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Factor VIIIa (LongAte)

✓ Approved

PolyTherics Limited · F8 · Recombinant Proteins

What is Factor VIIIa?

Factor VIIIa is a recombinant proteins developed by PolyTherics Limited. It is approved for therapeutic indications via injectable (others) or intravenous (iv) or subcutaneous injection.

Drug Profile

Brand NamesLongAte
CompanyPolyTherics Limited
Drug ClassRecombinant Proteins, Cell-based Therapies
Molecular TargetF8
RouteInjectable (Others), Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, PolyTherics Limited

Mechanism of Action

Molecular Targets

Factor VIIIa acts on 1 molecular target:

F8coagulation factor VIII (AHF, FVIII)
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Therapeutic Indications

Factor VIIIa is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersFactor VIII deficiency✓ Approved

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Cui Bono? Characterisation of the benefit concept and the justificatory narratives in animal research ethics literature.

Volonteri Micol M, Grimm Herwig H

Harm-benefit analysis (HBA) is one pillar of Directive 2010/63/EU, which regulates the use of animals in biomedical research. Despite HBA's central role in legislation governing in vivo studies, its regulatory adequacy is often questioned. In particular, it is widely acknowledged that the proper implementation of HBA is hampered by the vagueness of current policies, especially those related to assessing benefit. This review examined how benefit is interpreted in HBA, reconstructing the most prominent views emerging from the current debate and their implications for scientific practice. It reviews recent literature on this topic to identify the main issues arising from the ambiguity of the benefit concept and then reflects on their impact on the regulatory process for animal research. The artificial intelligence tool ChatPDF was used to facilitate the analysis of the sources. The findings suggest three central considerations: (1) scarce value is attributed to the epistemic benefits of preclinical trials, (2) the ethical evaluation of in vivo project proposals should better account for experimental quality and validity, and (3) it is essential to bridge the growing gap between the scientific community and society by promoting public understanding and engagement with biomedicine to rebuild trust in research.

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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-11-11

A Novel Immunosuppressive Effector Functions as a Bio-Adjuvant to Enhance the Activity of Bacillus Thuringiensis and Chemical Insecticides.

Liu Zhiyu Z, Chen Feng F, Wan Liting L, Chen Li L et al.

Host innate immunity is a major barrier to microbial infection and often limits the efficacy of biological and chemical pest-control agents. While microbial immunosuppressive effectors have been described, whether quorum-sensing systems coordinate virulence and immune suppression during host infection remains largely unknown. We demonstrated that the PlcR-PapR quorum-sensing system acts as a master regulator that promotes both processes (virulence and immune suppression) to enhance Bacillus thuringiensis (Bt) pathogenicity. During infection, PlcR-PapR signaling induces production of the heptapeptide PapR7, which activates expression of patatin-like protein PisP, a previously uncharacterized and widely conserved protein. PisP suppresses host immunity by inhibiting nuclear translocation of the transcription factor DAF-16, thereby attenuating the expression of antimicrobial defense genes. Consistent with this mechanism, Bt strains overexpressing pisP display enhanced virulence against both nematodes and insect hosts. Importantly, exogenous PisP markedly potentiates the activity of Bt Cry5Ba toxin and several commercial chemical insecticides, enabling effective pest control at reduced doses. Together, these findings reveal a quorum-sensing-controlled mechanism that links virulence regulation to immune suppression during Bt infection and identify PisP as a conserved Bt-encoded immunosuppressive effector with strong potential as a bio-adjuvant for improving the efficacy and sustainability of biological and chemical pest-management strategies.

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PubMedBMC neurology2026-11-11

Targeted biologics in muscle strength restoration and corticosteroid sparing for patients post-myasthenic crisis.

Wang Yuan Y, Jin Lei L, Huan Xiao X, Chen Ran R et al.

Myasthenic crisis (MC) represents a life-threatening condition in patients with myasthenia gravis (MG). Despite a substantial reduction in in-hospital mortality for MC, full restoration of muscle strength and quality of life usually requires months or years. It remains unknown whether the sequential use of targeted biologics improves clinical outcomes in patients post-MC compared with the standard of care (SOC). We prospectively followed patients from MC through 6 months post-discharge between November 2018 and November 2025. We then stratified patients into subgroups according to the use of either biologics-based therapy (C5 inhibitors, FcRn antagonists, or rituximab) (BIO) or SOC. The primary endpoint was the Myasthenia Gravis Foundation of America-quantitative MG (MGFA-QMG) score at 6 months after discharge. Secondary outcomes included Myasthenia Gravis Activities of Daily Living (MG-ADL), steroid dose, immunosuppressant (IS) use, cumulative steroid exposure, minimal symptom expression (MSE), and residual symptom burden. At 6 months after discharge, the BIO group (n = 56) had a lower MGFA-QMG score than the SOC group (n = 56) (4.51 ± 4.03 vs 6.28 ± 4.72; P = 0.038). Meanwhile, the BIO group required a lower dose of oral corticosteroid (14.74 ± 10.24 vs 21.96 ± 12.87 mg/day; P = 0.004), lower cumulative steroid burden (158.13 ± 64.71 vs 209.24 ± 96.81 mg/day·month; P = 0.001), and had a lower proportion of IS use (47.3% vs 67.9%; P = 0.028). MSE was achieved in 56.86% in the BIO and 60.38% in the SOC group, respectively. Targeted biologics were associated with better objective muscle strength and reduced corticosteroid and IS use after MC, although no significant between-group difference was observed in MG-ADL. A substantial proportion of patients in both groups continued to have residual symptoms at 6 months.

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PubMedNature communications2026-11-11

The mechanosensitive PIEZO1 channel promotes CD54+/iNOS+ neutrophil expansion in pulmonary fibrosis.

Zhuang Lili L, Shi Jia J, Lin Zhangmei Z, Ruan Xinyuan X et al.

Pulmonary fibrosis (PF) represents the common end-stage outcome of a broad range of interstitial lung diseases. The shared pathophysiologic mechanisms remain poorly understood. Here, we identify two phenotypically distinct neutrophil subsets in PF: a pro-inflammatory subset characterized by CD54 (human) or iNOS (mouse) expression, and an alternative subset marked by Arg1 expression. Notably, CD54+ and iNOS+ neutrophils were markedly expanded in PF patients and mice with bleomycin-induced PF, respectively. Adoptive transfer of iNOS+ neutrophils exacerbated fibrosis in bleomycin-induced PF, whereas transfer of Arg1+ neutrophils had no significant effect. Further, the expression of PIEZO1, a mechanically activated ion channel, is predominantly upregulated in CD54+ neutrophils from PF patients or iNOS+ neutrophils from PF mice. Piezo1 ablation in neutrophils selectively impairs iNOS+ neutrophil differentiation, thereby attenuating fibrosis progression. Mechanistically, PIEZO1 promotes the differentiation of these pro-inflammatory subsets through the transcription factor IRF4 in a calcium-dependent manner. We further identify the JAK/STAT pathway as an upstream regulator of PIEZO1 expression in neutrophils. Consequently, PIEZO1 expression and CD54+ neutrophils are markedly decreased in patients treated with JAK inhibitor baricitinib. Importantly, combined inhibition of JAK/STAT and calcium signaling exerts synergistic suppression on the iNOS+ neutrophil expansion and PF progression. Together, our findings reveal a mechanism in which PIEZO1 promotes PF by specifically driving the expansion of CD54+/iNOS+ neutrophils.

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PubMedJournal of biological engineering2026-11-11

Engineering an agrowaste-based multilayer bio-encapsulation system for sustained nutrient release and microbial biotransformation of chlorinated solvents.

Yang Dun-Sheng DS, Shen Meng-Wei MW, Huang Ya-Ling YL, Lin You-Ping YP et al.

Trichloroethylene (TCE), a known carcinogen, is denser than water, which explains its deep presence in groundwater. Limitations on long-term supplies of TCE degraders and nutrients often led to TCE dichlorination failures in the field. This study presents the development and evaluation of an agrowaste-based multilayer bioencapsulation system designed to prolong microbial activity and enhance nutrient availability for a more favorable TCE-dechlorination environment. TCE-degrading consortia were integrated with a nutrient-rich core derived from recycled fermented agrowastes and encapsulated within a structurally reinforced sodium alginate matrix to form bio-pellets. The acclimated microbial community exhibited a degradation rate constant of 0.33 day⁻¹, with confirmed transformation of TCE into dichloroethylene and vinyl chloride, indicating active reductive dechlorination pathways. Characterization of the encapsulated system revealed a nutrient profile of 410.4 ± 29.7 mg TOC g⁻¹, 9.1 ± 0.2 mg TN g⁻¹, and 20.5 ± 0.7 mg TP g⁻¹, which enabled sustained nutrient release to support microbial metabolic functions. Column reactor experiments demonstrated that the multilayer structure maintained physical integrity and functional stability for more than 74 days. The system achieved a total TCE removal efficiency of 98.5%, reducing concentrations from 600 mg L⁻¹ to 9.1 mg L⁻¹, while effectively alleviating mass transfer limitations commonly observed in non-encapsulated systems. Although microbial activity induced localized acidification, the incorporation of natural buffering capacity helped maintain system stability. These results demonstrate that the proposed bio-encapsulation platform provides a framework for integrating material design with microbial function, offering promising applications in environmental biotechnology and bioprocess engineering.

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PubMedAesthetic plastic surgery2026-11-11

ICAM-1 Mediates the Immunosuppressive Activity of Adipose-Derived Stem Cells in the Inflammatory Environment.

Cao Jiankun J, Wang Chuan C, Yang Zhigang Z, Chen Hui H

Adipose-derived mesenchymal stem cells have gained attention in plastic and reconstructive surgery because they are efficient immunoregulators and easily accessible with minimal invasion. However, the mechanism of their immunoregulatory role in the inflammatory environment is unclear. Adipose-derived stem cells (ASCs) and peripheral blood mononuclear cells (PBMCs) were co-cultured to confirm the immunosuppressive activity of ASCs. The effects of inflammatory cytokines on the expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) in ASCs were evaluated using flow cytometry. Nuclear factor-κB (NF-κB) and molecular target of rapamycin (mTOR) signaling inhibitors were used to evaluate the mechanism of tumor necrosis factor alpha (TNF-α) stimulated upregulation of ICAM-1 in ASCs. To evaluate the effect of ICAM-1 knockdown on the immunoregulatory capacity of ASCs, PBMCs were labeled with carboxyfluorescein succinimidyl ester (CFSE), and their proliferation was analyzed using flow cytometry. ASCs inhibited PBMC proliferation. ICAM-1, and not VCAM-1, responded to pro-inflammatory cytokines and was upregulated by TNF-α in a concentration- and time-dependent manner; the NF-κB pathway inhibitor specifically blocked this increase in ICAM-1 expression. Knocking down ICAM-1 attenuated the immunosuppressive effects of ASCs on PBMC proliferation. ICAM-1, and not VCAM-1, is an inflammation sensor on ASCs and plays a key role in the immunoregulatory potential of ASCs. Pro-inflammatory TNF-α significantly increases ICAM-1 expression on ASCs in a concentration- and time-dependent manner, which is mediated by the NF-κB signaling pathway. These data may provide a theoretical basis for the clinical administration of ASCs in inflammation-related diseases in plastic and reconstructive surgery. This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

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