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interferon

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HK inno.N · IFNAR2 · 重组蛋白

什么是 interferon？

interferon 是一种重组蛋白，由HK inno.N研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Topical。

药物档案

公司HK inno.N
药物类别重组蛋白
分子靶点IFNAR2
给药途径Injectable (Others), Topical
状态Approved
来源： ClinicalTrials.gov, HK inno.N

作用机制

分子靶点

interferon 作用于 1 个分子靶点：

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

interferon 针对 6 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
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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相关研究文献

PubMedNature communications2026-09-11

Modeling reptile virus infection in vitro using Python regius airway organoids.

Willemsen Sam S, van Son Gijs G, Rissmann Melanie M, Akkerman Ninouk N et al.

Zoonoses pose substantial global health risks, highlighting the need to better understand animal-to-human transmission. Reptiles are increasingly recognized as hosts of diverse pathogens, including numerous viruses, yet the diversity and prevalence of reptile pathogens, as well as their potential risk to humans, remain poorly understood. Here, we establish and characterize airway organoids derived from Python regius, providing an in vitro model to study reptile airway infection. Through de novo assembly of a Python regius reference genome, we characterize airway organoids at single-cell resolution, which suggests the presence of diverse cell populations including ionocytes, ciliated, secretory, goblet, endocrine, tuft, and basal cells. The organoids support productive infection with Ball Python Nidovirus (BPNV) and mount a robust epithelial antiviral response through the induction of interferon-stimulated genes, cytokines, and genes involved in chemical defense. As a proof-of-concept, treating organoids with antiviral drugs during infection reduces BPNV levels, highlighting the model's utility for drug testing. By providing a reductionist system of the serpentes airway, these organoids constitute a physiologically relevant in vitro model to study reptile viruses and host-pathogen interactions in their native host.

PMID 42722640
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PubMedFrontiers in medicine2026-09-11

Therapeutic expansion of JAK inhibitors in Chinese dermatological practice: beyond atopic dermatitis to novel autoimmune frontiers.

Lyu Xinyan X, Wang Yixi Y, Yang Jingyi J, Zhang Yiwen Y et al.

Janus kinase inhibitors (JAKi) have demonstrated clinical utility in managing atopic dermatitis (AD), yet their broader potential across immune-mediated dermatoses remains inadequately explored, particularly within China's restrictive regulatory landscape for dermatologic indications. This review examines pathogenic mechanisms and emerging evidence supporting JAKi repositioning in seven dermatological conditions beyond AD: alopecia areata (AA), vitiligo, psoriasis, dermatomyositis (DM), pemphigus, bullous pemphigoid (BP), and chronic spontaneous urticaria (CSU)-with emphasis on therapeutic gaps and opportunities specific to Chinese practice. We delineate disease-specific JAK-STAT dysregulation, including IFN-γ-driven cytotoxicity in AA/vitiligo, IL-23/STAT3 activation in psoriasis, and type I interferon hyperactivation in DM. Key clinical findings from rigorous trials indicate that oral tofacitinib achieves PASI75 in 58% of psoriatic patients within 16 weeks and topical ruxolitinib induces facial repigmentation exceeding 75% in vitiligo. In contrast, while current evidence is substantially limited to isolated case reports, emerging data suggest that baricitinib may resolve steroid-refractory BP lesions within one month. Persistent limitations include reliance on small-scale studies for pemphigus and CSU, along with unresolved safety concerns regarding thrombosis risks in susceptible populations. Crucially, we identify therapeutic gaps in segmental vitiligo and juvenile DM where clinical data are absent. This synthesis advocates for randomized controlled trials to validate JAKi efficacy against biologics in high-burden diseases currently dependent on glucocorticoids.

PMID 42724161
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PubMedJournal of thoracic disease2026-09-11

New approaches for cryptococcosis treatment and prevention-a systematic review.

Li Yong-Ming YM, Chen Zhen Z, Zeng Shuxin S, Ye Feng F et al.

Cryptococcosis remains a life-threatening fungal infection with high mortality despite current antifungal therapy. The toxicity, limited accessibility, poor tissue penetration, and increasing resistance associated with conventional antifungals highlight the need for innovative preventive and therapeutic strategies. This systematic review summarises recent advances in cryptococcosis management and identifies priorities for future research and clinical translation. PubMed, Embase, Web of Science, Cochrane Library, and ClinicalTrials.gov were systematically searched for studies published between January 2005 and December 2025. Data on study characteristics, therapeutic strategies, mechanisms, and outcomes were extracted. Because of substantial heterogeneity among clinical and preclinical studies, quantitative synthesis and certainty-of-evidence assessment were not performed. Eighty-six studies were included. Promising advances were identified in vaccines, immunotherapy, nanotechnology-based drug delivery, novel antifungal agents, drug repurposing, and non-pharmacological interventions. Vaccine candidates induced protective immunity in animal models but remain preclinical. Adjunctive interferon-γ is the only immunotherapy supported by clinical evidence, whereas programmed cell death protein 1 (PD-1) blockade, chimeric antigen receptor T-cell (CART) therapy, most of monoclonal antibodies, and other immunomodulators remain under preclinical investigation. MAT2203 demonstrated non-inferior efficacy with improved safety compared with intravenous amphotericin B. Several novel antifungal agents have entered clinical development, whereas repurposed drugs have shown limited clinical benefit. Most non-pharmacological approaches also remain experimental. Emerging strategies are reshaping cryptococcosis management beyond conventional antifungal therapy. Although most remain at the preclinical or early clinical stage, advances in host-directed immunotherapy, nanomedicine, and novel antifungal development provide promising opportunities to improve treatment efficacy, safety, and accessibility. Well-designed clinical studies are needed to facilitate clinical translation.

PMID 42724278
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PubMedClinical and molecular hepatology2026-09-11

RNAi-mediated HBV antigen shutdown enhances the antiviral immune effects of PEGIFNα via T and B cell crosstalk remodeling.

Zai Wenjing W, Hu Kongying K, He Mengying M, Song Ziyang Z et al.

PEGylated interferon-α (PEGIFNα) shows promise in treating chronic hepatitis B (CHB), yet patient response remains suboptimal. While suppressing hepatitis B virus (HBV) antigens by RNA interference (RNAi) could enhance PEGIFNα efficacy in CHB patients, the underlying immunological mechanisms remain obscure. Using our newly established extracellular humanized IFNAR (IFNAR-hEC) mouse model of chronic HBV infection, we evaluated the efficacy of a GalNac-conjugated siRNA (GalNac-siHBV) alone or in combination with PEGIFNα. Phenotypic and functional characteristics of immune cells were assessed by flow cytometry, ELISpot, and single-cell RNA sequencing (scRNA-seq). High circulating HBsAg reduced antiviral effects and immune responsiveness of PEGIFNα. Combined PEGIFNα and RNAi therapy synergistically and durably suppressed HBsAg (~4log10 IU/mL, vs PBS) and achieved HBsAg seroconversion in ~30% of mice, outperforming either monotherapy. Mechanistically, PEGIFNα enhanced global T and B cell function, whereas combined therapy further amplified HBV-specific T and B cell responses. scRNA-seq analysis indicated that combined therapy attenuated inhibitory B cell-B cell interactions, strengthened MHC-I-mediated T cell crosstalk, and enhanced MHC-II signaling networks across B cells and hepatocytes/Cd8+ T cells, collectively improving the lymphocyte functionality and facilitating HBsAg seroconversion. Reinforcing MHC-I/II signaling with agonistic antibodies (α4-1BB, αCD40) or IL-2-Fc further potentiated antiviral immune responses of combinational regimen. Combined RNAi and PEGIFNα therapy exerts synergistic antiviral effects by relieving HBV antigen-induced immune tolerance and orchestrating a functional T cell-B cell crosstalk network centered on MHC-I/II signaling. Enhancing antigen presentation pathways represents a promising adjunctive strategy to improve functional cure rate of CHB.

PMID 42723512
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PubMedJournal of clinical and translational hepatology2026-09-11

Comparison of Peg-INF plus TDF versus TDF Monotherapy in Indeterminate-phase Chronic Hepatitis B Patients with High HBsAg levels, HBeAg-negative status, and Normal ALT Levels.

Liu Min M, Xiao An A, Bu Bing B, Zuo Lili L et al.

Chronic hepatitis B patients with baseline hepatitis B surface antigen (HBsAg) <1500 IU/mL are considered as the favorable population for achieving functional cure. This trial aimed to explore a treatment strategy to help the unfavorable population characterized by high HBsAg levels (>3000 IU/mL), hepatitis B e antigen-negative status, and normal alanine transaminase levels in the indeterminate phase (HBeIP), transition to the favorable group. In this investigator-initiated, open-label clinical trial, we randomly assigned participants aged 18 to 60 years with HBeIP characteristics to receive either tenofovir disoproxil fumarate (TDF) monotherapy (monotherapy group) or pegylated interferon alfa-2b (Peg-IFNα-2b) plus TDF (combination group). The primary endpoints were the HBsAg loss rate and the proportion of participants with HBsAg <1,500 IU/mL through week 96. From May 2021 to November 2023, we enrolled 263 participants, with 131 randomly assigned to the combination group and 132 to the monotherapy group. In the primary analysis, none of the 132 participants (0%) in the monotherapy group achieved HBsAg loss, compared with 10 of 131 (7.6%) in the combination group (P = 0.001). Through week 96, 48.9% (64/131) of participants in the combination group achieved HBsAg <1,500 IU/mL, and a reduction in HBsAg level greater than 1 log10 IU/mL between baseline and week 24 was an independent predictor of this endpoint (Odds Ratio = 16.957, 95% Confidence Interval: 3.002-95.797, P = 0.001). In contrast, only two participants (1.5%) in the monotherapy group achieved HBsAg <1,500 IU/mL. Compared with TDF monotherapy, combination therapy with Peg-IFNα-2b and TDF significantly improved both HBsAg <1,500 IU/mL and HBsAg loss rates in HBeIP patients.

PMID 42724027
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PubMedTranslational cancer research2026-09-11

Midkine restrains T-cell mediated anti-tumor immunity by suppressing macrophage M1 polarization in lung adenocarcinoma.

Qian Ting T, Sun Zijian Z, Wang Xin X, Sun Yan Y

Lung adenocarcinoma (LUAD) is characterized by a highly immunosuppressive tumor microenvironment (TME), which limits the efficacy of current anti programmed cell death protein 1 (anti-PD-1) immunotherapy. Midkine (MDK), a heparin-binding growth factor, is frequently overexpressed in various malignancies; however, its specific role in regulating anti-tumor immunity in LUAD remains unclear. This study aimed to investigate the immunomodulatory role of MDK in LUAD, and to evaluate the therapeutic potential of MDK neutralization. In this study, we analyzed single-cell sequencing datasets and validated MDK expression across multiple non-small cell lung cancer (NSCLC) cell lines. To explore the immunomodulatory functions of MDK, we established ex vivo co-culture models using human peripheral blood mononuclear cells (PBMCs) and LUAD cells. We assessed the impact of recombinant MDK and an MDK-neutralizing antibody (α-MDK) on T cell proliferation, differentiation, and cytotoxicity, as well as macrophage polarization, using flow cytometry, lactate dehydrogenase (LDH) release assays, and multiplex cytokine measurement. We confirmed that MDK is significantly upregulated in malignant LUAD cells compared to normal lung epithelial cells. Functional analysis revealed that MDK signaling suppresses T cell-mediated anti-tumor immunity by inhibiting the expansion of cytotoxic CD8+ T cells and restricting T helper type 1 cell (TH1) polarization. Furthermore, MDK impaired the polarization of macrophages towards the pro-inflammatory M1 phenotype, and dampened antigen-presenting cell function. Notably, blocking MDK signaling with a neutralizing antibody effectively reversed these immunosuppressive effects, restoring T cell cytotoxicity and enhancing the secretion of pro-inflammatory cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). Our findings demonstrate that MDK acts as a key regulator in the LUAD TME by simultaneously restraining T cell activation and M1 macrophage polarization. These data suggest that targeting MDK offers a promising therapeutic strategy to overcome immune suppression and improve clinical outcomes in LUAD.

PMID 42724375
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