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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

PubMed[Rinsho ketsueki] The Japanese journal of clinical hematology2026-08-30

[Predictors of treatment-free remission (TFR) and second TFR attempts in chronic myeloid leukemia].

Ureshino Hiroshi H

The introduction of tyrosine kinase inhibitors (TKIs) has made long-term survival achievable for patients with chronic myeloid leukemia (CML). In patients who achieve a deep molecular response, treatment-free remission (TFR), defined as sustained remission without molecular relapse after TKI discontinuation, has emerged as an important therapeutic goal. Accumulating evidence indicates that the establishment and maintenance of TFR are strongly influenced by host immunity, particularly immune surveillance mediated by natural killer (NK) cells. This review summarizes the clinical and immunological factors associated with successful TFR and discusses the potential of killer immunoglobulin-like receptor/human leukocyte antigen genetic polymorphisms as predictive biomarkers that regulate NK cell function and TFR outcomes. It also highlights immunomodulatory strategies using interferon-α, the feasibility of second attempts at TFR after initial discontinuation failure, and emerging therapeutic approaches targeting CML stem cells to achieve more durable disease control.

PMID 42669513
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PubMediScience2026-08-30

CLEC-1 promotes early IFN response in cDC1s and favors immune dysregulation during sepsis in mice.

Ogor Thomas Teja TT, Porée Esther E, Saenz Javier J, Davieau Marion M et al.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host immune response, characterized by both hyperinflammation and immunosuppression. Here, we show that the absence of the C-type lectin receptor CLEC-1-expressed particularly by lung cDC1s-improves mouse recovery following E. coli infection. Mechanistically, phenotypic and transcriptomic analyses revealed that Clec1a loss is characterized by an attenuated type I interferon response in lung cDC1s as well as reduced CXCL10 expression and monocyte infiltration during the acute phase of sepsis. Additionally, Clec1a deficiency is associated with an enhanced antigen presentation profile of lung myeloid cells and lower accumulation of regulatory T cells upon secondary infection, suggesting reduced immunoparalysis. Importantly, we demonstrate that blocking CLEC-1 using an anti-human CLEC-1 monoclonal antibody mitigates hyperinflammation in CLEC-1 humanized mice. Together, these findings uncover a role for CLEC-1 in the dysregulation of the inflammatory response during sepsis and suggest its potential as an immunotherapeutic target.

PMID 42668608
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PubMediScience2026-08-30

Harnessing biological variability for mechanistic inference: A stochastic framework applied to neural stem cell dynamics.

Wang Ren-Yi RY, Danciu Diana-Patricia DP, Klawe Filip Z FZ, Marciniak-Czochra Anna A

Inter-individual heterogeneity is often treated as noise, yet its temporal evolution can reveal regulatory mechanisms hidden from mean-field behavior. We present a stochastic framework that exploits variability for mechanistic inference in cell population dynamics. Using adult neurogenesis as a case study, we develop a state-dependent stochastic model of transitions between quiescent and active states and derive a diffusion approximation for the dynamics of both mean and variance. Applied to repeated cross-sectional data from wild-type and interferon-receptor knockout mice, we show that distinct regulatory mechanisms can produce similar mean dynamics but different fluctuation patterns. Jointly fitting mean and variance identifies proliferation-rate regulation as the dominant contributor to variability, while activation and self-renewal primarily govern average and long-term dynamics. Wild-type mice exhibit regulation of all three processes, whereas knockout mice lose activation control. These results show that population-level variability provides mechanistic information beyond average dynamics and helps distinguish between competing mechanistic models.

PMID 42668621
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-08-30

IFI27 and BAX are Essential for GSDME-Mediated Myeloma Cell Pyroptosis.

Cui Yaoli Y, Sun Yuening Y, Liu Ziyang Z, Lai Xuntao X et al.

Induction of pyroptosis is a novel strategy for multiple myeloma (MM) treatment, but the underlying mechanism remains elusive. In the analysis of the transcriptomic profile in pyroptotic MM cells, we find the interferon-alpha inducible protein IFI27 is strikingly upregulated. IFI27 is downregulated in MM cells in association with poor prognosis, but its overexpression displays great potency to trigger pyroptosis in both MM cell lines and newly diagnosed MM cells in a GSDME-dependent manner. Moreover, ectopic IFI27 impairs mitochondrial structure and function. Interestingly, when mitochondria are depleted, IFI27 almost fails to induce MM cell pyroptosis. Mechanistic studies show that IFI27 recruits N-GSDME to mitochondria via BAX, therefore triggering pyroptosis. When IFI27 is knocked down, MM cells hardly undergo pyroptosis even when triggered by N-GSDME, BAX, or chemotherapeutic agents. Although GSDMD induces cell pyroptosis independent of BAX, BAX is required for IFI27- and N-GSDME-induced cell pyroptosis. Lastly, ectopic IFI27 promotes GSDME activation and triggers MM cell pyroptosis in vivo and strikingly prolongs the survival of mice with MM. In summary, the present study finds that IFI27 and BAX are essential for GSDME-mediated cell pyroptosis, and induction of IFI27 may represent a promising strategy for the treatment of MM expressing GSDME.

PMID 42669156
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PubMedAging cell2026-08-30

SIRT1 Silences L1 Retrotransposons by Stabilizing Heterochromatin-Modifying Complexes.

Wang Xiaona X, Li Tianbo T, Tang Huanyin H, Liu Meng Xiao MX et al.

SIRT1, a sirtuin family member, has been extensively documented to be closely linked to aging and aging-related disease. Cellular senescence is a state of irreversible cell cycle arrest that functions as a key driver of aging. During cellular senescence, LINE-1 (L1) retrotransposable elements become transcriptionally activated and stimulate a type-I interferon (IFN-I) response. L1 activity has been strongly linked to aging and a variety of age-related disorders. However, whether SIRT1 influences cellular senescence through the transposable element L1 remains unknown. In this study, we discovered that SIRT1 significantly suppresses L1 retrotransposition. Under quiescent conditions, SIRT1 exhibits increased enrichment at the L1 5'-UTR region. This recruitment enhances its interaction with the heterochromatin-regulatory factors Lamin B1 and KAP1, subsequently elevating H3K9me3 levels. This repressive chromatin mark inhibits L1 transcription, thereby maintaining genomic stability and delaying cellular senescence. Consistent with these observations, SIRT1-deficient cell lines exhibited a marked reduction of the interaction of Lamin B1 and KAP1 and a reduced presence of these factors at the L1 5'-UTR. Consequently, the elevated L1 transcription resulting from SIRT1 deficiency activated the cGAS-STING pathway and ultimately triggered cellular senescence, an effect that was rescued by treatment with 3TC (a nucleoside reverse transcriptase inhibitor). In summary, our findings demonstrate that SIRT1 suppresses L1 retrotransposition by recruiting heterochromatin factors, thereby delaying cellular senescence and providing new insights with implications for delaying aging and mitigating age-related pathologies.

PMID 42669067
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PubMedKidney medicine2026-08-30

Metabolomic Signatures of Inflammation in Chronic Kidney Disease.

Chen Teresa K TK, Surapaneni Aditya L AL, Estrella Michelle M MM, Appel Lawrence J LJ et al.

Inflammation is associated with adverse kidney, cardiovascular, and mortality outcomes. Investigation of the metabolic milieu as it relates to inflammation may provide important insights into these disease processes. Prospective cohort. African American Study of Kidney Disease and Hypertension (AASK), Atherosclerosis Risk in Communities (ARIC) study, and Boston Kidney Biopsy Cohort (BKBC) participants with available metabolomics and inflammatory protein data. Baseline blood levels of 718 metabolites. Baseline and longitudinal changes in blood levels of tumor necrosis factor receptors 1 and 2 (TNFR1, TNFR2), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), interleukins 6, 8, and 10 (IL-6, IL-8, IL-10), uromodulin (UMOD), and epidermal growth factor (EGF). Multivariable linear regression and linear mixed-effects models. Among 491 AASK participants (mean age 54 years; 37% women; mean glomerular filtration rate, 45 mL/min/1.73 m2), 367 cross-sectional associations between metabolites and inflammatory proteins were significant after correction for multiple comparisons. The direction of association was mostly positive for TNFR1 (97%), TNFR2 (97%), IL-8 (77%), and IL-10 (100%); negative for UMOD (80%) and EGF (97%); and variable for TNF-⍺, IFN-γ, and IL-6. Pathways were distinct for several inflammatory proteins (eg, tryptophan metabolism for TNFR2). Forty-five associations between metabolites and longitudinal change in inflammatory proteins were identified. Notable metabolites included tigylcarnitine and N 2,N 5-diacetylornithine, which were associated with 2-year increases in TNFR1 and/or TNFR2, and 1,5-anhydroglucitol, where lower levels were associated with decreases in UMOD. In ARIC (n = 3,773) and BKBC (n = 413), replication of cross-sectional associations was excellent for TNFR1 (ARIC 83%; BKBC 85%) and TNFR2 (ARIC 64%; BKBC 79%) but poor for IL-8 (ARIC 3%; BKBC 3%). Metabolite data limited to baseline visit; potential for residual confounding. Using an untargeted approach, multiple metabolites were cross-sectionally and longitudinally associated with inflammatory proteins in persons with chronic kidney disease.

PMID 42668601
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