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recombinant human interferon alfa-2a

✓ Approved

BioGeneric Pharma · IFNAR2 · Recombinant Proteins

What is recombinant human interferon alfa-2a?

recombinant human interferon alfa-2a is a recombinant proteins developed by BioGeneric Pharma. It is approved for therapeutic indications via injectable (others).

Drug Profile

CompanyBioGeneric Pharma
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, BioGeneric Pharma

Mechanism of Action

Molecular Targets

recombinant human interferon alfa-2a acts on 1 molecular target:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
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Therapeutic Indications

recombinant human interferon alfa-2a is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Neoplasm malignant✓ Approved

Related Research Articles

PubMedPediatric allergy, immunology, and pulmonology2026-11-11

Successful Reintroduction of Olipudase Alfa Following Anaphylaxis Using a 12-Step Desensitization Protocol in a Child With Chronic Neurovisceral Acid Sphingomyelinase Deficiency.

Cimi Burcu Sarigul BS, Akyüzlüer Güneş Merve Setenay MS, Ozturk Gokcan G, Gurlek Erkut E et al.

Background:Olipudase alfa is the first disease-specific enzyme replacement therapy (ERT) approved for the treatment of noncentral nervous system manifestations of acid sphingomyelinase deficiency (ASMD); however, experience with the management of olipudase alfa-induced anaphylaxis remains limited.Case Presentation:We report a 13-year-old girl with chronic neurovisceral ASMD who developed anaphylaxis during an olipudase alfa infusion, presenting with periorbital edema, generalized urticaria, and hypotension. Following successful treatment with intramuscular adrenaline, olipudase alfa was reintroduced using a 12-step desensitization protocol. After two successful infusions at 2 mg/kg, the dose was re-escalated to the full therapeutic dose of 3 mg/kg, which has since been maintained every 2 weeks without recurrence of hypersensitivity reactions.Conclusion:In contrast to the previously reported real-world pediatric case, in which recurrent anaphylactic reactions ultimately necessitated omalizumab therapy, our patient successfully achieved and maintained the full therapeutic dose with desensitization alone. This case suggests that individualized desensitization may enable the safe continuation of olipudase alfa following anaphylaxis, thereby avoiding permanent discontinuation of ERT.

PMID 43010577
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PubMedAnalytical chemistry2026-11-11

Single-Step Sample-Activated Alternating Sequential Flow Enables Autonomous Multistep Electrochemical Lateral Flow Detection of Mpox Virus DNA.

Lapee-E Vasita V, Phimdee Piyathida P, Jung Hyo-Il HI, Pasomsub Ekawat E et al.

The 2022 multinational mpox virus (MPXV) outbreak and continued cross-border transmission have highlighted limitations of laboratory-confined PCR diagnostics. Here, we report an alternating lateral flow architecture (ALFA) that transforms traditional single-pass lateral flow into a programmable platform for autonomous multistep electrochemical nucleic acid detection following a single prepared-sample introduction. By regulating passive fluid delivery, ALFA enables sequential molecular processing and in situ signal generation without external intervention. Coupled with Ag(I)-mediated mismatch DNA nanocomplexes (MDNs), the system provides electrochemical signal amplification without nucleic acid amplification. ALFA detected MPXV DNA with a limit of detection (LOD) of 1.55 pM and a linear range of 101-105 pM. In urine and saliva spiked with structurally intact viral particles, the lowest statistically distinguishable concentration was 10 copies mL-1. Clinical evaluation of 50 PCR-characterized lesion swab samples yielded 92.11% sensitivity, 100% specificity, and 94.0% accuracy. The platform also maintained stable performance over an estimated 112 days. ALFA therefore provides a programmable lateral flow framework for rapid, amplification-free, decentralized nucleic acid diagnostics.

PMID 43010552
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PubMedClinical pharmacology and therapeutics2026-11-11

Antiviral Activity and Safety of Molnupiravir in Healthy Participants Inoculated With Influenza Virus: A Phase 2a, Randomized, Human Challenge Trial.

Nussbaum Jesse J, Mann Alex J AJ, Liao Laura E LE, Zhao Tian T et al.

Influenza viruses cause substantial global morbidity and mortality. Molnupiravir, an orally administered prodrug of β-D-N4-hydroxycytidine, has broad activity against RNA viruses, including influenza. A phase 2a, randomized, two-part human challenge trial in healthy adults (NCT05818124) was conducted to evaluate molnupiravir for influenza infection. In Part 1, 20 participants were inoculated with 106.26TCID50 of A/France/759/21 (H1N1) to establish infectivity, pathogenicity, and safety. After assessment of Part 1, a 10-fold lower virus dose was selected for Part 2 to delay time to peak viral load (PVL). In Part 2, 141 participants were randomized 1:1:1:1 to receive molnupiravir (5 days, 800 mg twice daily) postexposure prophylaxis (PEP; initiated 12 hours after inoculation), molnupiravir treatment (initiated 48 hours after inoculation), oseltamivir treatment (5 days, 75 mg twice daily, initiated 48 hours after inoculation), or placebo. Primary endpoints, assessed by quantitative viral culture, were PVL in all participants for PEP and viral load area under the curve (VL-AUC) in participants with confirmed infection for treatment. Lowering the viral inoculum delayed PVL by ~12 hours, although infection rates in the Part 2 placebo arm (40%) were lower than in Part 1 (75%). Molnupiravir PEP did not significantly reduce PVL compared with placebo but was associated with lower viral burden (difference in mean log10 VL-AUC -2.21 day*log10TCID50/mL; P = 0.03). No significant antiviral effect was observed with molnupiravir or oseltamivir treatment compared with placebo. Molnupiravir was well tolerated, with an adverse event profile similar to placebo. Although primary endpoints were not met, early administration of molnupiravir showed antiviral activity.

PMID 43010566
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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.

PMID 43009724
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PubMedFrontiers in cellular and infection microbiology2026-11-11

A single-cell atlas of the human respiratory system identifies a monocyte-centered HSPA1B+ inflammatory primed state associated with WTAP.

Wang Ying Y, Zhu Lin L, Zhu Yejin Y, Chen Guoping G

Chronic obstructive pulmonary disease (COPD) is characterized by persistent pulmonary inflammation and tissue remodeling, yet the cellular states and regulatory mechanisms underlying monocyte functional heterogeneity remain incompletely understood. Here, we generate a high-resolution single-cell transcriptomic atlas of the human respiratory system and identify a diverse monocyte functional landscape in healthy lungs containing a HSPA1B+ inflammatory monocytes state. This population exhibits enhanced inflammatory programs, cytokine and chemokine activity, and shows a distinct position within the inferred transcriptional landscape of the continuous monocyte functional spectrum. Cell-cell communication analysis further reveals that HSPA1B+ inflammatory monocytes function as active communication nodes within a stromal-immune-vascular network, integrating MIF, extracellular matrix, and immune-regulatory signals while mediating CXCL and adhesion-associated interactions with surrounding cellular compartments. Comparative analysis of COPD lung tissues and bronchoalveolar lavage fluid demonstrates selective enrichment of this inflammatory monocyte program in disease-associated environments, whereas peripheral blood monocytes from healthy individuals and COPD patients show limited representation of this state. Integrated transcriptomic and m6A regulator-associated analyses identify WTAP, a core component of the m6A methyltransferase complex, as a factor associated with the inflammatory monocytes program. WTAP silencing in inflammatory monocyte models suppresses pro-inflammatory mediators while enhancing interferon-response and antigen-presentation programs. Collectively, these findings define an inflammatory monocyte state landscape in the human respiratory system and identify a WTAP-associated transcriptional program linked to monocyte inflammatory activation and functional remodeling in COPD. This study provides new insights into the organization of pulmonary immune states and the potential regulatory mechanisms underlying chronic inflammatory regulation in COPD.

PMID 43011278
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PubMedFrontiers in immunology2026-11-11

Fractalkine produced by Shiga toxin type 2-stimulated human glomerular endothelial cells modulates γδ T lymphocyte migration.

Rosso David Antonio DA, Rosato Micaela M, Ledesma Martín M, Gómez Fernando Daniel FD et al.

γδ T cells play a critical role in tissue immunosurveillance through their capacity to sense cellular stress. However, their recruitment dynamics to peripheral organs such as kidney during Shiga toxin (Stx)-induced renal damage, remain undefined. Since the CX3CL1/CX3CR1 axis is vital for leukocyte homing into inflamed organs, we investigated its participation in mediating γδ T cell trafficking to the Stx-damaged kidney. We integrated in vitro functional assays using Stx2a-stimulated human glomerular endothelial cells (HGEC) with in silico single-cell RNA sequencing (scRNA-seq) analysis of public human kidney injury datasets. CX3CL1/CX3CR1 expression was evaluated via qPCR, ELISA, and flow cytometry, while the functional recruitment γδ T cells recruitment was quantified using transwell migration assays. In vitro, Stx2a significantly upregulates CX3CL1 mRNA and protein secretion in HGEC. In silico profiling of acute kidney injury (AKI) tissues confirmed widespread CX3CL1 upregulation in the damaged parenchyma and identified a distinct TRGV9+ cell cluster expressing CX3CR1 transcripts. Contingency analysis showed that TRGV9+ cells were substantially more likely to express CX3CR1 than other T/NKT cells. Importantly, flow cytometry analysis confirmed that γδ T cells express high levels of CX3CR1 protein. Finally, transwell assays demonstrated that both Stx2a-conditioned HGEC media and recombinant CX3CL1 potently induce γδ T cell migration, an effect that was completely abrogated upon disruption of the chemokine gradient. Together, these findings suggest that CX3CL1 release by Stx2a-stimulated endothelial cells contributes to a chemotactic gradient that may mediate the targeted recruitment of circulating CX3CR1+ TRGV9/TRDV2 cells to the injured kidney.

PMID 43010887
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