Drug Database
IN

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)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

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

PubMedAdvances in protein chemistry and structural biology2026-05-24

Transcriptomic profiling reveals immune pathway dysregulation and key interferon-responsive genes in Systemic Lupus Erythematosus.

Selvam Prasanna Kumar PK, Mohan Supraja S, Vasudevan Karthick K

Systemic Lupus Erythematosus (SLE) is a complex autoimmune disorder characterized by chronic inflammation, multi-organ involvement, and a strong type I interferon (IFN) signature. To elucidate immune-specific molecular drivers of SLE, we performed transcriptomic profiling using RNA sequencing (RNA-seq) data from 117 samples (99 SLE patients, 18 healthy controls) obtained from the European Nucleotide Archive (PRJNA294187). Following quality control, alignment to GRCh38, and read quantification, differential expression analysis with DESeq2 identified 2150 differentially expressed genes (DEGs), including 1361 upregulated and 789 downregulated genes (FDR<0.01, |log₂FC=>1). Reactome pathway enrichment isolated 41 immune-related DEGs enriched in cytokine signaling, interferon response, antigen processing, and innate immune activation. Notably, interferon-stimulated genes (ISGs) such as EIF2AK2, ISG15, CXCL10, CXCL11, IFI44L, RSAD2, and HERC5 emerged as central nodes in immune regulatory networks. Gene Ontology analysis highlighted overactivation of defense response, chemokine-mediated cell trafficking, and Jak-STAT signaling pathways typically induced by viral infection but aberrantly sustained in SLE, driving chronic inflammation and autoimmunity. Several genes, including HERC5, HERC6, and IL5RA, exhibited regulatory roles in ubiquitination and cytokine receptor signaling, suggesting potential as biomarkers for disease activity. These findings support targeting type I IFN signaling and related immune circuits as therapeutic strategies, aligning with emerging clinical success of IFN-blockade in SLE. By prioritizing immune-focused DEGs and integrating pathway-level interpretation, our study refines the transcriptomic landscape of SLE and provides actionable molecular insights for precision medicine approaches aimed at disease modulation and patient stratification.

PMID 42177068
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PubMedAdvances in protein chemistry and structural biology2026-05-24

Identification of common hub genes and pathways in systemic lupus erythematosus and cervical cancer using bioinformatics approach.

Loganathan Tamizhini T, Madhulekha S S, Zayed Hatem H, C George Priya Doss GPD

Systemic lupus erythematosus (SLE) is a complex autoimmune condition characterized by multifactorial pathogenesis involving dysregulated immune responses. It has been associated with an elevated risk of various cancers, notably cervical cancer (CC), one of the most common cancers in women globally. Despite this association, the molecular mechanisms linking SLE and CC remain incompletely defined. To investigate this intersection, we employed integrative bioinformatics approaches to analyze transcriptomic datasets relevant to both SLE and CC, including GSE112087, GSE154851, GSE46907, GSE49454, GSE50772, GSE63514, GSE64217, GSE63678, GSE7803, and GSE9750 . We performed differential gene expression analysis, constructed Protein-Protein Interaction (PPI) networks, and carried out functional annotation to pinpoint pivotal hub genes and signaling pathways implicated in both diseases. Our analysis revealed significant differentially expressed genes (DEGs) in SLE, predominantly associated with cytokine and interferon alpha/beta signaling pathways, as well as the innate immune response. Notable hub genes included MX1, ISG15, and STAT1. In CC, DEGs were chiefly enriched in the mitotic cell cycle and cytokine signaling processes, with CDK1 and DLGAP5 standing out as key hub genes. The cross-disease analysis identified shared DEGs between SLE and CC, particularly in the interferon-alpha/beta and cytokine signaling pathways. This suggests a shared molecular architecture that underlies both autoimmune and cancer pathogenesis. Our study underscores the common molecular pathways between SLE and CC, highlighting the significance of interferon and cytokine signaling in the pathogenesis of both diseases. These insights set the stage for future research into potential therapeutic targets for the treatment of both SLE and CC.

PMID 42177067
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PubMedKidney international2026-05-24

Role of the Post-translational ISGylation of Interferon Regulatory Factor 9 in Diabetes-Induced Podocyte Injury.

Lv Zhimei Z, Hu Jinxiu J, Lang Yating Y, Fan Xiaoting X et al.

Diabetic kidney disease (DKD) is the most common cause of kidney failure, with podocyte injury being a key event in its progression. Here, by performing single-cell regulatory network inference and clustering analysis between DKD and normal kidney samples, we found a significant increase in interferon regulatory factor 9 (IRF9) transcriptional activity in the podocytes of DKD kidneys. However, the role of IRF9 in DKD remains poorly understood. Kidney tissue from patients with DKD and high glucose-cultured conditionally immortalized human podocyte cell line (HPC) were employed to investigate IRF9 expression and localization. RNA sequencing was performed to elucidate the role of IRF9 in podocyte injury. Co-immunoprecipitation, in-situ proximity ligation assay, and surface plasmon resonance were performed to confirm the binding between IRF9 and interferon-stimulated gene 15 (ISG15). ISGylation and ubiquitination assays were used to examine the potential effects of ISG15 on IRF9 expression. Podocyte-specific IRF9 deletion and overexpression mice and podocyte-specific ISG15 knockdown mice were established to assess kidney injury in vivo. IRF9 protein expression was increased in the podocytes of patients with DKD, without changes in IRF9 mRNA expression, and IRF9 expression was negatively correlated with eGFR and positively correlated with 24-hour urinary protein. In cultured human podocytes, high glucose conditions stimulated IRF9 protein expression without affecting IRF9 mRNA expression. Silencing IRF9 alleviated high glucose-induced podocyte injury, whereas IRF9 overexpression exacerbated podocyte injury. IRF9 induced podocyte injury via inflammasome activation and pyroptosis. Interestingly, high glucose exposure increased IRF9 protein expression by stimulating ISG15 expression, which promoted IRF9 ISGylation and subsequently inhibited IRF9 ubiquitination to increase IRF9 protein stability. In vivo, the podocyte-specific deletion of IRF9 or podocyte-specific knockdown of ISG15 attenuated podocyte and glomerular injury in streptozotocin-induced diabetic mice fed a high-fat diet; in contrast, the podocyte-specific overexpression of IRF9 exacerbated podocyte and glomerular injury in these diabetic mice. Targeting ISG15-IRF9 could be a potential novel therapy for podocyte injury in DKD.

PMID 42176776
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PubMedAntiviral research2026-05-24

Identification of Nsp15 Inhibitors Restoring Interferon-Dependent Antiviral Activity Against SARS-CoV-2.

Maloccu Stefania S, Otsuka Yuka Y, Molchan Elizabeth E, Foti Michelle M et al.

The endoribonuclease Nsp15 is essential for coronavirus pathogenesis and evasion of host defenses and is therefore a promising drug target. We determined optimal parameters for an endoribonuclease FRET biochemical assay and use it for a high-throughput drug screen. Measurement of Z'-factor confirmed robust assay performance (Z'= 0.7- 0.9). We screened a commercially available library (LOPAC 1280) and identified three molecules able to inhibit the catalytic endonuclease activity of Nsp15 in the low micromolar range. Among them, a promising hit compound, Reactive Blue 2 showed also anti-SARS-CoV-2 activity with EC50 value of 2 μM, and low cytopathic effect in multiple cell types (CC50 >28 μM). More importantly, SARS-CoV-2 replication was inhibited in cells with an intact IFN system, but not in IFN-deficient cell lines.

PMID 42176900
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PubMedAdvances in therapy2026-05-24

Efficacy and Safety of Pegylated Interferon as Rescue Therapy for Patients with Chronic Hepatitis B Who Failed to Achieve Functional Cure After Antisense Oligonucleotides or Small Interfering RNA: A Prospective, Multicentre, Open-Label Randomized Controlled Trial (SPHERE) Protocol.

Zhang Qiran Q, Sun Feng F, Sui Shulan S, Lin Jianmei J et al.

Although novel targeted therapies such as antisense oligonucleotides (ASO) or small interfering RNA (siRNA) can rapidly reduce hepatitis B surface antigen (HBsAg), only a subset of patients can achieve HBsAg seroclearance, and recurrence is common after discontinuation. This trial aims to evaluate the efficacy and safety of sequencing pegylated interferon alpha (Peg-IFNα) as rescue therapy for patients who have not achieved functional cure after initial therapy with ASO or siRNA. This is a prospective, multicentre, open-label, non-inferiority randomized controlled trial. Patients with chronic hepatitis B (CHB) who have previously completed a full course of ASO or siRNA therapy with HBsAg level of 1-500 IU/mL at screening will be enrolled. Participants will be randomized 1:1 to two arms: those in arm A (immediate treatment arm) will receive 24 weeks of Peg-IFNα starting at enrolment, followed by 24 weeks off-treatment observation; participants in arm B (delayed treatment arm) will firstly be observed for 24 weeks then followed by 24 weeks of Peg-IFNα treatment. At week 48, those with HBsAg seroclearance will enter a 48-week treatment-free follow-up, while those without seroclearance, regardless of initial arm, will receive an additional 24 weeks of Peg-IFNα, followed by 24 weeks off-treatment observation after week 72. The primary endpoint is the proportion of participants achieving HBV DNA < 20 IU/mL, HBsAg < 0.05 IU/mL and normal ALT at week 72. Secondary endpoints are HBsAg clearance rates, changes in clinical indicators, and safety evaluation results at other time points including weeks 24, 48 and 96. Sample size was calculated using Bayesian methods with the following parameters: experimental group response rate 0.57, control group response rate 0.47, non-inferiority margin 0.1, power 0.8, α = 0.05 and required posterior probability ≥ 80%. The single-group sample size was 33, and considering a 10% dropout rate, the total sample size was set to 72 (36 per group). Statistical analysis will be based on Bayesian non-inferiority test, with the primary judgment criterion being a posterior probability of ≥ 80% that the experimental group is non-inferior to the control group. Successful completion of this trial will provide a viable rescue treatment option for patients who have not met treatment goals after ASO or siRNA therapy. It may complete the future therapeutic framework, bringing more patients, especially those who are difficult-to-treat, within the scope of functional cure. ClinicalTrials.gov identifier NCT06923280.

PMID 42176181
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PubMedPediatric radiology2026-05-24

Imaging findings in pediatric interferonopathies.

Tsujioka Yuko Y, Nishimura Gen G, Hattori Shinya S, Kim Ok Hwa OH et al.

Type I interferon (IFN-I) is a proinflammatory cytokine that activates signalling pathways crucial for antiviral defence in innate immunity. The IFN-I system is a self-preserving mechanism that normally responds to exogenous nucleic acids derived from pathogens, but not to endogenous nucleic acids from host cells. However, genetic defects that constitutively activate this pathway can lead to aberrant IFN-I production (the "IFN signature") and sterile inflammation (autoinflammation), giving rise to a group of monogenic disorders collectively termed "autoinflammatory interferonopathies." This emerging perspective was initially prompted by the phenotypic similarities between Aicardi-Goutières syndrome and congenital toxoplasmosis, other infections, rubella, cytomegalovirus, and herpes simplex (TORCH) infection. Autoinflammatory interferonopathies can manifest with variable combinations of cutaneous changes, encephalopathy, vasculopathy, interstitial lung disease, and other features (e.g., skeletal changes), and are commonly accompanied by autoimmunity. More recently, the IFN signature has also attracted attention in autoimmune diseases such as systemic lupus erythematosus and dermatomyositis, which have been increasingly referred to as "autoimmune interferonopathies." Collectively, interferonopathies provide a novel framework for immune-mediated diseases spanning an autoinflammatory-autoimmune continuum. Here, we outline the clinical, imaging, and pathogenic features of paediatric interferonopathies. While each disorder has distinctive imaging findings, many share common patterns reflecting common underlying pathophysiology.

PMID 42176059
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