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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)
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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

PubMedIndian journal of ophthalmology2026-10-16

Visual and refractive outcomes of Eyecryl phakic intraocular lens in myopia and myopic astigmatism.

Sachdev Gitansha Shreyas GS, Pandey Ujjwala U, Palan Parth P

To assess the refractive accuracy and safety profile of posterior chamber Eyecryl phakic intraocular lens (pIOL) implantation. Tertiary eye care hospital in South India. Retrospective study. Patients undergoing posterior chamber Eyecryl pIOL (Biotech Healthcare) implantation for the correction of myopia or myopic astigmatism were evaluated, provided a minimum follow-up duration of 24 months was achieved. Preoperative and postoperative assessments included uncorrected and corrected distance visual acuity, manifest refraction, intraocular pressure, and endothelial cell density measured with specular microscopy (Topcon SP-1A). Visual and refractive outcomes, safety indices, refractive stability, and postoperative complications were evaluated at 1, 6, 12, and 24 months postoperative visit. The analysis included 377 eyes of 197 patients with a mean age of 25.9 ± 4.9 years. At 24 months, mean UDVA was log MAR 0.042 ± 0.10, with 92% of eyes achieving 20/25 or better and 96% achieving 20/32 or better. The efficacy and safety indices were 1.03 ± 0.49 and 1.06 ± 0.48, respectively. Ninety four percent of the eyes were within ± 0.50 D of the intended spherical equivalent, and an MRSE of -0.03 ± 0.14 D was achieved. Refractive outcomes stabilized after 6 months and remained unchanged through 24 months. Cataract formation occurred in 0.8% of eyes, while rotational instability was observed in 0.013% and managed successfully with lens repositioning or exchange. The Eyecryl pIOL is a safe, effective, and predictable option for the correction of myopia and astigmatism, demonstrating refractive stability over a 2-year follow-up period.

PMID 42885960
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PubMedNutrients2026-10-16

Bempedoic Acid Treatment in Four Adult Patients with Glycogen Storage Disease Type 1a: A Retrospective, Exploratory Case Series.

Hempel Julya J, Meyer Uta U, Menke Christian C, Mindermann Charlotte C et al.

Background: Glycogen storage disease type 1a (GSD 1a) is an inborn error of metabolism due to glucose-6-phosphatase deficiency. Treatment consists of frequent, carbohydrate-rich meals, intake of glucose polymers like uncooked cornstarch, or drip feeding in small infants. Although dietary treatment is challenging, it has improved the long-term outcomes for patients with GSD 1a. Nevertheless, several complications, including dyslipidaemia, remain difficult to manage, and early atherosclerosis with risk for ischemic stroke is a potential long-term concern. We propose bempedoic acid (BA) as a potential treatment option for dyslipidaemia in adult patients with GSD 1a. BA is an approved lipid-lowering therapy and may have additional beneficial metabolic effects in patients with GSD 1a. We hypothesize that BA may reduce malonyl-CoA concentrations and thereby alleviate the inhibition of mitochondrial fatty acid oxidation. This could potentially contribute to improved metabolic stability in patients with GSD 1a. Methods: Four adult female patients with GSD 1a and dyslipidaemia received BA at a dose of 180 mg once daily for 2-5 years. In this retrospective case series, we explored potential additional effects of BA treatment beyond its established lipid-lowering effect. Results: Under BA treatment, patients reported prolonged fasting periods, and carbohydrate intake could be reduced in some patients. Plasma lactate concentrations decreased during treatment, while triglyceride concentrations decreased in two patients but increased in the others. Two patients experienced a slight, clinically irrelevant increase in serum uric acid concentrations, a known adverse effect of BA. No other adverse effects were observed. Conclusions: In this retrospective, uncontrolled, single-center case series, BA was associated not only with its expected lipid-lowering effect, but also with potential improvements in metabolic control and prolonged fasting tolerance in adults with GSD 1a. However, these preliminary observations require confirmation in larger, prospective, controlled studies. Future studies should include standardized metabolic assessments and direct measurements of key metabolites involved in the pathophysiology of GSD 1a. Preclinical studies using appropriate animal models may further contribute to elucidating the underlying mechanisms and potential metabolic effects of BA.

PMID 42884635
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PubMedNature metabolism2026-10-16

IRF7 signalling in tanycytes controls brain-body-immune response across the ovarian cycle.

Nampoothiri Sreekala S, Fernandois Daniela D, Journiac Nathalie N, Delahaye Fabien F et al.

Sex-specific differences in metabolic and immune function are shaped by endocrine-immune interactions, yet the complexity of this relationship remains poorly understood. Here, we identify an immune cell-like state of tanycytes, an ependymoglial cell type lining the third ventricle that mediates brain-body communication1,2 in both mice and humans. Using single-cell transcriptomics, we provide a high-resolution cellular map of the mouse and human mediobasal hypothalamus with cross-species comparison of tanycytes. We capture dynamic sex-, oestrous cycle- and high-fat diet-dependent transcriptomic changes in tanycytes, including a cyclic interferon response in tanycytes during the physiological oestrous cycle in female mice. We found that the oestrous cycle, with its changing hormonal milieu, especially oestradiol, affected the brain's immune responses, characterized by the temporal and cyclic expression of interferon regulatory factor 7 (Irf7) gene, as well as downstream interferon-stimulated genes such as Cxcl10 in tanycytes of female mice, which are associated with increased infiltration of leukocytes and cytokine responses. Irf7 expression in tanycytes of physiological males remained stable and markedly lower, suggesting a distinct immune activation pattern in the brains of cycling females. By targeting oestrogen and interferon signaling in tanycytes, we show that balanced, cyclic leukocyte infiltration into the median eminence may have a role in oestrous cycle maintenance, whereas Irf7 in tanycytes modulates circulating monocyte proportions, revealing brain-immune system communication through tanycytes. Our findings reveal an immune-associated role for tanycytes, with potential implications for understanding the endocrine and immunological mechanisms underlying sex-biased diseases.

PMID 42881274
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PubMedCell communication and signaling : CCS2026-10-16

A Toxoplasma gondii-derived ROP38 protein engages Ser15/Thr18-linked p53 activation and DNA damage-associated apoptotic signaling in human cancer cells.

Seo Seung-Hwan SH, Lee Ji-Eun JE, Cho Eun-Ji EJ, Shin Eun-Hee EH

The tumor suppressor p53 integrates diverse cellular stresses to regulate DNA damage responses, cell-cycle progression, and apoptosis-associated signaling. Toxoplasma gondii secretes rhoptry effectors that remodel host signaling networks, but the host targets and signaling functions of the rhoptry kinase ROP38 remain poorly defined. GFP-tagged T. gondii ME49 ROP38 full-length protein (ROP38 Full) and its kinase-domain fragment (ROP38 KiD) were stably expressed in HCT116 and HepG2 human cancer cells. Kinase-associated activity was assessed in anti-GFP immunoprecipitates, and a candidate co-immunoprecipitation screen was used to identify ROP38-associated host proteins. ROP38-p53 association and phospho-p53 species were further examined by co-immunoprecipitation. Purified recombinant ROP38 and human p53 were used for direct interaction and in vitro phosphorylation assays. Whole-cell p53 signaling, DNA damage/apoptosis-associated markers, and cell-cycle distribution were also analyzed. Statistical analyses used one- or two-way ANOVA, as appropriate, followed by Tukey's multiple comparisons test. ROP38 Full- and ROP38 KiD-containing immunoprecipitates showed increased kinase-associated activity. Among the candidate proteins examined, p53 was the only ROP38-associated host factor detected in both cell lines. ROP38 Full and ROP38 KiD co-immunoprecipitated with total p53 and preferentially enriched p53 phosphorylated at Ser15 and Thr18. Purified recombinant ROP38 directly associated with recombinant p53 and promoted Ser15/Thr18 phosphorylation in the presence of ATP. At the whole-cell level, ROP38 expression increased p53 abundance and multisite phosphorylation, with prominent Ser15/Thr18 induction, and was accompanied by increased γH2AX, PUMA, cleaved caspase-3, and p21 expression. ROP38-expressing cells also showed decreased G1-phase populations with increased S- and G2/M-phase populations. These data identify a candidate ROP38-associated p53 signaling module in human cancer cells and provide biochemical evidence that ROP38 can directly associate with p53 and promote Ser15/Thr18 phosphorylation in vitro. The requirement for intrinsic ROP38 catalytic activity and the physiological relevance of this relationship during T. gondii infection remain to be established.

PMID 42881414
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PubMedCommunications psychology2026-10-16

Task-specific theta enhancement and domain-general alpha/beta suppression as oscillatory signatures of cognitive flexibility.

Hülsemann Mareike M, Löffler Christoph C, Schubert Anna-Lena AL

Cognitive flexibility-the ability to adapt to changing situational or task demands-is a fundamental aspect of human cognition and a potential source of individual differences in higher-order cognitive abilities. To further understand the neural mechanisms underlying this ability, we examined event-related spectral perturbations (ERSP) in three cued switching tasks (parity/magnitude, global/local, number/letter) in a sample of 148 adults. Employing a data-driven approach that combined mass-univariate time-frequency analysis, cluster-based permutation testing, and latent change structural equation modeling, we identified two robust neural signatures: a transient frontal theta increase and a sustained alpha/beta suppression. Both effects were more pronounced in switch compared to repeat trials. Frontal theta reflected task-specific control processes, whereas parietal alpha/beta indexed domain-general attentional processes that persisted from cue onset through target processing-consistent with two-stage models of task switching. Notably, flexibility-related alpha/beta dynamics did not correlate with measures of intelligence or working memory capacity. However, stronger cue-elicited alpha/beta suppression correlated with reduced non-decision-time switch costs, indicating more effective task preparation, underscoring that alpha/beta suppression captures a neurally coherent but behaviorally distinct dimension of cognitive flexibility. These findings provide evidence that alpha/beta suppression constitutes a reliable, cross-task generalizable neural signature of attentional reconfiguration during task switching, while highlighting the multi-component nature of individual differences in cognitive flexibility.

PMID 42881249
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PubMedCells2026-10-16

TRPs-NCX2 Axis Jointly Preserves Pancreatic Beta Cell Susceptibility/Sensitivity to Elevated Glucose.

Sagintayev Adlet A, Oflaz Furkan E FE, Kanlinuro Andra A, van Amsterdam Savina S et al.

Background: For appropriate glucose sensing, pancreatic beta-cells essentially establish a constant mitochondria-directed endoplasmic reticulum (ER) Ca2+ leak via phosphorylated presenilin-1 (PS1). In the current work, we investigated how cells maintain the ER Ca2+ content during this continuous Ca2+ leak. Methods: Ca2+ imaging for ER, cytosolic and subplasmalemmal Ca2+, high resolution respirometry, and ELISA for insulin secretion were used. Results: A novel ER Ca2+ refilling mechanism driven by reverse-mode NCX2, which is fueled by local Na+ influxes through TRPC3 and TRPV4 channels that are independent of STIM-ORAI1 was found in pancreatic rodent and human beta cell lines. Disrupting this TRPs-NCX2 axis reduces subplasmalemmal Ca2+ levels, abolishes glucose-induced cytosolic Ca2+ oscillations, suppresses glucose-triggered elevation in mitochondrial energetics, and impairs first-phase insulin secretion. Conclusions: We identified a novel, ORAI1-independent "TRPs-NCX2" relay that couples Na+ influx via TRPC3 and TRPV4 to NCX2 reverse mode to maintain ER Ca2+ stores during physiological basal ER Ca2+ leakage, which is fundamental to beta-cell responsiveness to elevated glucose.

PMID 42882464
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