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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

PubMedJournal of microbiological methods2026-08-30

Development of an A7G variant of recombinant human G-CSF for improved fibroblast-mediated wound healing.

Thota Sujani S, Myneni Praveen P, Venkateswarulu T C TC

Recombinant human granulocyte colony-stimulating factor (rh-G-CSF) is useful in tissue regeneration due to its angiogenic and anti-inflammatory actions. The current study focused on the downstream process of A7G mutant rh-G-CSF (m-rh-G-CSF) and the effects of m-rh-G-CSF on human fibroblasts. The m-rh-G-CSF was purified and had 97.24% purity, a final protein concentration of 0.814 g/L and a molecular weight of 18,784 Da. The addition of m-rh-G-CSF significantly elevated the ATP level in the treated cells in a concentration-dependent manner. The maximal ATP level was achieved at a concentration of 2.5 μg/mL and was 89% higher than in the control cells and 13% higher than in reference rh-G-CSF. In the scratch-wound assay, 92.67% and 98.69% wound closure were observed at 24 and 48 h after the addition of m-rh-G-CSF, respectively, compared with 49.93% in control cells at 48 h. These findings support the potential of m-rh-G-CSF as a therapeutic candidate for fibroblast-mediated wound healing.

PMID 42669396
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PubMedPediatric research2026-08-30

A recombinant fragment of human surfactant protein D reduces lung inflammation in preterm lambs.

Castillo-Hernandez Tania F TF, Finkielsztein Ariel A, Bhatt Reena R, Panichi Daniele D et al.

Bronchopulmonary dysplasia (BPD), the major chronic respiratory morbidity in extremely preterm infants, is largely driven by inflammation. Preterm lungs are deficient of surfactant protein D (SP-D), an immunomodulatory protein absent in current commercial surfactant preparations. We hypothesised that using a recombinant fragment of human SP-D (rfhSP-D) as an adjuvant to exogenous surfactant therapy would reduce ventilator-induced inflammation. We utilised a preterm lamb model of ventilator-associated lung injury. Mechanically ventilated preterm lambs were randomised into control and two treated groups, receiving endotracheal surfactant at 15 min post-delivery. Physiological parameters were measured throughout the experiment. Lung tissue was analysed for changes in alveolar architecture and expression levels of pro-inflammatory cytokines. Bronchioalveolar lavage (BAL) was analysed for SP-D concentration, and inflammatory cells. Intratracheal administration of rfhSP-D improved respiratory outcomes, significantly increased airspace and lung compliance in treated groups. Treated lambs also showed a reduction in lung tissue gene expression of inflammatory cytokines and inflammatory cell counts. Intratracheal administration of rfhSP-D did not negatively impact standard surfactant therapy and appeared to complement it. The administration of rfhSP-D as an adjuvant to standard surfactant therapy effectively reduced lung inflammation supporting the potential therapeutic use of rfhSP-D for preterm infants at risk of developing BPD. We have successfully developed and tested a novel recombinant fragment of human surfactant protein D (rfhSP-D) capable of reducing ventilator-associated lung inflammation in a pre-term lamb model. These results suggest rfhSP-D may be a novel potentially useful therapy for Bronchopulmonary dysplasia (BPD) in combination with currently available surfactant replacement therapies and serves as justification for a first in human clinical trial in mechanically ventilated infants. If successful, rfhSP-D could become a therapeutic candidate to mitigate pulmonary inflammation and improve lung outcomes, potentially offering a novel therapeutic avenue in the prevention or management of BPD.

PMID 42668280
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PubMed[Rinsho ketsueki] The Japanese journal of clinical hematology2026-08-30

[Predictors of treatment-free remission (TFR) and second TFR attempts in chronic myeloid leukemia].

Ureshino Hiroshi H

The introduction of tyrosine kinase inhibitors (TKIs) has made long-term survival achievable for patients with chronic myeloid leukemia (CML). In patients who achieve a deep molecular response, treatment-free remission (TFR), defined as sustained remission without molecular relapse after TKI discontinuation, has emerged as an important therapeutic goal. Accumulating evidence indicates that the establishment and maintenance of TFR are strongly influenced by host immunity, particularly immune surveillance mediated by natural killer (NK) cells. This review summarizes the clinical and immunological factors associated with successful TFR and discusses the potential of killer immunoglobulin-like receptor/human leukocyte antigen genetic polymorphisms as predictive biomarkers that regulate NK cell function and TFR outcomes. It also highlights immunomodulatory strategies using interferon-α, the feasibility of second attempts at TFR after initial discontinuation failure, and emerging therapeutic approaches targeting CML stem cells to achieve more durable disease control.

PMID 42669513
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PubMediScience2026-08-30

CLEC-1 promotes early IFN response in cDC1s and favors immune dysregulation during sepsis in mice.

Ogor Thomas Teja TT, Porée Esther E, Saenz Javier J, Davieau Marion M et al.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host immune response, characterized by both hyperinflammation and immunosuppression. Here, we show that the absence of the C-type lectin receptor CLEC-1-expressed particularly by lung cDC1s-improves mouse recovery following E. coli infection. Mechanistically, phenotypic and transcriptomic analyses revealed that Clec1a loss is characterized by an attenuated type I interferon response in lung cDC1s as well as reduced CXCL10 expression and monocyte infiltration during the acute phase of sepsis. Additionally, Clec1a deficiency is associated with an enhanced antigen presentation profile of lung myeloid cells and lower accumulation of regulatory T cells upon secondary infection, suggesting reduced immunoparalysis. Importantly, we demonstrate that blocking CLEC-1 using an anti-human CLEC-1 monoclonal antibody mitigates hyperinflammation in CLEC-1 humanized mice. Together, these findings uncover a role for CLEC-1 in the dysregulation of the inflammatory response during sepsis and suggest its potential as an immunotherapeutic target.

PMID 42668608
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PubMedJournal of invertebrate pathology2026-08-30

Bombyx mori lipase-1 reduces viral replication and proliferation by inhibiting the expression of the DNA-binding protein (dbp) gene.

Chen Haiyu H, Ding Xiangrui X, Wang Jinyang J, Zhao Qiaoling Q et al.

Bombyx mori lipase-1 (Bmlipase-1) has strong anti-BmNPV activity, but the mechanism by which Bmlipase-1 resists BmNPV invasion has not been elucidated so far. In this paper, based on the construction of recombinant viruses overexpressing Bmlipase-1, we analyzed the effects of the recombinant viruses on the genes related to recombinant virus replication as well as viral replication and proliferation after the recombinant viruses infected BmN cells. In the presence of the virus, Bmlipase-1 localizes to the cell nucleus. Quantitative polymerase chain reaction (qPCR), northern blotting and western blot analyses showed that Bmlipase-1 inhibited the expression of BmNPV DNA-binding protein (dbp) as well as the replication and proliferation of the recombinant virus. DBP is a key factor for normal viral DNA replication and for the stabilization of nascent viral DNA. A biotin-labeled probe was synthesized around the c-Myb transcription factor binding site in the upstream promoter region of dbp and analyzed by EMSA with prokaryotically expressed and purified Bmlipase-1. It was found that Bmlipase-1 could bind to CACTTCAATT in the dbp promoter region, while the activity of the dbp promoter lacking CACTTCAATT was significantly reduced. In conclusion, Bmlipase-1 can bind to the CACTTCAATT motif on the dbp promoter in vitro, and this motif contributes positively to the activity of the dbp promoter. Overexpression of Bmlipase-1 significantly downregulates dbp expression and inhibits viral replication. Based on these findings, we propose the following hypothesis: Bmlipase-1 may inhibit viral replication by binding to the CACTTCAATT motif and interfering with the transcriptional regulation of dbp. However, this regulatory model requires further validation in the context of viral infection. This paper provides a new theoretical basis for the prevention and control of lepidopteran insect viruses, and also opens up a new way to study the antiviral mechanism of the silkworm, Bombyx mori.

PMID 42669400
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PubMedThe Journal of antimicrobial chemotherapy2026-08-30

Clinical outcomes of beta-lactam monotherapy versus beta-lactam plus azithromycin in hospitalized patients with community-acquired pneumoniae-right-to-reply.

Zhygalova Zhygalova Ilona I, Blanco López Iago I, Dopazo Sotillo Silvia S, Carreira Sampayo Uxía U et al.

PMID 42669627
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