included 1223 females (347 cases) who were postmenopausal at blood collection. For each biomarker, risk ratios (RRs) and 95% confidence intervals (CIs) for ER-positive breast cancer were estimated (1) per-doubling in biomarker concentration and (2) for quartiles of concentration with the lowest category as the reference, using weighted Poisson regression with a robust variance estimator. The risk of postmenopausal ER-positive breast cancer increased per doubling in blood concentrations of leptin (RR: 1.13, 95% CI: 1.03, 1.25), adiponectin (RR: 1.10, 95% CI: 0.90, 1.34), tumour necrosis factor-alpha (RR: 1.27, 95% CI: 0.96, 1.68), and interleukin-10 (RR: 1.14, 95% CI: 1.01, 1.29). The RR for a doubling of the leptin-to-adiponectin ratio was 1.07 (0.99, 1.16). RRs for other biomarkers were 1.04 (0.93, 1.17) for interferon-gamma, 1.01 (0.88, 1.17) for interleukin-6, 0.98 (0.83, 1.16) for interleukin-8, and 1.03 (0.95, 1.11) for C-reactive protein. Systemic inflammation may be important in the risk of developing ER-positive breast cancer for postmenopausal females.

PMID 42763311
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PubMedCureus2026-09-20

Candidate MicroRNA Regulatory Axes in Melanoma CD8+ T Cell Exhaustion: A Network-Based In Silico Stratification.

Javed Muhammad Zain U MZU, Hussain Muhammad M

Background Anti-programmed cell death protein-1 (anti-PD-1) immunotherapy has transformed the treatment of advanced melanoma, but durable benefit remains limited to a subset of patients. CD8+ T cell exhaustion contributes to immune escape in the melanoma tumor microenvironment, while the post-transcriptional regulation of exhaustion-associated genes by microRNAs (miRNAs) remains incompletely understood. Objective We characterized miRNA-mRNA regulatory associations in CD8+ T cell exhaustion-enriched melanoma transcriptomes, classified inverse associations as loss-of-repression (LoR) or active suppression (AS), extended the network to candidate long non-coding RNA (lncRNA)-miRNA-mRNA relationships, and examined whether network-derived transcriptomic scores were associated with anti-PD-1 outcomes in independent cohorts. Methods The TCGA-SKCM bulk transcriptomes were filtered by single-sample gene set enrichment analysis (ssGSEA), yielding 121 CD8+ T cell exhaustion-enriched cases and 115 cases with paired miRNA and mRNA measurements. Differentially expressed miRNAs (DEmiRNAs) were identified between fixed high- and low-exhaustion tertiles (n = 38 each) using two-sided Mann-Whitney U tests with Benjamini-Hochberg correction (|log₂FC| ≥ 0.5; false discovery rate (FDR) ≤ 0.05). Database-supported inverse Spearman's correlations (ρ ≤ -0.30; FDR ≤ 0.05) were assembled into a bipartite network. Edges were classified as LoR or AS, and a competing endogenous RNA (ceRNA) extension incorporated DIANA-LncBase/ENCORI lncRNA-miRNA interactions. Nine biologically anchored axes underwent continuous-score analysis and HC3 regression adjusted for tumor purity, CD8, fibroblast/CAF, myeloid, interferon-gamma, and sample type, together with four sensitivity analyses. Exploratory clinical testing used GSE78220 and the pre-PD-1 biopsy subset of the DFCI melanoma cohort (cBioPortal study identifier: mel_dfci_2019). Results Twenty-six DEmiRNAs (20 upregulated and 6 downregulated) formed 326 inverse miRNA-mRNA edges, comprising 263 AS and 63 LoR associations. Six of nine focused axes met the adjusted-support criterion, and all six were AS-classified including upregulated miR-155-5p as the dominant hub, with inverse associations involving FOXO3 (ρ = -0.305, adjusted p = 0.020) and MEIS1, the strongest priority edge (ρ = -0.470, adjusted p < 0.0001). NEAT1, MALAT1, and XIST emerged as the top-degree lncRNA hubs, all classified as AS-sponge type. Exclusion of one solid-tissue-normal specimen left 114 paired tumors, retained 25 DEmiRNAs, and supported seven of nine axes in the tumor-only sensitivity analysis. Relational integration with lncRNA-miRNA records yielded 29,274 candidate chains, including 790 containing a focused miRNA-mRNA edge. Transcriptomic score analyses were negative and exploratory in GSE78220 (mRNA proxy area under the curve (AUC) = 0.631; Mann-Whitney p = 0.269) and in the DFCI melanoma cohort (mRNA topology AUC = 0.453, p = 0.451; lncRNA topology AUC = 0.388, p = 0.0695). Conclusions The LoR/AS framework offers a transparent means of organizing correlative miRNA-mRNA hypotheses in melanoma bulk transcriptomes. The adjusted results favored an AS pattern among the focused axes, but they did not establish CD8+ T-cell-intrinsic regulation, direct miRNA targeting, ceRNA activity, or clinical predictive utility. Experimental testing in sorted or single-cell melanoma CD8+ tumor-infiltrating lymphocyte systems is required.

PMID 42763729
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PubMedInternational immunopharmacology2026-09-19

Elevated ISG15 reinforces RIG-I/MDA5-linked macrophage-microglia crosstalk during blood-brain barrier disruption in neuromyelitis optica spectrum disorder.

Niu Yunfeng Y, Sun Jing J, Han Yusen Y, Guo Ruoyi R et al.

Neuromyelitis optica spectrum disorder (NMOSD) is an AQP4-IgG-mediated astrocytopathy characterized by blood-brain barrier (BBB) injury and myeloid inflammation. We investigated whether interferon-stimulated gene 15 (ISG15) contributes to myeloid activation through RIG-I-like receptor (RLR) signaling. Single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from patients with NMOSD was combined with validation in monocytes, serum, and cerebrospinal fluid. THP-1-derived macrophages and HMC3/BV2 microglia underwent LPS and/or IFN-β stimulation and ISG15 knockdown or overexpression. To assess macrophage-derived ISG15 effects on microglial polarization, ISG15-manipulated macrophages were non-contact cocultured with microglia in Transwell inserts, and microglial M1/M2 markers were measured. Western blotting quantified free and conjugated ISG15. ISG15-RIG-I association were examined by co-IP. An AQP4-IgG/human complement passive-transfer mouse model provided in vivo validation. NMOSD PBMCs showed monocyte expansion and an ISG15-high interferon/RLR signature, with increased ISG15 in CD14+ monocytes, serum, and cerebrospinal fluid. In macrophages, LPS plus IFN-β increased inflammatory cytokines, migration, and both free/conjugated ISG15. ISG15 overexpression or knockdown bidirectionally altered macrophage and microglial phenotypes; the Transwell coculture confirmed that macrophage ISG15 status directly modulated microglial M1/M2 polarization. ISG15 modulated RIG-I/MDA5/LGP2 expression, with RIG-I overexpression partially rescuing the RLR program after knockdown. Co-IP confirmed physical association between ISG15 and RIG-I. In vivo, BBB disruption coincided with ISG15-high infiltrating and resident myeloid cells and RLR upregulation. Elevated ISG15 following BBB injury reinforces RIG-I/MDA5/LGP2 signaling and drives macrophage-microglia inflammatory crosstalk in NMOSD, establishing the ISG15-RLR axis as a key amplification pathway that bridges peripheral and central myeloid responses.

PMID 42763248
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PubMedVirology2026-09-19

Transcriptional decoupling of the epithelial-immune bridge is associated with suboptimal influenza B virus immunogenicity.

Rowe Thomas T, Ross Ted M TM

Influenza B viruses (IBV) elicit weaker, less durable antibody responses than influenza A viruses (IAV) in ferrets. Using an ex vivo primary ferret nasal epithelial cell (FNEC) and peripheral blood mononuclear cell (PBMC) co-culture model, we demonstrate that this deficit is not caused by poor viral fitness. IAV and IBV replicate to equivalent apical titers (p = 0.190) and trigger equivalent basolateral interferon lambda (IFNλ) protein (p > 0.98) and induction of RIG-I, IFNλ3, and TSLP (p > 0.83) at 48 h post-infection (hpi). However, subsequent downstream signaling in recruited PBMC diverges. At 48 hpi, IBV induces uncoupled signaling featuring 1160.1-fold TYK2 induction (p = 0.032). By 72 hpi, IAV maintains pro-inflammatory output, whereas IBV shifts toward a regulatory phase marked by GZMA (3.24-fold; p = 0.001), STAT3 (7.59-fold, p = 0.003) and TGFß (3.97-fold, p = 0.003). Spearman's analysis confirms the TYK2 vs. CCL5 axis is decoupled during IBV infection (rs = 0.5, p = 0.450) compared to robust coupling in IAV (rs = 0.89, p = 0.033). This signaling decoupling across the "epithelial-immune bridge" drives suboptimal IBV immunogenicity.

PMID 42762643
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