interferon beta-1b is a recombinant proteins developed by Generium Pharmaceutical. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.
interferon beta-1b is developed for 1 unique indication across 1 therapeutic area.
Therapeutic Area
Condition
Phase
Nervous system disorders
Multiple sclerosis
✓ Approved
Related Research Articles
PubMedACG case reports journal2026-07-17
Colonic Ischemia Without Mesenteric Occlusion: A Case Implicating Interferon-β.
Siegel Alexander A, Tun Kyaw Min KM, Gamache Jennifer J, Kizer Robert R
Type I interferons are commonly used immunomodulatory agents. Interferon-α (interferon-α) has been associated with ischemic colitis, but cases linking interferon-β (IFN-β) to ischemic colitis are rare. We present a 66-year-old woman with multiple sclerosis treated with IFN-β who developed acute abdominal pain and diarrhea. Imaging demonstrated right-sided colonic inflammation with pneumatosis. Colonoscopy with tissue biopsy confirmed ischemic colitis, despite patent mesenteric vasculature on angiographic imaging. Her symptoms resolved after discontinuation of IFN-β. This case highlights IFN-β as a potential cause of nonocclusive ischemic colitis and underscores the importance of recognizing ischemic complications in patients treated with IFN-β.
Autoimmunity and peginterferon therapy for polycythemia vera.
Rivière Etienne E, Guy Alexandre A, Mansier Olivier O, Mediavilla Clémence C et al.
Peginterferon‑α is useful to treat myeloproliferative neoplasms (MPNs) but can precipitate broad autoimmunity. By promoting beta-cell, thyroid, and systemic immune injury, it can lead to Type 1 diabetes, autoimmune thyroiditis, systemic lupus erythematosus, or Sjögren's syndrome. Onset typically occurs within the first months but may be delayed until after treatment cessation. Type 1 diabetes is usually irreversible and requires lifelong therapy, whereas thyroiditis and lupus more often improve after interferon withdrawal, though autoantibodies frequently persist. In this narrative review, we provide an overview of how peginterferon can induce autoimmunity in genetically susceptible individuals with pre-existing subclinical autoimmunity. Pre-treatment risk assessment, including personal/family history of autoimmune disease and consideration of baseline thyroid function and anti-GAD antibodies in high-risk patients, may identify those at elevated risk for irreversible complications, particularly Type 1 diabetes. Targeted clinical and laboratory monitoring throughout therapy and for 12-24 months post-cessation can enable early detection and appropriate intervention.
PubMedbioRxiv : the preprint server for biology2026-07-17
Distinct macrophage and T cell programs shape pancreatic inflammation during metabolic stress and aging.
Sai Somesh S, Omar Ibrahim I, Barone Matthias M, Mühle Kerstin K et al.
Type 2 diabetes is linked to systemic inflammation driven by metabolic stress and aging. Although pancreatic inflammation associated with these factors is well documented, the dynamics of immune cell populations and their molecular changes remain poorly understood. We characterized immune cell alterations in the pancreas and pancreatic islets during Western diet (WD) feeding and aging using imaging mass cytometry (IMC) and single-cell RNA sequencing (scRNA-seq). Spatial and transcriptional analyses were performed to define immune cell subtype composition, activation states, and inferred cell-cell communication programs under metabolic and age-related stress conditions. Our analyses identified expansion of an F4/80 low macrophage subtype and activated effector-like CD8 + T cells throughout the pancreas during WD feeding and aging. Within pancreatic islets, single-cell RNA sequencing identified a type I interferon-responsive macrophage population with low F4/80 expression that expanded during overnutrition. Notably, the type I interferon responses elicited by these stressors diverged: aging was associated with a more canonical type I interferon response, whereas overnutrition induced a broader response that included STAT3-associated transcriptional programs. We further provide evidence for enhanced cytokine-mediated communication between macrophages and a CD8 + cytotoxic T-cell population under overnutrition and aging. These findings show that metabolic stress and aging remodel pancreatic inflammation through overlapping but distinct immune mechanisms, involving expansion of F4/80 low macrophages, activation of divergent type I interferon programs, and enhanced macrophage-CD8 + T-cell communication. Together, these findings suggest that distinct therapeutic approaches may be required to preserve islet function in type 2 diabetes driven by metabolic stress versus aging.
Metabolic stress and aging remodel pancreatic inflammation through overlapping but distinct immune mechanisms.Spatial and single-cell analyses identified conserved remodeling of pancreatic macrophage populations accompanied by activation of cytotoxic T-cell responses during metabolic stress and aging.In pancreatic islets, macrophages exhibited distinct type I interferon-associated transcriptional programs, with aging showing a more canonical interferon response and metabolic stress eliciting a broader inflammatory program that included STAT3-associated transcriptional signatures.These findings provide a framework for understanding how metabolic stress and aging differentially shape pancreatic inflammation.
PubMedMonaldi archives for chest disease = Archivio Monaldi per le malattie del torace2026-07-17
Removal of Expression of Concern for 'Interferon-γ release assay'.
Publisher The T
Removal of Expression of Concern for 'Interferon-γ release assay' by Malay Sarkar and Jasmine Sarkar, Accepted Manuscript, https://doi.org/10.4081/monaldi.2025.3258 The Publisher of the Monaldi Archives for Chest Disease is publishing this removal of expression of concern to inform readers that the investigation is complete and all earlier issues have been addressed. This notice supersedes the information provided in the Expression of Concern related to this article (https://doi.org/10.4081/monaldi.2025.3712).
Biallelic mutations in SUPV3L1 cause a variable leukodystrophy due to impaired mitochondrial degradosome function.
Green Lydia L, Hamilton Noémie N, Elpidorou Marilena M, Maroofian Reza R et al.
Purpose Sensing and degradation of double stranded RNA (dsRNA) in the cell is tightly regulated to avoid activation of type I interferon signalling. The mitochondrial dsRNA degradosome complex is formed by PNPT1 and SUPV3L1. While biallelic PNPT1 mutations are an established cause of early-onset encephalopathy, the clinical and radiological impact of SUPV3L1 dysfunction is yet to be fully defined. Methods Through an international collaboration, we identified 21 patients with biallelic SUPV3L1 mutations. Available clinical and radiological data were compared. A supv3l1 knock-out zebrafish was generated to investigate the impact of supv3l1 loss in vivo . Results Fifteen different biallelic loss-of-function SUPV3L1 variants were identified in twenty-one individuals presenting with a wide clinical spectrum including neonatal haematological disturbance, infant-onset motor disorder and acute encephalopathy. Most individuals demonstrated significant neurodevelopmental involvement, manifesting as moderate to severe motor delay with intellectual impairment. Other common clinical features include microcephaly and spasticity. Three out of four patients tested showed an increased interferon signature in peripheral blood. A supv3l1 knock-out zebrafish exhibited defective mitochondria morphology and microglial function, with a significant activation of type 1 interferon signalling. Conclusion We define the genetic, clinical and radiological spectrum of SUPV3L1 -asociated disease and suggest activation of the type 1 interferon innate immune pathway by dysplastic microglia as a possible underlying cause.