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interferon beta-1b (Infibeta)

✓ Approved

Generium Pharmaceutical · Recombinant Proteins · Recombinant Proteins

What is interferon beta-1b?

interferon beta-1b is a recombinant proteins developed by Generium Pharmaceutical. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesInfibeta
CompanyGenerium Pharmaceutical
Drug ClassRecombinant Proteins
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Generium Pharmaceutical

Therapeutic Indications

interferon beta-1b is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Nervous system disordersMultiple sclerosis✓ Approved

Related Research Articles

PubMedFrontiers in immunology2026-10-15

Hemin suppresses interferon responses in periodontal cell models through JAK2-STAT1 inhibition.

Huang Xiaoyu X, Gruber Reinhard R, Panahipour Layla L

Hemin, an oxidized heme species released during erythrocyte breakdown, is detectable in gingival crevicular fluid during periodontal inflammation, but its effects on local immune signaling remain unclear. We investigated whether hemin modifies cytokine-induced interferon responses in HSC-2 oral squamous cell carcinoma cells and primary human gingival fibroblasts. Cells were stimulated with interleukin-1β and tumor necrosis factor-α, or with interferon-γ, in the presence or absence of hemin. Transcriptomic changes were assessed by RNA sequencing and pathway analysis, and selected transcripts and proteins were validated by reverse-transcription quantitative PCR, enzyme-linked immunosorbent assay, immunoblotting, and immunofluorescence. Ligand-kinase interactions were examined by molecular docking and molecular dynamics simulations, and recombinant Janus kinase 2 activity was measured in a cell-free assay. Hemin preferentially suppressed an interferon-associated gene network, including CXCL10, CXCL11, MX1, OAS1, IFIT1, IFIT3, and ISG15, while nuclear factor κB-associated responses were comparatively preserved. Hemin also reduced signal transducer and activator of transcription 1 Tyr701 phosphorylation and nuclear accumulation induced by either the cytokine combination or interferon-γ. Computational analyses predicted stable hemin interactions within conserved ATP-binding pockets of Janus kinases, and the cell-free assay demonstrated inhibition of recombinant Janus kinase 2. Together, these findings show that hemin attenuates interferon-associated transcription in periodontal cell models, consistent with inhibition of the Janus kinase 2-signal transducer and activator of transcription 1 axis. This mechanism may enable blood-derived hemin to modify local mucosal immune signaling, although its relevance to periodontal tissues and antiviral defense requires confirmation in organotypic, infection, and in vivo models.

PMID 42876722
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PubMedFrontiers in immunology2026-10-15

Anti-interferon-γ autoantibodies: immunopathogenesis, diagnostic innovation, and emerging therapeutic strategies in an adult-onset immunodeficiency.

Tsai Chin-Shiang CS, Cheng Aristine A, Naz Farha F

Adult-onset immunodeficiency with anti-interferon-γ autoantibodies (AIGA) is a rare acquired immunodeficiency increasingly recognized in East and Southeast Asia, characterized by disseminated infections with nontuberculous mycobacteria and other intracellular pathogens. Recent studies have refined our understanding of its immunopathogenesis, including HLA-linked susceptibility, epitope-specific neutralization of IFN-γ, and molecular mimicry, while highlighting persistent gaps in diagnosis and treatment. This Perspective synthesizes emerging evidence into a clinically oriented framework spanning diagnosis, monitoring, and immunomodulatory therapy. We discuss functional confirmation of AIGA, repurposing of the QuantiFERON-TB platform as an accessible screening strategy, and quantitative titers and ¹8F-FDG PET as complementary biomarkers of disease activity and treatment response. We propose a clinical decision pathway in which refractory or progressive infection, rather than a fixed titer threshold, triggers immunomodulation, with rituximab and cyclophosphamide as the best-supported induction strategies, daratumumab reserved for refractory cases, and emerging AIGA-specific evidence supporting azathioprine for maintenance. Recognizing heterogeneous access to specialized testing and biologics across AIGA-endemic regions, we propose a resource-stratified approach integrating widely available markers with referral-based testing and resource-adapted treatment. We also highlight emerging antigen-specific strategies, including chimeric autoantibody receptor T cells engineered to eliminate autoantibody-producing B cells, as a future direction toward durable remission. Finally, we outline priorities for prospective validation and biomarker-guided therapy.

PMID 42876531
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PubMedFrontiers in immunology2026-10-15

Activation of cytosolic DNA sensing in NCM460 intestinal epithelial cells induces antiviral factors that restrict HIV infection in macrophages.

Majid Safah S, Khan Shazheb S, Wang Xu X, Khan Raheeb R et al.

The gastrointestinal tract is an important site of HIV persistence and contains susceptible target cells, including macrophages. Crosstalk between intestinal epithelial cells and macrophages may contribute to mucosal innate defense. NCM460 human intestinal epithelial cells were transfected with poly(dA). Expression and production of interferons, interferon-stimulated genes, and CC chemokines were assessed by quantitative RT-PCR, western blotting, and ELISA. Primary human macrophages were treated with conditioned supernatants from NCM460 cells, and HIV infection was assessed using cytopathic effects, luciferase activity, and HIV Gag RNA expression. Poly(dA) induced IFN-β, IFN-λ1, IFN-λ2/3, ISG15, viperin, OAS1, RANTES, and MIP-1α in NCM460 cells. Supernatants from poly(dA)-stimulated NCM460 cells induced GBP5, viperin, and MX2 in primary macrophages and significantly inhibited HIV infection. Activation of cytosolic DNA sensing in intestinal epithelial cells induces soluble antiviral factors that enhance innate antiviral responses in macrophages and may contribute to mucosal defense against HIV.

PMID 42876517
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PubMedImmunological reviews2026-10-15

Oxidative Stress, Post-Translational Modifications, and Type 1 Diabetes Pathogenesis.

Winstead Colleen J CJ, Hodel Miki M, Tse Hubert M HM

Type 1 diabetes (T1D) is an organ-specific autoimmune disease that destroys insulin-producing beta-cells. Insulin is a vital hormone for regulating glycemia that often undergoes post-translational modifications during processing from pre-proinsulin to biologically active insulin. While necessary for proper glucose homeostasis, insulin is also an autoantigen recognized by autoreactive T cells in T1D. Cellular stress pathways including endoplasmic reticulum stress and oxidative stress mediated by an increase in reactive oxygen species (ROS) synthesis and/or a concomitant decrease in antioxidant function can further drive post-translational modifications of various autoantigens in T1D including insulin. Innate immune-derived ROS generation is an essential frontline defense against microbial infections, but ROS can also function as signaling intermediates to properly stimulate T cell responses. Oxidative stress-induced post-translational modifications are thought to trigger autoreactive T cells in T1D by generating novel neoepitopes, eliciting epitope spreading, or enhancing autoantigen interactions with antigen-presenting cells. With the current technology, detecting post-translationally modified proteins is challenging. In this review, we will explore the role of ROS and other post-translational modifications involved in T1D. We will also discuss islet transplantation strategies being used for patients with T1D including novel cell sources for beta-cell replacement and management of oxidative stress after transplantation.

PMID 42876362
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PubMedAmerican journal of therapeutics2026-10-15

The Evolving Landscape of Hypertrophic Cardiomyopathy Treatment: Are Guidelines Keeping Pace?

Shusterman Vlad V, Salamatbad Gidon G, Weintraub Spencer S, Wharton Ronald R

Hypertrophic cardiomyopathy (HCM) is a common inherited cardiovascular disorder associated with morbidity. Rapid advances in therapeutics-particularly the emergence of cardiac myosin inhibitors (CMIs)-suggest that current management guidelines are lagging best practices. Cardiac myosin inhibitors have revolutionized the management of patients with obstructive HCM. Patients with nonobstructive HCM have had limited therapeutic options historically; however, the recently published ACACIA-HCM trial demonstrated significant benefit in these patients and may represent a new treatment option in these patients, although more long-term data and research are needed in this population. A literature review was performed using PubMed/MEDLINE, Google Scholar, society guidelines, and recently published clinical trials evaluating HCM, cardiac myosin inhibitors, beta blockers, calcium channel blockers, septal reduction therapy, and emerging therapies for obstructive and nonobstructive HCM. Historically, HCM management has centered on negative inotropic/chronotropic agents to alleviate left ventricular outflow tract obstruction by decreasing the force of contraction and increasing diastolic filling time. The introduction of CMIs represents a paradigm shift by directly targeting the underlying hypercontractility, representing the first therapy specifically designed to treat obstructive HCM, obviating the need for earlier agents, which had limited data and at best modest therapeutic benefit. There may finally be an available treatment for diastolic heart failure in patients with nonobstructive HCM with myosin inhibition, as results from a recent trial ACACIA-HCM were favorable. Furthermore, ongoing investigations are exploring novel approaches such as metabolic modulators. The management of HCM is undergoing substantial transformation, yet guideline recommendations continue to prioritize beta blockers as first-line therapy despite mounting evidence supporting CMIs. Although treatment strategies for obstructive HCM have evolved significantly, optimal approaches for nonobstructive disease remain unclear. Addressing this gap represents a critical priority for future research.

PMID 42875832
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PubMedFrontiers in immunology2026-10-15

Myeloid cell expression of the VDR and parathyroid hormone control the host response to influenza infection in mice.

Tang Mengzhu M, Froelich Nicole E NE, Hanna Nicholas J NJ, Weaver Veronika C VC et al.

Respiratory infections caused by seasonal influenza viruses remain a major global health burden. Vitamin D receptor (VDR) signaling regulates immune responses, but the role of the VDR and its interaction with parathyroid hormone (PTH) in host resistance to H1N1 influenza infection is not understood. Global VDR knockout (KO) mice, or myeloid (M) deletion of the VDR (M-VDR KO) and the respective wildtype (WT) littermates were infected with H1N1 influenza virus. Additional experiments treated WT mice with intermittent PTH or vehicle and then infected them with a H1N1 influenza A virus. Disease severity, mortality, viral burden and clearance, lung pathology, and inflammatory cytokine responses were evaluated. H1N1 influenza infection of WT mice resulted in non-lethal disease, whereas VDR KO mice had 21% mortality, delayed viral clearance, more severe symptoms and lung pathology. The increased severity of respiratory disease was accompanied by higher type I and II interferon responses in the lungs. M-VDR KO mice had increased disease severity and delayed viral clearance compared to WT littermates. PTH-treated WT mice had increased clinical scores, influenza M gene, and cytokine responses compared to vehicle treated WT mice. The work describes a novel paradigm in which the vitamin D-PTH axis governs host resistance to influenza virus disease by controlling the amount of inflammation and the amount of virus in the lung. In addition, the data suggest that VDR expression in myeloid cells is critical for controlling the early innate immune response to influenza viruses.

PMID 42876719
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