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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

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

PubMedBritish journal of cancer2026-09-19

Genomic and transcriptomic landscape of spread through air spaces in stage 1 lung adenocarcinoma.

Saw Stephanie P L SPL, Pang Mengyuan M, Patteri Clare C, Takano Angela A et al.

Spread through air spaces (STAS) is an adverse histologic feature in early-stage lung adenocarcinoma (LUAD) incorporated into the ninth edition TNM staging. Despite its clinical significance, the molecular features underlying STAS in stage 1 LUAD remain incompletely characterised. Patients with stage 1 LUAD and known STAS status were identified. Whole exome and RNA sequencing were performed on tumour samples with matched normal controls. Disease-free survival (DFS) was analysed using the Kaplan-Meier method and Cox regression. Among 378 patients, 54.2% had STAS+ tumours, with similar incidence between EGFR-mutant and EGFR-wildtype LUAD. STAS+ tumours were significantly associated with stage 1B disease, lymphovascular invasion, higher histological grade, micropapillary or solid predominant adenocarcinoma subtype and PD-L1 tumour proportion score ≥1%. STAS+ remained independently associated with inferior DFS after multivariable adjustment (hazard ratio 2.32, 95% CI 1.16-4.63; p = 0.017). At the molecular level, STAS+ tumours were enriched for TP53 co-mutations, whole genome doubling, non-TRU transcriptomic subtypes and upregulation of cell cycle-related pathways, with directionally consistent findings across EGFR-mutant and EGFR-wildtype tumours. STAS+ in stage 1 LUAD is associated with a distinct molecular phenotype characterised by genomic instability and cell cycle dysregulation, consistent with a more aggressive biological phenotype with implications for risk stratification and adjuvant therapy selection.

PubMedMedicine2026-09-19

The NF-κB pathway in inflammatory responses in preeclampsia: A systematic review and meta-analysis.

Zhang Hui H, Nong Yanhua Y, Huang Meiqi M, Wei Riyuan R et al.

Preeclampsia is a pregnancy-specific hypertensive disorder associated with systemic inflammation, endothelial dysfunction, and adverse maternal and fetal outcomes. The nuclear factor kappa B (NF-κB) signaling pathway has been implicated in inflammatory activation, but its role in preeclampsia remains incompletely defined. This systematic review and meta-analysis aimed to evaluate the association between NF-κB pathway activation and inflammatory responses in preeclampsia. This meta-analysis reviewed 15 peer-reviewed articles focusing on the involvement of the NF-κB pathway in preeclampsia. Quantitative assessments included changes in systolic and diastolic blood pressure and levels of key inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta, interleukin-6 (IL-6), and NF-κB. Systolic and diastolic blood pressure were significantly elevated in patients with preeclampsia. TNF-α and NF-κB levels were also significantly increased, indicating enhanced inflammatory activation associated with the disease. In contrast, interleukin-1 beta and IL-6 levels did not differ significantly, although IL-6 showed a nonsignificant trend toward increased levels. This meta-analysis suggests that NF-κB activation, together with increased TNF-α levels, may contribute to the inflammatory pathophysiology of preeclampsia. These findings support further investigation of NF-κB-related pathways, including Sirtuin 1-mediated regulation, as potential biomarkers and therapeutic targets.

PubMedCancer medicine2026-09-19

Association Between BMI and Tumour Regression After Neoadjuvant Therapy in Oesophageal Cancers: Insights From a German Nationwide Registry.

Otto Susanne D SD, Pozios Ioannis I, Rayya Wael W, Schineis Christian H W CHW et al.

For locally advanced oesophageal carcinoma, multimodal therapy is the standard of care, but prognosis remains poor. Obesity has risen markedly in the last decades. The impact of obesity on response to neoadjuvant treatment remains unclear. This study evaluates the association between body mass index (BMI) and histopathological tumour regression following neoadjuvant therapy in oesophageal cancer. We performed an analysis using the prospective database from the DGAV|registry oesophageal surgery provided by the German Society for General and Visceral Surgery (Deutsche Gesellschaft für Allgemein- und Viszeralchirurgie, DGAV). The primary outcome was histopathological tumour regression grade by the Becker classification. The primary explanatory variable was BMI. Descriptive statistics were followed by uni- and multivariate regression analyses adjusted for tumour histology, neoadjuvant regimen, age, sex, ECOG status, comorbidities, dysphagia and weight loss. Associations were evaluated using a multivariate regression (partial proportional odds) model. Six hundred and forty-seven patients were included, comprising 432 adenocarcinomas (including AEG I/II) and 215 squamous cell carcinomas (SCC). After adjustment for clinical and tumour-related covariates, higher BMI was independently associated with a favourable histopathological response: No association was observed for the transition to Becker grade ≥ 1b; however, higher BMI was associated with reduced odds of Becker grade ≥ 2 (OR 0.97, 95% CI 0.94-1.00, p = 0.04) and Becker grade ≥ 3 (OR 0.93, 95% CI 0.90-0.96, p < 0.001). In addition, SCC, absence of dysphagia, radiochemotherapy and low ECOG score were independently associated with favourable regression, whereas no independent associations were observed for age, sex, diabetes status, comorbidities or pretherapeutic weight loss. Analysis of the German DGAV|registry revealed that higher BMI was significantly associated with improved histopathological tumour regression following multimodal therapy for oesophageal cancer. These findings suggest potential differences in tumour biology among patients with elevated BMI, underscoring the need for further mechanistic investigation.

PubMedCognitive, affective & behavioral neuroscience2026-09-19

Who is to blame? Outcome controllability and error attribution differentially shape cognitive preparation and feedback evaluation.

Grote Luisa A LA, Schneider Daniel D, Wascher Edmund E, Arnau Stefan S

Sense of agency (SoA), the experience of controlling one's actions and their consequences, is crucial for self-representation and adaptive goal-directed behavior. Much of today's cognitive work is performed through interaction with systems that are not entirely reliable or are prone to operator error. Against this background, it is of particular interest to understand how perceived outcome-controllability and attribution of action-outcome disruptions feed back into cognitive processing as states of perceived agency. In this EEG study, we manipulated performance feedback in a color-discrimination task to dissociate self-attributed from system-attributed errors. Thirty-five participants completed blocks with veridical feedback, feedback suggesting increased error rates due to impaired personal performance, and feedback indicating malfunctioning response buttons. Behavioral performance was decomposed using the EZ-diffusion model, and time-frequency analyses focused on preparatory alpha and beta oscillations and feedback-locked theta activity. Both manipulated feedback conditions led to slower responses compared to veridical feedback. Diffusion modeling revealed that general performance slowing was driven by reduced drift rates, whereas differences between self- and system-attributed errors were reflected in nondecision time. In the EEG, manipulated feedback attenuated cue-related decreases in occipital alpha and sensorimotor beta power during the cue-target interval. In addition, system- versus self-attributed errors elicited stronger feedback-related midfrontal theta responses. Our findings suggest a functional dissociation within the agency inference process, where perceived controllability regulates preparatory investment of cognitive resources on a global level, while the attribution of action-outcome discrepancies seem to modulate evaluative processing.

PubMedJournal of molecular medicine (Berlin, Germany)2026-09-19

MicroRNA-122 as a regulator and biomarker of liver disease.

Ahmadova Sara S, Wicik Zofia Z, Mucha Joanna J, Palatini Jeff J et al.

MicroRNA-122 (miR-122) is the most abundant liver-specific microRNA, comprising ~ 70% of the hepatic miRNA pool, and a central regulator of lipid metabolism, inflammation, fibrosis, viral replication, and hepatocarcinogenesis. This review synthesizes experimental, clinical, and molecular evidence on the role of miR-122 across the spectrum of liver disease, including metabolic dysfunction-associated fatty liver disease (MAFLD) and steatohepatitis (MASH), drug-induced acute liver injury, hepatitis B and C virus (HBV/HCV) infection, hepatocellular carcinoma (HCC), and colorectal cancer liver metastasis. Mechanistically, miR-122 governs hepatic lipogenesis through the Sirt1/LKB1/AMPK axis, modulates inflammation via LPS/TLR-4/FoxO3 signaling, and exerts tumor-suppressive and antiviral effects through Cyclin G1/p53, HO-1, NDRG3, GALNT10, PEG10, and NEGR1. A recurring theme is the compartment- and stage-dependent behavior of miR-122: hepatic expression declines with disease progression, whereas circulating levels rise with hepatocyte injury, reconciling apparently contradictory reports and underscoring the importance of specimen source and disease stage in biomarker interpretation. We further contrast the etiology-specific regulation of miR-122 in HBV- versus HCV-associated disease, in which epigenetic silencing and interferon-linked mechanisms drive divergent expression. Finally, we critically appraise the failed clinical translation of anti-miR-122 therapeutics (miravirsen, RG-101), highlighting viral resistance, safety liabilities, and the tumor-suppressor paradox that constrains inhibition-based strategies. Collectively, miR-122 emerges as a minimally invasive biomarker and a biologically informative, though therapeutically challenging, target in liver disease.

PubMedWorld journal of surgical oncology2026-09-19

Stress-driven reprogramming of plasmacytoid dendritic cells in intrahepatic cholangiocarcinoma defines a reversible targetable immunosuppressive state.

Chen Mei-Ru MR, Xie Xiao-Li XL, Zhou Yan-Li YL, Tian Jin-Mei JM et al.

Plasmacytoid dendritic cells (pDCs) have been implicated in both restraining and promoting intrahepatic cholangiocarcinoma (iCCA), leaving their clinical relevance and therapeutic potential unresolved. Mendelian randomization was used to assess the causal association between circulating pDC levels and iCCA risk. Bulk and single-cell transcriptomic analyses were performed to characterize pDC-related programs and tumor-conditioned states, and multiplex immunofluorescence was used to define spatial distribution and clinical associations in iCCA tissues. To assess reversibility of stress-associated pDC features, IRE1α RNase activity was pharmacologically inhibited with 4µ8C under tumor-conditioned stress in vitro. Genetically predicted higher circulating pDC levels were associated with lower iCCA risk, consistent with a systemic protective association. In bulk cohorts, higher expression of pDC markers (CLEC4C, NRP1, IL3RA) was associated with an immune-inflamed microenvironment and improved survival in early-stage disease. Single-cell analyses indicated that intratumoral pDCs acquired stress-associated transcriptional programs, including enrichment of endoplasmic reticulum stress and unfolded protein response pathways. In vitro, 4µ8C reduced IRE1α-dependent XBP1 splicing and partially restored type I interferon-linked activation and pDC immunogenic readouts under tumor-conditioned stress. Spatial profiling further showed that higher intratumoral CD303⁺IRF7⁺ pDC activation was associated with advanced stage and poorer overall survival, whereas higher activation in adjacent non-tumor tissues correlated with more favorable outcomes. Together, these findings support a context-dependent, stress-associated pDC program in iCCA and provide a rationale for further evaluating the IRE1α-XBP1 stress axis as a potential approach to modulate pDC-associated immune states within the tumor microenvironment.

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