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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

PubMedCardiology research and practice2026-11-11

Beyond the Infection: The Immunopathological Cascade and Novel Therapeutic Avenues in Viral Myocarditis.

Chen Yi Y, Liu Mengnan M, Wu Jinwen J, Li Yirui Y et al.

Viral myocarditis (VMC) is an inflammatory disease of the myocardium induced by infection with cardiotropic viruses. Its pathogenesis encompasses direct virus-induced myocardial injury and excessive host immune-mediated pathological responses. This review systematically delineates the dynamic progression of VMC, from viral invasion and immune activation to chronic myocardial remodeling. Special emphasis is placed on pattern recognition receptors (PRRs) in sensing viral components, and how mechanisms like cytokine storms, autoimmunity, and macrophage polarization imbalances drive myocardial injury and fibrosis. Furthermore, we summarize current and emerging therapeutic strategies-highlighting etiology-guided stratification based on myocardial viral genome status. For virus-positive cases, direct pathogen-targeted antivirals (e.g., interferon-beta [IFN-β], telbivudine), viral entry decoys, mitochondrial protectants, novel antiheart failure agents (SGLT2 inhibitors, ARNI), and blood component apheresis (TPE/IA) offer promising avenues. Conversely, immunosuppressive regimens, CAR-Treg therapies, and cytokine antagonists (e.g., IL-1β, TNF-α, IL-17) are strictly indicated for virus-negative inflammatory cardiomyopathy. The clinical translation potential and challenges in these multitarget interventions are discussed in detail. Despite advances in elucidating VMC immunopathology, precise management remains ch.allenging due to difficulties in balancing antiviral defense and inflammatory injury. Future research should leverage multiomics technologies and personalized multitarget approaches to improve clinical outcomes.

PMID 43011511
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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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PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-11-11

Aryl Hydrocarbon Receptor Is Dispensable for the Early Transcriptional Response of Mouse Macrophages to Type I Interferon.

Tabtim-On Darawan D, Segura Elodie E

Type I interferon (IFN-I) signaling is essential in the homeostasis and activation of immune cells, and macrophages play a central role in the IFN-I system. Dysregulation leads to tissue damage and autoimmunity, and IFN-I signaling needs to be tightly fine-tuned. One reported mechanism involves interactions with the transcription factor aryl hydrocarbon receptor (AhR). However, it remains to be determined whether AhR is required for the early transcriptional response of macrophages to IFN-I. Here we used macrophages from genetically deficient mice to investigate the involvement of AhR in the induction of early IFN-I-driven responses. We show that constitutive AhR deficiency does not impair the canonical transcriptional response to IFN-I in bone marrow-derived macrophages nor the expression of IFN-stimulated molecules by peritoneal macrophages upon in vivo exposure. These findings contrast with observations made in other cell types, in particular astrocytes and lung cancer cells, and support the notion of a context-dependent crosstalk between AhR and IFN-I-dependent signaling.

PMID 43012672
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PubMedBioscience reports2026-11-11

From genome guardian to immune modulator: the dual faces of DNA-PKcs.

Li Qiang Q, Zhan Pei-Wen PW, Hong Xian X, Qu Ying Y et al.

The DNA-dependent protein kinase catalytic subunit (DNA-PKcs) has long been recognized as a genome guardian, serving as a master regulator of non-homologous end joining (NHEJ), safeguarding genomic integrity and enabling adaptive immunity through V(D)J recombination. Beyond this nuclear function, DNA-PKcs is now increasingly appreciated as a context-dependent immune modulator, acting at the interface between the DNA damage response and inflammatory signaling. This review synthesizes recent advances that redefine DNA-PKcs as a versatile "molecular integrator." We delineate its structural dynamics and multifaceted regulation, and dissect its dual function in the cytoplasm, where it can either potentiate or suppress the cyclic GMP-AMP synthase and stimulator of interferon genes (cGAS-STING) pathway and even initiate STING-independent interferon responses. We further explore how dysregulation of DNA-PKcs underpins a spectrum of pathologies, from immunodeficiency and autoimmunity to cancer and neurodegeneration. Finally, we discuss the translational promise of DNA-PKcs inhibitors, which not only act as classical chemo- and radio-sensitizers but also remodel the tumor microenvironment by activating antitumor immunity. Decoding the context-dependent logic behind these dual faces is therefore paramount for developing novel therapeutics that leverage DNA-PKcs across oncology, autoimmunity, and neurodegeneration.

PMID 43012527
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PubMedAntimicrobial agents and chemotherapy2026-11-11

Rosmarinic acid exerts anti-CVB3 effects by inducing HO-1 via the SIRT1/AMPKα/Nrf2 pathway.

Huang Junbo J, Song Qing Q, Di Yanjun Y, Cheng Zhiyun Z et al.

Coxsackievirus B3 (CVB3) is the primary pathogen of viral myocarditis (VMC), and there is no specific therapy. Rosmarinic acid (RA) has anti-inflammatory and antioxidant properties, but its anti-CVB3 activity and mechanism remain unclear. This study examined the inhibitory effect of RA on CVB3 replication and VMC, and the underlying mechanism. In CVB3-infected HeLa cells and a mouse VMC model, RA blocked viral replication dose-dependently, with an EC50 of 26.49 μM and a selectivity index of 21.72, which was more effective than ribavirin. Time-of-addition experiments showed that RA interfered with the post-entry replication stage. Mechanistically, RA directly bound sirtuin 1 (SIRT1), with an affinity of -10.2 kcal/mol, increasing its conformational stability and inhibiting ubiquitin-proteasome degradation, thereby reversing CVB3-induced SIRT1 downregulation. Antiviral and anti-inflammatory effects of RA were abolished by SIRT1 knockdown. RA activated the AMPK/Nrf2/HO-1 cascade in a SIRT1-dependent manner. Notably, the HO-1 metabolite biliverdin (BV) stimulated STAT1/2 phosphorylation and interferon-stimulated gene expression. In vivo, RA effectively ameliorated CVB3-induced myocardial injury and restored SIRT1/AMPK/Nrf2/HO-1 expression. In conclusion, RA prevents CVB3 replication and VMC via direct binding and stabilization of SIRT1, activation of the SIRT1/AMPK/Nrf2/HO-1/BV signaling pathway, and stimulation of interferon response through STAT1/2.

PMID 43012511
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PubMedJournal of education & teaching in emergency medicine2026-11-11

Ruptured Hemorrhagic Ovarian Cyst Mimicking Ruptured Ectopic Pregnancy in a Post-Transplant Patient: A Case Report.

Shah Saloni S, Lewis Kristin K, Hseuh Andy A

The incidence of syncope in the setting of ruptured ectopic pregnancy can vary widely; however, data specifically focusing on syncope as the primary presenting symptom without accompanying abdominal pain or vaginal bleeding are scarce.1,2 Our 23-year-old female patient, who is post-liver transplant and currently on immunosuppressive therapy, experienced syncope without significant pain or bleeding and presented to the ED with stable vital signs. Initial investigations revealed mild left lower quadrant tenderness, a serum beta-hCG of 95 mIU/mL, and moderate free pelvic fluid with a 28 mm left ovarian "cyst" on transvaginal ultrasound. These findings raised concerns for a ruptured ectopic pregnancy. Diagnostic laparoscopy, however, ultimately revealed a ruptured ovarian hemorrhagic cyst. Subsequent negative urine beta-hCG tests confirmed the initial serum beta-hCG as a false positive likely due to heterophile antibody interference, which is common in immunosuppressed patients. This case represents a rare mimic of a ruptured ectopic pregnancy which can occur in post-transplant patients and a nuanced interpretation of clinical workup. Syncope in reproductive-age women, ruptured ovarian cyst, ectopic pregnancy mimics, false-positive beta-hcg, heterophile antibody interference, emergency ultrasonography, diagnostic laparoscopy, immunosuppression and diagnostic challenges, atypical presentations of gynecologic emergencies.

PMID 43011960
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