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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

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

PubMedScandinavian journal of immunology2026-11-11

Type I Interferonopathies in Inborn Errors of Immunity: Pathogenesis, Clinical phenotype, Diagnosis and Management.

Zeinali Fatemeh F, Rezaei Nima N, Yazdani Reza R

Type I interferonopathies represent a heterogeneous group of inborn errors of immunity (IEI), characterized by dysregulated and persistent activation of the Type I interferon pathway. These patients present a broad spectrum of clinical phenotypes involving the nervous system, skin, lungs, and haematopoietic system. Diagnosis is often challenging owing to overlap with other autoinflammatory and autoimmune conditions. In parallel with the expanding molecular spectrum of these disorders, their classification within IEI has continued to evolve. This review provides an updated synthesis of Type I interferonopathies in the context of the 2024 International Union of Immunological Societies (IUIS) classification, linking the underlying genetic defects and dysregulated interferon pathways to their characteristic and overlapping clinical phenotypes. Particular emphasis is placed on a practical diagnostic framework integrating clinical recognition, interferon-based biomarkers, and molecular testing, as well as on the transition from conventional immunomodulation toward pathway-directed therapies, including the growing clinical experience with Janus kinase inhibitors. This review integrates current knowledge on the pathogenesis, clinical features, diagnostic approaches, and treatment strategies in patients with Type I interferonopathies, providing an updated clinically oriented framework for their recognition, diagnosis, and management within the expanding spectrum of IEIs.

PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-11-11

Aryl Hydrocarbon Receptor Is Dispensable for the Early Transcriptional Response of Mouse Macrophages to Type I Interferon.

Tabtim-On Darawan D, Segura Elodie E

Type I interferon (IFN-I) signaling is essential in the homeostasis and activation of immune cells, and macrophages play a central role in the IFN-I system. Dysregulation leads to tissue damage and autoimmunity, and IFN-I signaling needs to be tightly fine-tuned. One reported mechanism involves interactions with the transcription factor aryl hydrocarbon receptor (AhR). However, it remains to be determined whether AhR is required for the early transcriptional response of macrophages to IFN-I. Here we used macrophages from genetically deficient mice to investigate the involvement of AhR in the induction of early IFN-I-driven responses. We show that constitutive AhR deficiency does not impair the canonical transcriptional response to IFN-I in bone marrow-derived macrophages nor the expression of IFN-stimulated molecules by peritoneal macrophages upon in vivo exposure. These findings contrast with observations made in other cell types, in particular astrocytes and lung cancer cells, and support the notion of a context-dependent crosstalk between AhR and IFN-I-dependent signaling.

PubMedBioscience reports2026-11-11

From genome guardian to immune modulator: the dual faces of DNA-PKcs.

Li Qiang Q, Zhan Pei-Wen PW, Hong Xian X, Qu Ying Y et al.

The DNA-dependent protein kinase catalytic subunit (DNA-PKcs) has long been recognized as a genome guardian, serving as a master regulator of non-homologous end joining (NHEJ), safeguarding genomic integrity and enabling adaptive immunity through V(D)J recombination. Beyond this nuclear function, DNA-PKcs is now increasingly appreciated as a context-dependent immune modulator, acting at the interface between the DNA damage response and inflammatory signaling. This review synthesizes recent advances that redefine DNA-PKcs as a versatile "molecular integrator." We delineate its structural dynamics and multifaceted regulation, and dissect its dual function in the cytoplasm, where it can either potentiate or suppress the cyclic GMP-AMP synthase and stimulator of interferon genes (cGAS-STING) pathway and even initiate STING-independent interferon responses. We further explore how dysregulation of DNA-PKcs underpins a spectrum of pathologies, from immunodeficiency and autoimmunity to cancer and neurodegeneration. Finally, we discuss the translational promise of DNA-PKcs inhibitors, which not only act as classical chemo- and radio-sensitizers but also remodel the tumor microenvironment by activating antitumor immunity. Decoding the context-dependent logic behind these dual faces is therefore paramount for developing novel therapeutics that leverage DNA-PKcs across oncology, autoimmunity, and neurodegeneration.

PubMedAntimicrobial agents and chemotherapy2026-11-11

Rosmarinic acid exerts anti-CVB3 effects by inducing HO-1 via the SIRT1/AMPKα/Nrf2 pathway.

Huang Junbo J, Song Qing Q, Di Yanjun Y, Cheng Zhiyun Z et al.

Coxsackievirus B3 (CVB3) is the primary pathogen of viral myocarditis (VMC), and there is no specific therapy. Rosmarinic acid (RA) has anti-inflammatory and antioxidant properties, but its anti-CVB3 activity and mechanism remain unclear. This study examined the inhibitory effect of RA on CVB3 replication and VMC, and the underlying mechanism. In CVB3-infected HeLa cells and a mouse VMC model, RA blocked viral replication dose-dependently, with an EC50 of 26.49 μM and a selectivity index of 21.72, which was more effective than ribavirin. Time-of-addition experiments showed that RA interfered with the post-entry replication stage. Mechanistically, RA directly bound sirtuin 1 (SIRT1), with an affinity of -10.2 kcal/mol, increasing its conformational stability and inhibiting ubiquitin-proteasome degradation, thereby reversing CVB3-induced SIRT1 downregulation. Antiviral and anti-inflammatory effects of RA were abolished by SIRT1 knockdown. RA activated the AMPK/Nrf2/HO-1 cascade in a SIRT1-dependent manner. Notably, the HO-1 metabolite biliverdin (BV) stimulated STAT1/2 phosphorylation and interferon-stimulated gene expression. In vivo, RA effectively ameliorated CVB3-induced myocardial injury and restored SIRT1/AMPK/Nrf2/HO-1 expression. In conclusion, RA prevents CVB3 replication and VMC via direct binding and stabilization of SIRT1, activation of the SIRT1/AMPK/Nrf2/HO-1/BV signaling pathway, and stimulation of interferon response through STAT1/2.

PubMedBreast cancer research : BCR2026-11-11

CD39-associated myeloid-T-cell coordination within an immunoregulatory neighborhood linked to treatment resistance in triple-negative breast cancer.

Hu Zihan Z, Zheng Haoyu H, Jin Cheng C, Shang Guoguo G et al.

Immunotherapy efficacy in triple-negative breast cancer (TNBC) remains limited, partly due to mechanisms of immune suppression within the tumor microenvironment (TME). Ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1, encoding cluster of differentiation 39, CD39) is a key immunoregulatory ectonucleotidase, but its treatment-associated distribution and coordination across myeloid and T-cell states in TNBC remain incompletely characterized. We re-analyzed a single-cell RNA sequencing (scRNA-seq) dataset comprising 156120 immune cells from 27 tumor and metastatic samples across 14 patients with TNBC. Trajectory and cell-cell communication analyses were complemented by NicheNet, independent single-cell and bulk transcriptomic validation, CosMx spatial transcriptomics, and multiplex immunofluorescence. CD39 protein expression and its association with survival were evaluated in an independent cohort of 112 patients with TNBC using immunohistochemistry (IHC), Kaplan-Meier analysis, and multivariable Cox proportional hazards regression. Three signed-R2-based summary indices-treatment contribution (TC), ENTPD1 dynamic index (EDI), and tumor response index (TRI)-were applied to summarize treatment-associated immune dynamics. ENTPD1 expression was observed across macrophage and regulatory T-cell states, including CD4+CD39+ Tregs. Higher macrophage ENTPD1 expression was associated with M2-related programs, attenuated stimulator of interferon genes (STING)-type I interferon signaling, and reduced antigen-presentation programs. Cell-cell communication analysis revealed preferential interactions between myeloid cells and CD4+CD39+ T cells. Inferred lymphotoxin (LT) signaling involving CD4+CD39+ T cells and myeloid populations was higher in non-responders. Cross-cohort and patient-level analyses supported coordinated CD39-associated immune programs, while spatial transcriptomics and representative multiplex immunofluorescence imaging visualized the implicated populations within shared tumor regions. In the independent IHC cohort, high tissue-level CD39 expression remained independently associated with shorter overall survival (OS) after adjustment for age group and American Joint Committee on Cancer (AJCC) stage. ENTPD1/CD39 was associated with coordinated myeloid and T-cell states, an adenosine-related immunoregulatory context, and reduced response to anti-programmed death-ligand 1 (PD-L1) therapy plus chemotherapy in TNBC. These findings support further evaluation of ENTPD1/CD39-associated immune states in the context of immune checkpoint blockade (ICB). High tissue-level CD39 expression was independently associated with shorter OS in an independent clinical cohort.

PubMedJournal of virology2026-11-11

Fish TRAF6 shapes interferon antiviral response by targeting the background MAVS for protein degradation.

Gong Xiu-Ying X-Y, Zhao Xiang X, Dan Cheng C, Guo Wen-Hao W-H et al.

The interferon (IFN)-mediated antiviral immune response is tightly regulated to prevent insufficient or excessive immune activation. In mammals, the E3 ubiquitin ligase tumor necrosis factor receptor-associated factor 6 (TRAF6) is generally considered a positive regulator of IFN signaling although its role in fish may differ. In this study, zebrafish TRAF6 showed opposing regulatory effects on different retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) signaling components in overexpression assays, but knockdown and knockout experiments further supported its overall negative regulatory role in the fish IFN response. To investigate this inhibitory mechanism, we uncovered a previously unrecognized role of zebrafish TRAF6 in promoting the degradation of mitochondrial antiviral-signaling protein (MAVS) under basal conditions in an E3 ligase activity-dependent manner. Zebrafish TRAF6 bound to the N-terminal caspase recruitment domain (CARD) of MAVS in the cytoplasm and promoted lysosome-dependent MAVS degradation. Lys286 and Lys293 contributed to this degradation and were required for TRAF6-enhanced K48-linked polyubiquitination of MAVS. Simultaneous mutation of both residues increased basal MAVS protein levels and enhanced its ability to activate the IFN response. Our data also suggest that TRAF6 may promote MAVS degradation through a proteasome-dependent pathway involving the C-terminal region of MAVS. TRAF6 knockout (TRAF6-KO) zebrafish exhibited significantly enhanced resistance to spring viremia of carp virus (SVCV) infection. Basal MAVS protein levels were also significantly higher in TRAF6-KO tissues than in wild-type (WT) zebrafish. Collectively, our results reveal a critical role of zebrafish TRAF6 in regulating basal MAVS expression to fine-tune IFN-mediated antiviral innate immunity.IMPORTANCEInterferon (IFN)-mediated innate immunity is essential for protecting fish against viral infection, but excessive IFN activation can also be harmful to the host. Here, we identify zebrafish TRAF6 as a dual regulator of IFN-mediated antiviral signaling. In overexpression assays, TRAF6 enhanced RIG-I-mediated signaling and increased K63-linked ubiquitination of the RIG-I signaling complex while suppressing MAVS-mediated signaling by promoting MAVS degradation through distinct degradation pathways. In vivo, TRAF6 deficiency enhanced antiviral gene expression, reduced infectious viral titers, and significantly improved survival following SVCV infection. These findings reveal a previously unrecognized dual regulatory role for TRAF6 in fish antiviral immunity and highlight the importance of TRAF6-mediated MAVS degradation under basal conditions in regulating IFN-mediated antiviral responses.

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