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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)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

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

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

Related Research Articles

PubMedFrontiers in microbiology2026-10-15

Effects of long-term application of traditional compost and bio-compost on soil microbial community structure and life-history strategies.

Liu Lizhan L, Yang Tao T, Wu Xiaofang X, Fan Yang Y et al.

Long-term compost application is an important strategy for improving soil fertility and regulating soil microbial communities, but the comparative effects of traditional compost and bio-compost on microbial life-history strategies remain unclear, which is a valuable framework for linking community shifts to soil carbon and nutrient cycling. In this study, a long-term (30-year) field experiment established in 1993 under a winter wheat-summer maize cropping system was used to evaluate the effects of high-rate bio-compost, high-rate traditional compost, low-rate bio-compost, low-rate traditional compost, and an unfertilized control on soil properties, enzyme activities, microbial community structure, and oligotrophic/copiotrophic groups. Compost application significantly increased soil organic carbon, total nitrogen, total phosphorus, and soil moisture, with soil organic carbon content in the high-rate bio-compost treatment being 33.8% higher than that of the control. Soil oxidative enzyme activities, including catalase, lignin peroxidase, manganese peroxidase, and laccase, were also enhanced by compost addition. Bacterial diversity was highest under low-rate bio-compost, whereas fungal diversity and trophic strategies showed stronger responses to fertilization. Principal coordinate analysis and permutational multivariate analysis of variance indicated that both bacterial and fungal community compositions were significantly altered by 30 years of compost application. The bacterial oligotroph/copiotroph ratio remained relatively stable among treatments, while the fungal oligotroph/copiotroph ratio decreased significantly under low-rate bio-compost. Specifically, this treatment significantly decreased the relative abundance of the oligotrophic fungal phylum Basidiomycota while increasing the copiotrophic phylum Ascomycota, indicating a shift toward copiotrophic fungal groups. Co-occurrence network analysis showed that the high-rate bio-compost significantly enhanced microbial network complexity, increasing the number of nodes from 419 (control) to 753 and edges from 828 to 1841 in the bacterial network, suggesting enhanced microbial connectivity under high-rate bio-compost application. Correlation, Mantel, and redundancy analyses further identified soil total phosphorus and oxidative enzyme activities, especially manganese peroxidase, lignin peroxidase, and laccase, as key factors associated with microbial community variation and trophic group distribution. Overall, long-term bio-compost application improved soil fertility, stimulated oxidative enzyme activities, enhanced microbial network complexity, and regulated microbial life-history strategies, with different responses between bacterial and fungal communities.

PMID 42876575
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PubMedFrontiers in cellular and infection microbiology2026-10-15

Streptococcus anginosus extracellular vesicles deliver protein to promote gastric cancer progression.

Li Feng F, Chen Xiling X, Huang Hao H, Sun Xiaowei X et al.

Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide. Although Helicobacter pylori (Hp) is considered a major etiological factor, only 3% of Hp-infected individuals develop GC, implying additional microbial drivers. Streptococcus anginosus (SA) exhibits independent pro-carcinogenic properties, but its mechanism in regulating GC malignant phenotypes remains elusive. This study investigated the roles and molecular mechanisms of SA-derived extracellular vesicles (SA-EVs) in GC progression. SA-EVs were isolated and characterized, followed by in vitro and in vivo functional assays, transcriptomic analysis and rescue experiments to explore their pro-tumor effects and key components. SA-EVs were efficiently internalized by GC cells, which markedly promoted GC cell proliferation, migration and invasion in vitro, and accelerated tumor growth in vivo. Mechanistically, the protein cargos of SA-EVs specifically triggered the activation of the JAK-STAT signaling pathway, which further upregulated the expression of genes associated with cell proliferation and epithelial-mesenchymal transition (EMT). Moreover, pharmacological inhibition experiments verified that removal of SA-EV protein components or pharmacological blockade of JAK-STAT signaling effectively eliminate the pro-tumor effects of SA-EVs. Streptococcus serves as a core signature genus in Hp-independent GC. SA drives GC malignancy by delivering functional proteins via EVs to activate JAK-STAT signaling. This study reveals a novel bacteria-host interaction mechanism mediated by SA-EVs, providing a potential target for GC intervention.

PMID 42876538
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PubMedArtificial organs2026-10-15

Economic Evaluation of Prolonged Hypothermic Oxygenated Machine Perfusion Enabling Daytime Liver Transplantation.

Woltjes Linda C LC, Bonnema Marijke I MI, Brüggenwirth Isabel M A IMA, Lantinga Veerle A VA et al.

Short-duration (1-2 h) dual hypothermic oxygenated machine perfusion (DHOPE) reduces ischemia-reperfusion injury-related complications. Prolonged DHOPE preservation (DHOPE-PRO) may facilitate logistics. We assessed the economic impact of DHOPE-PRO versus conventional short-duration DHOPE, hypothesizing that DHOPE-PRO would not be associated with increased one-year transplantation-related costs. This post hoc economic evaluation of the prospective DHOPE-PRO trial (NL8740) included adult recipients of livers donated after brain death. All transplantation-related medical expenses up to one year post-transplant were collected. The cost of resource use was calculated using 2022 full hospital prices indexed to 2024. Time-driven variable costing was applied to perfusion, surgery, and intensive care costs. The primary outcome was total one-year transplantation-related cost. Of 24 patients, 12 received a liver after DHOPE and 12 after DHOPE-PRO. Median one-year total costs were €83 583 [interquartile range (IQR) 78 400-104 158] for DHOPE and €78 582 [IQR 73123-92 855] for DHOPE-PRO (p = 0.347). Perfusion costs were higher with DHOPE-PRO (€23 926 [IQR 22711-24 697] versus €17 306 [IQR 16928-17 594]; p < 0.001), while surgery costs were lower (€18 560 [IQR 17806-20 747] versus €21 303 [IQR 19535-25 418]; p = 0.033). Costs related to other medical activities did not differ between groups. In this exploratory single-center economic evaluation, DHOPE-PRO enabled daytime liver transplantation without evidence of increased one-year transplantation-related costs compared with short-duration DHOPE. Higher perfusion-related costs were accompanied by lower surgery-related costs in this cohort. These findings warrant confirmation in larger studies. Netherlands Trial Registry number: NL8740.

PMID 42875815
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PubMedFrontiers in immunology2026-10-15

The effect of low-temperature-induced immune activation in elderly idiopathic facial palsy: the association between Th1/Th2 imbalance and facial nerve inflammation.

Tang Xing X, Ji Ziqin Z, Xiao Xueling X, Zhu Tongtong T et al.

The pathogenesis of idiopathic facial palsy in the elderly has not been fully elucidated. Recent studies have shown that exposure to low temperatures may participate in the pathological process through immune-mediated pathways. This article reviews that cold stimulation can disrupt the Th1/Th2 immune balance, manifested as reduced secretion of Th1-type cytokines and upregulation of Th2-type cytokines, thereby inducing peripheral inflammatory responses around the facial nerve, leading to nerve edema, demyelination, and conduction dysfunction. Due to the immune aging characteristics of the elderly population, including the reduction of the initial T cell pool, the imbalance of pro-inflammatory and anti-inflammatory factor ratios, and the decline in regulatory T cell function, they are more sensitive to the immune dysregulation induced by low temperatures and have a significantly increased risk of facial palsy. Clinical and animal experimental evidence supports this mechanism, suggesting that the serum IL-4/IFN-γ ratio may serve as a prognostic marker. Future multi-center studies are needed to verify the effectiveness of targeted immune regulation intervention through the Th2 pathway and explore the application value of low-temperature warning and individualized warming strategies in the prevention of facial palsy in the elderly.

PMID 42876459
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PubMedThe Egyptian journal of immunology2026-10-15

Assessment of serum levels of vitamin D and tumor necrosis factor alpha in ulcerative colitis patients at Egyptian Military Hospitals: Cross-sectional observational study.

Eldahan Wedad W, Hassan Mohamed Z H MZH, Asaad Ahmed M AM, Salaheldin Mohamed M et al.

Ulcerative colitis (UC) is a chronic inflammatory disorder confined to the colonic and rectal mucosa. The disease is marked by infiltration of immune cells, leading to excessive production of inflammatory mediators. A key pro-inflammatory cytokine that plays a vital role in the pathophysiology of ulcerative colitis is tumor necrosis factor alpha (TNF-alpha). Low levels of vitamin D have been associated with several autoimmune disorders. This study aimed to assess vitamin D serum levels in UC patients as regard TNF-alpha serum levels and the Severity of UC (UCDAI). This cross-sectional observational research was carried out at Military healthcare facilities in Cairo, Egypt, over six months, from 1 July 2025 to 31 December 2025. Utilizing a convenience sample of 50 adults aged 15 to 70 years with a confirmed diagnosis of ulcerative colitis, newly diagnosed. They were divided into two groups according to disease severity (UCDAI or Mayo score): 26 patients in the mild group & 24 patients in the moderate/severe group. Demographic data were collected from patients' interviews. Colonoscopy for ulcerative colitis disease activity index (UCDAI) score, CBC, ESR, CRP, and Fecal calprotectin (FC) were investigated at Egyptian Military hospitals. Serum levels of 25-hydroxyvitamin D (using CLIA) and TNF-alpha (using ELISA) were measured at central laboratories of the armed forces and blood bank. Correlation analysis showed Serum Vitamin D had a moderate negative correlation with UCDAI (r = -0.466, p-value= 0.001), and a strong negative correlation with serum TNF-alpha (r = -0.669, p-value <0.001). Serum TNF-alpha showed a moderate positive correlation with UCDAI (r = 0.472, p-value= 0.001). Fecal calprotectin had a strong positive correlation with UCDAI (r = 0.704, p-value <0.001) and a weak positive correlation with serum TNF-alpha (r = 0.388, p-value= 0.005). In conclusion, this study demonstrates that patients with moderate to severe ulcerative colitis had pronounced mucosal and systemic inflammation, reflected by markedly elevated fecal calprotectin and TNF-alpha levels, concomitant with significantly lower vitamin D concentrations compared with those in mild disease.

PMID 42875905
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PubMedEndocrinology and metabolism (Seoul, Korea)2026-10-15

Link between Circulating CCL2 Levels and Sarcopenia: Evidence from a Cohort Study, the UK Biobank, and Human GTEx Transcriptomic Data.

Kwak Mi Kyung MK, Kim Sung-Jin SJ, Park So Jeong SJ, Dao Tam T et al.

Chronic inflammation is a hallmark of aging, but the role of inflammatory mediators such as C-C motif chemokine ligand 2 (CCL2) in skeletal muscle health remains unclear. Although CCL2 is often considered a detrimental pro-aging factor, it is also essential for myogenesis. This study aimed to clarify the complex role of CCL2 in human muscle metabolism. We used a multimodal approach integrating clinical, proteomic, transcriptomic, and genetic analyses. The association between circulating CCL2 and sarcopenia-related parameters was examined in 323 community-dwelling older adults and validated using UK Biobank data (n=54,219). Genotype-Tissue Expression (GTEx) transcriptomic data (n=818) were used for tissue-level analysis, and Mendelian randomization (MR) was performed to assess causality. In the cohort study, serum CCL2 levels were significantly higher in participants with sarcopenia, weak muscle strength, or poor physical performance (P<0.001 to 0.042) and were inversely correlated with skeletal muscle index, grip strength, and gait speed (P<0.001 to 0.003). Each standard deviation increase in circulating CCL2 level was associated with 1.37-1.71-fold higher odds of sarcopenia-related outcomes (all P≤0.028). UK Biobank data also showed higher plasma CCL2 levels in participants with sarcopenia (P=0.005). In contrast to these observational findings, tissue-level analysis using GTEx data showed that higher skeletal muscle CCL2 expression was correlated with greater muscle cross-sectional area. MR further supported an inverse causal association between genetically predicted plasma CCL2 levels and sarcopenia risk (P=0.029). These divergent findings raise the possibility that elevated circulating CCL2 levels in sarcopenia reflect a compensatory response to muscle deterioration rather than a direct pathogenic driver, highlighting the need for further mechanistic validation.

PMID 42875904
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