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Human recombinant interferon beta-1a (Megavex)

✓ Approved

AMEGA Biotech · IFNB1 · Recombinant Proteins

What is Human recombinant interferon beta-1a?

Human recombinant interferon beta-1a is a recombinant proteins developed by AMEGA Biotech. It is approved for therapeutic indications via intramuscular (im) injection.

Drug Profile

Brand NamesMegavex
CompanyAMEGA Biotech
Drug ClassRecombinant Proteins
Molecular TargetIFNB1
RouteIntramuscular (IM) Injection
StatusApproved
Sources: ClinicalTrials.gov, AMEGA Biotech

Mechanism of Action

Molecular Targets

Human recombinant interferon beta-1a acts on 1 molecular target:

IFNB1interferon beta 1 (IFN-beta, IFNB)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

Human recombinant interferon beta-1a is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Nervous system disordersMultiple sclerosis✓ Approved

Related Research Articles

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Efficacy of recombinant growth hormone therapy in children born small for gestational age (SGA): a retrospective analysis.

Pałysa Aleksandra A, Kopiec-Burdecka Monika M, Pyrżak Beata B

Children born small for gestational age (SGA) present with a birth weight or length below -2 standard deviations (SD) relative to population norms for gestational age and sex. In Poland, such patients are eligible for recombinant human growth hormone (rhGH) therapy reimbursed by the National Health Fund. To retrospectively assess the effectiveness of rhGH therapy in children diagnosed with SGA based on clinical data from 39 patients treated with rhGH between 2016 and 2025. Anthropometric data were analysed at therapy initiation and completion. Treatment duration and changes in height and weight SD score (SDS) were evaluated. The influence of age at treatment initiation and sex on therapy outcomes was also assessed. The mean treatment duration was 3 years and 9 months. The average annual height gain was 6.9 cm/year and weight gain 5.3 kg/year. Boys showed a significantly higher annual height gain than girls (p = 0.013), while weight gain differences were not significant (p = 0.08). An improvement in both height and weight SDS was observed across all age groups, with the most pronounced benefits among children who began therapy before the age of 10 years. The most frequent reason for treatment discontinuation was reduced growth velocity. rhGH therapy in children born SGA is effective and safe, resulting in an improvement in growth parameters. The best outcomes are achieved when treatment is initiated in early childhood. The therapy is safe when accompanied by appropriate metabolic monitoring.

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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-22

Astrocytic Ketogenesis Protects Central Nervous System Injury via CPT1A Stabilization and Epigenetic Regulation.

Pan Dishui D, Shu Haoming H, Gao Rui R, Ren Yilong Y et al.

Following central nervous system (CNS) injury, reactive astrocytes proliferate and encapsulate the lesion to facilitate repair. However, the specific metabolic characteristics remain unknown. Here, through integrated single-cell and spatial transcriptomics, we uncovered a subset of astrocytes that undergo enhanced lipid and ketone metabolic reprogramming following spinal cord injury (SCI). The ketone body β-hydroxybutyrate (β-OHB) inhibited autophagic degradation of carnitine-palmitoyltransferase-1A (CPT1A) via P300-mediated lysine β-hydroxybutyrylation (Kbhb). Astrocyte-specific deletion of Cpt1a led to impaired wound healing, reduced axonal sparing and worsened locomotor recovery after SCI, effects rescued by exogenous β-OHB. Mechanistically, ketogenesis promotes wound repair and lipid metabolic reprogramming, forming a positive feedback loop via H3K9bhb-dependent epigenetic remodeling in astrocytes after SCI. Furthermore, ketogenic diet (KD) promoted tissue repair across multiple CNS injury models. Clinically, elevated β-OHB levels were associated with better tissue preservation and functional recovery in SCI patients. Collectively, our findings underscore the critical role of astrocytic lipid metabolic and epigenetic reprogramming after CNS injury and identify KD as a promising therapeutic strategy.

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PubMedBrain and behavior2026-10-22

Multi-Metric EEG Connectivity and Graph Analysis Reveal Altered Resting-State Networks in Major Depressive Disorder.

Rose Sushmit Jahan SJ, Imon A H M Rahmatullah AHMR, Bushra Rushdania R, Ahmed Nafis N et al.

EEG functional-connectivity studies in major depressive disorder (MDD) have produced inconsistent findings, partly because different estimators capture distinct aspects of neural coupling. We implemented a multi-metric resting-state EEG approach combining linear, phase-based, nonlinear, and graph-theoretical measures to characterize frequency-dependent sensor-level connectivity alterations and identify sensor-level network patterns relevant to depression-related dysconnectivity. Resting-state EEG from 30 DSM-IV MDD participants and 28 healthy controls was analyzed using a 19-channel 10-20 montage. After MNE-Python preprocessing, including filtering, ICA-based artifact removal, current source density (CSD) transformation, and symmetric orthogonalization, coherence, PLV, PLI, and MI were computed across theta, alpha, and beta bands. Edge-wise differences were tested using Brunner-Munzel with Holm correction, confirmed with Westfall-Young maxT correction, and summarized using Hedges' g and graph measures. MDD showed frequency- and metric-dependent sensor-level connectivity alterations. Theta coherence, PLV, and PLI were dominated by lower connectivity across frontal-to-posterior, fronto-central, temporal/posterior-temporal, parieto-occipital, and central-to-occipital sensor pairs, whereas theta MI showed few increased frontal/fronto-temporal effects. Alpha findings were more selective, with mainly lower coherence and PLV across frontopolar/frontal-to-central, fronto-midline, and posterior links, while alpha MI showed a limited mixed pattern. In beta, coherence, PLV, and PLI showed sparse robust reductions, whereas beta MI showed widespread increased statistical dependence. Graph-theoretical summaries at 20% proportional density showed mainly lower mean weighted strength and global efficiency in theta- and alpha-band networks. These findings indicate frequency- and metric-dependent resting-state EEG sensor-level connectivity alterations in MDD. The dominant pattern was lower theta/alpha connectivity across distributed sensor pairs, alongside increased beta MI-based dependence. The results provide corrected, effect-size-informed evidence of altered inter-sensor coordination without establishing dysfunction of specific cortical regions or named networks. This framework may support future hypothesis-driven research in independent, clinically annotated, higher-density EEG or multimodal datasets.

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PubMedFrontiers in artificial intelligence2026-10-22

scTIME: single-cell-informed interpretable modeling of immunotherapy-associated immune states in non-small cell lung cancer.

Chen Guozhi G, You Chenqiu C, Gao Hong H, Xu Chengjie C

Immune checkpoint inhibitor response in non-small cell lung cancer (NSCLC) reflects coordinated tumor and immune states that are not fully captured by single biomarkers. We developed scTIME, an interpretable model that translates single-cell immune programs into bulk transcriptomic scores, and integrated public single-cell, T-cell receptor, transcriptomic, survival, and proteogenomic cohorts. Response modeling used two cohorts with different endpoints (40 patients) and compared six algorithms. ElasticNet was selected as a sparse reporting model, achieving a pooled five-fold out-of-fold ROC-AUC of 0.810; nested model selection yielded 0.772. Matched held-out stratification identified response-enriched scTIME groups in a direct descriptive comparison with CD274, while the fitted score emphasized cytotoxic CD8, natural killer, SPP1 macrophage, interferon-response, and antigen-presentation programs. Single-cell analyses and external projections linked these programs to CXCL10-CXCR3 recruitment, exclusion-associated states, and T-cell receptor ecology across molecular contexts. Exploratory survival and cross-omics analyses extended the framework beyond the response cohorts but were interpreted as projection rather than independent validation. Together, the results show how cell-resolved immune biology can support transparent, multi-omic biomarker development without reducing response to a single pathway. scTIME remains exploratory because model choice was post hoc, cohorts were small and clinically heterogeneous, and endpoint-matched external validation was unavailable.

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PubMedPediatric endocrinology, diabetes, and metabolism2026-10-22

Refractory hypoparathyroidism in paediatric autoimmune polyglandular syndrome type 1: successful long-term use of teriparatide.

Perez Carolina C, Adarme Nicolas N, Hernandez Catalina C, Sarmiento Maria Paula MP

Autoimmune polyglandular syndrome type 1 (APS-1) is a rare monogenic disorder caused by pathogenic variants in the autoimmune regulator (AIRE) gene. It typically manifests in childhood with at least two features of the classic triad: chronic mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency. We present the case of an 11-year-old girl from a consanguineous family, with severe hypocalcaemia and chronic oral candidiasis. Despite high-dose calcium and calcitriol therapy, she experienced recurrent symptomatic hypocalcaemia requiring multiple hospitalisations. Genetic testing confirmed homozygosity for the pathogenic AIRE variant c.967_979del, establishing the diagnosis of APS-1. Due to poor biochemical control, teriparatide (parathyroid hormone, PTH [1-34]) was initiated at 20 g twice daily, leading to rapid improvement in calcium-phosphate homeostasis, a 75% reduction in oral calcium requirements, and no further hospitalisations over a two-year period. The therapy was well tolerated with no adverse events. This is the first paediatric case reported in Colombia using recombinant PTH (1-34) for APS-1-related hypoparathyroidism, supporting its therapeutic role in refractory cases.

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PubMedZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics2026-10-22

[Post-discharge fortified human milk feeding in preterm infants with moderate-to-high nutritional risk: a retrospective cohort study].

Wang Yun-He YH, Yao Yi Y, Chi Yun-Qian YQ, Zhang Zi-Han ZH et al.

To investigate the effects of post-discharge fortified human milk feeding on growth, common complications, and neuropsychological development in preterm infants with moderate-to-high nutritional risk. Clinical data were retrospectively collected from 320 preterm infants with moderate-to-high nutritional risk who were discharged from the Department of Neonatology, Provincial Hospital Affiliated to Shandong First Medical University between January 2021 and December 2023 and completed a 6-month follow-up. Infants were classified into four groups by nutritional risk level and feeding method: moderate-risk fortified human milk, moderate-risk formula, high-risk fortified human milk, and high-risk formula. Comparisons were conducted between fortified human milk and formula within the same risk level, and between moderate- and high-risk groups within the same feeding method. Within the same feeding method, gestational age at birth and birth weight differed significantly between moderate- and high-risk infants (P<0.001). Within the same nutritional risk level, no significant differences were found between fortified human milk and formula groups in gestational age at birth and birth weight (P>0.05). In the fortified human milk groups, corrected gestational age at discharge differed significantly between moderate- and high-risk infants (P<0.05). No significant differences were noted among the four groups in discharge weight, length, or head circumference (P>0.05). Analysis of covariance, adjusting for discharge weight, length, head circumference, and corrected gestational age at discharge, showed no significant differences among the four groups during the 6-month follow-up in growth velocities of weight, length, or head circumference, nor in hemoglobin, 25-hydroxyvitamin D, or alkaline phosphatase measured at 1, 3, and 5 months (P>0.05). Multivariable logistic regression indicated that fortified human milk feeding did not increase the risk of infection (OR=0.66, 95%CI: 0.40-1.08, P=0.097) or feeding intolerance (OR=0.70, 95%CI: 0.45-1.08, P=0.107). At 6 months' corrected age, mental, motor, and behavioral scores did not differ significantly among groups (P>0.05). In preterm infants at moderate-to-high nutritional risk, post-discharge fortified human milk feeding does not increase the risk of infection or feeding intolerance, does not differ significantly from formula feeding in short-term catch-up growth or neuropsychological development, and appears clinically feasible and safe.

PMID 42902717
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