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interferon beta-1b (Infibeta)

✓ Approved

Generium Pharmaceutical · 重组蛋白 · 重组蛋白

什么是 interferon beta-1b?

interferon beta-1b 是一种重组蛋白,由Generium Pharmaceutical研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)、Subcutaneous Injection。

药物档案

商品名Infibeta
公司Generium Pharmaceutical
药物类别重组蛋白
给药途径Injectable (Others), Subcutaneous Injection
状态Approved

治疗适应症

interferon beta-1b 针对 1 个适应症,涉及 1 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersMultiple sclerosis✓ Approved

相关研究文献

PubMedClinics and practice2026-10-26

The Relationship Between Interferon Status and HPV Infection in Patients with Oral Epithelial Dysplasia: An Observational Study.

Khisamieva Guzel G, Sologova Diana D, Svitich Oxana O, Diachkova Ekaterina E et al.

Background/Objectives: Oral potentially malignant diseases (OPMDs) with signs of epithelial dysplasia are characterized by a high risk of malignancy. However, there are still no algorithms for their early diagnosis and prediction, due to the many possible predisposing factors, including human papillomavirus (HPV) infection and decreased immunity. There is a need to assess the relationship between the manifestations of oral epithelial dysplasia (OED), HPV invasion in the oral cavity, and interferon status to improve the identification and characterization of patients with different degrees of dysplasia. Methods: This study was designed and reported with reference to the STROBE checklist. The study aimed to assess the association between interferon status and HPV invasion in patients with OED. As per the inclusion and exclusion criteria, this observational study included 180 patients with histologically confirmed oral epithelial dysplasia associated with leukoplakia or oral lichen planus. Interferon (IFN) status was assessed by measuring serum interferon activity, spontaneous interferon production, IFN-α/β, and IFN-γ activity in peripheral blood. HPV DNA was detected and genotyped in biopsy specimens using polymerase chain reaction. Results: HPV-positive patients demonstrated significantly lower IFN-α/β and IFN-γ activity compared with HPV-negative patients (p < 0.001). Severe OED was more frequently observed in HPV-positive individuals, whereas mild dysplasia predominated among HPV-negative patients (p < 0.05). Interferon activity progressively decreased with increasing dysplasia severity, with the lowest IFN-α/β and IFN-γ activity detected in patients with severe dysplasia (p < 0.001 and p < 0.05, respectively). A significant positive correlation between IFN-α/β and IFN-γ activity was identified in patients with moderate dysplasia (p = 0.003). Multivariate binary logistic regression analysis demonstrated that HPV positivity (adjusted OR = 4.62, 95% CI: 2.18-9.79; p < 0.001) and reduced IFN-α/β activity (adjusted OR = 1.34 per 10-unit decrease, 95% CI: 1.14-1.58; p < 0.001) were independently associated with severe dysplasia. The multivariable model demonstrated acceptable discriminatory ability for identifying patients with severe dysplasia (AUC = 0.736), with a sensitivity of 89.4% and a specificity of 56.1%. Conclusions: The findings suggest that HPV-associated OED is linked to reduced interferon status, particularly lower IFN-α/β and IFN-γ activity in more severe dysplastic lesions. Combined assessment of interferon status and HPV detection may help identify patients at higher risk of severe OED.

PMID 42930365
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PubMedHepatology (Baltimore, Md.)2026-10-26

Phase 1b study of miricorilant in patients with presumed metabolic dysfunction-associated steatohepatitis (MASH).

Alkhouri Naim N, Rudraraju Madhavi M, Leibowitz Mark M, Jenders Robert A RA et al.

Miricorilant, an oral nonsteroidal selective glucocorticoid receptor modulator, is being investigated as a therapy that modulates hepatic cortisol activity in patients with metabolic dysfunction-associated steatohepatitis (MASH). This phase 1b study evaluated miricorilant's efficacy and safety. Seventy patients with presumed MASH received oral miricorilant daily (30-150 mg) or intermittent (100-200 mg once, twice, or thrice weekly) dosing regimens for 12 or 24 weeks. Across dosing regimens, reductions in relative liver fat content (LFC) ranged from 10.1% to 76.6%. Improvements in MASH liver function markers and the enhanced liver fibrosis (ELF) score were observed across regimens. Treatment-emergent adverse events (TEAE) leading to drug interruption/discontinuation occurred in 12.9% of patients (n=9) each; most were due to aminotransferase elevations during an excessively rapid drop in LFC (up to 70.2% at week 6) and in patients receiving daily dosing. Intermittent dosing enabled more patients to complete 12 weeks of treatment without discontinuation due to TEAEs. Intermittent dosing with miricorilant 100 mg twice weekly had the best benefit-risk profile; this cohort demonstrated a mean LFC reduction of 28.2% at week 12, with a corresponding decline in liver enzymes (ALT, -3.8 U/L; AST, -6.0 U/L). Patients in this cohort also had numerical improvement in lipid profiles, glycemic markers, and fibrosis biomarkers. Intermittent miricorilant dosing of 100 mg twice weekly achieved meaningful reductions in LFC and improved liver health markers with a favorable safety profile. This regimen is being evaluated in the phase 2b MONARCH study (NCT06108219).

PMID 42929711
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PubMedCells2026-10-26

Antagonistic TGR5 and FXR Signaling Shapes STAT1-Dependent Interferon Responses in Intestinal Epithelial Cells.

Jia Huilin H, Wu Nannan N, Yan Yufeng Y, Kong Fanzhi F

Bile acids function not only as digestive metabolites but also as signaling molecules that influence mucosal immunity. However, how the bile acid receptors Takeda G-protein-coupled receptor 5 (TGR5; also known as GPBAR1) and farnesoid X receptor (FXR) coordinate intestinal epithelial interferon (IFN) responses remains incompletely understood. Here, we investigated the impact of TGR5 and FXR on IFN signaling in porcine IPEC-J2 and murine MODE-K intestinal epithelial cells. Pharmacological activation of TGR5 with INT-777 induced type I and type III IFNs together with multiple interferon-stimulated genes (ISGs), among which IFNλ3 and ISG15 showed the most prominent responses. Mechanistically, TGR5 enhanced STAT1 phosphorylation and nuclear accumulation, and both STAT1 silencing and pharmacological blockade of STAT1 phosphorylation attenuated TGR5-driven IFNλ3 and ISG15 expression. Inhibition of adenylate cyclase or protein kinase A further placed a cAMP-PKA-STAT1 axis downstream of TGR5. By contrast, activation of FXR with GW4064 suppressed poly(I:C)-induced IFNλ3 and ISG15 transcription and antagonized TGR5-mediated STAT1 activation and downstream gene expression. Confocal imaging further suggested that FXR restrains STAT1 nuclear trafficking through cytoplasmic colocalization with STAT1. Collectively, our findings identify a bile acid receptor rheostat in which TGR5 amplifies, whereas FXR dampens, epithelial IFN signaling through STAT1. This work provides a mechanistic framework for understanding how bile acid sensing may tune antiviral readiness at the intestinal mucosa.

PMID 42929875
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PubMedEcology2026-10-26

Community history modifies how plant diversity shapes beta multifunctionality.

He Yan Y, Yang Rui R, Mao Lingfeng L

Research on ecosystem multifunctionality (EMF) has mainly quantified the magnitude of multiple functions within local communities (alpha multifunctionality [alpha-EMF]), whereas less is known about variation in function profiles among communities (beta multifunctionality [beta-EMF]). We asked how plant diversity affects variation in ecosystem function profiles among communities and whether this relationship depends on community history. We analyzed 5-year means of six ecosystem functions from 240 subplots in the DELTa-BEF, short for DEterminants of Long-Term Biodiversity Effects on Ecosystem Functioning Experiment, comparing new communities without experimental plant or soil history, resown communities retaining soil history, and old communities with continuous plant and soil histories. We adapted a variance-based beta diversity framework to quantify beta-EMF and partition it into local contributions to beta multifunctionality (LCBM) and function contributions to beta multifunctionality (FCBM). Plant diversity increased alpha-EMF in all treatments, with stronger increases in resown and old than in new communities. Richness was not detectably related to LCBM in new communities but was associated with lower LCBM in resown communities and higher LCBM in old communities, with the clearest contrast between the resown and old treatments. Leaf area index contributed more to beta-EMF than expected under equal contributions (20.2%), whereas basal respiration contributed less (13.2%); the other four functions did not differ from the equal-contribution expectation. Thus, similar gains in local multifunctionality can be accompanied by contrasting patterns of spatial functional heterogeneity, depending on community history. Partitioning beta-EMF into local and function contributions provides a practical way to identify which communities and functions contribute to spatial heterogeneity.

PMID 42928695
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-26

Large Oncosomes Induce Pro-Metastatic Stromal-Myeloid Reprogramming.

Silva Taylon Felipe TF, Concato-Lopes Virginia Marcia VM, Bedier Fatima F, Newman Lauren L et al.

Bone metastasis can be facilitated by systemic remodeling, yet the tumor-derived signals that influence the bone marrow microenvironment remain incompletely understood. Large oncosomes (LOs) are atypically large (> 1 µm), tumor-derived extracellular vesicles shed by amoeboid cancer cells. Here, we demonstrate that LOs function as systemic mediators of metastatic niche formation by activating innate immune sensing in bone marrow mesenchymal stem cells (BM-MSCs). Systemic administration of LOs to immunocompetent tumor-bearing mice did not affect primary tumor growth but increased metastatic burden. LOs induced a robust, dose-dependent interferon-driven inflammatory program, characterized by interferon-stimulated genes and neutrophil chemokines. Mechanistically, this response was driven by LO-associated nucleic acids activating convergent cytosolic DNA- and RNA-sensing pathways in recipient stromal cells. LO-conditioned BM-MSCs promoted the accumulation and polarization of neutrophils toward an immunosuppressive, polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC)-like phenotype. In vivo, genetic suppression of LO shedding in tumor cells reduced PMN-MDSC accumulation in the bone marrow, which was reversed by systemic LO administration. Together, these findings support a model in which LO-associated signals reprogram the bone marrow microenvironment to support metastatic colonization, identifying a previously unrecognized mechanism linking tumor vesiculation to immune remodeling at distant sites.

PMID 42928450
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PubMedJournal of psychiatry & neuroscience : JPN2026-10-26

Dissociable anterior and posterior beta-burst dynamics track thought disorder in schizophrenia.

Wei Hsi T H, Power Lindsey L, Dou Rukun R, Baillet Sylvain S et al.

Thought disorder in schizophrenia likely reflects disrupted maintenance of internal models during predictive processing. Beta oscillations have been proposed to index top-down predictive signalling, but prior resting-state studies have focused on spectral power, overlooking transient burst dynamics that potentially stabilize and reinstate internal representations, especially in the default mode network (DMN). Resting-state magnetoencephalography was acquired from 25 patients (7 females) with schizophrenia and 25 matched controls (8 females) between May 2024 and October 2025. Beta bursts (15-30 Hz) were extracted from source-localized cortical time series, and burst rate, duration, power, and inter-regional synchrony were quantified. Associations with computationally derived semantic and syntactic speech features reflecting thought disorder were assessed using principal-component regression in the patient group. Conventional beta power did not differ between groups after correction. In contrast, beta-burst dynamics showed significant group-by-anterior-posterior-position interactions for burst rate (p = 0.018), power (p = 0.0014), and duration (p < 0.001). Within the DMN, patients showed shorter inferior parietal burst duration (t(46.0) = -2.74, FDR-adjusted p = 0.0343) and increased burst synchrony within left prefrontal cortex (t(31.0) = 2.81, FDR-adjusted p = 0.0343) and between prefrontal cortices (t(29.8) = 2.73, FDR-adjusted p = 0.0423). Within the patient group, burst components were associated with speech organization (R2 = 0.47, F(3,19) = 5.66, p = 0.006), driven by the inferior parietal burst-duration component (β = -0.55, p = 0.0036), but did not relate to overall clinical severity. The modest patient sample, short resting-state recording, cross-sectional design, and lack of laminar specificity limit causal and mechanistic inference; burst-speech associations require replication. Schizophrenia is associated with dissociable anterior and posterior beta-burst abnormalities that track objective speech markers of thought disorder. These findings suggest impaired hierarchical coordination of predictive beta signalling as a candidate neurophysiological account linking intrinsic network dysfunction to disorganized thought.

PMID 42929455
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