Drug Database
FA

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

PubMedWater research2026-07-17

Overlooked properties difference of biogenic sulfur resulting in distinct performance in serving as an electron donor for microbial denitrification.

Zhang N N, Yi G G, Ren R R, Zhang G G et al.

Biogenic sulfur (bio-S0) is recognized as a more efficient electron donor compared to its chemical counterpart in microbial denitrification. However, the performance differences among various types of bio-S0 remain poorly understood, posing a challenge in identifying the optimal variant. In this study, we comparatively investigated three distinct bio-S0 samples-bio-S0-A1 and bio-S0-A2, both obtained from single-reactor bio-S0 production processes with varying organic coating thicknesses, and bio-S0-B, sourced from a dual-reactor bio-S0 production process-alongside chemical sulfur (chem-S0) in terms of property characterization, denitrification performance, and microbial composition. Our results showed that bio-S0-B exhibited an elevated denitrification rate compared to the chem-S0, but was less effective than bio-S0-A1 and bio-S0-A2. This discrepancy could be attributed to the differing sulfur-related properties, such as polysulfane content and crystallinity. Regarding the other two bio-S0 samples (bio-S0-A1 and bio-S0-A2), our findings indicated that the organic coating negatively impacted denitrification performance. Inspired by this, we further demonstrated that bio-S0 can be optimized by destroying the organic coating, leading to an increase of up to 3.2-fold in denitrification rate. Variations of microbial composition were noted among different bio-S0 samples, with the relative abundance of Moheibacter showing a positive correlation with the denitrification rate. This study offers a property-based guideline for optimizing the selection of bio-S0 and further refining raw bio-S0 to enhance its effectiveness as an electron donor for denitrification.

PMID 42462649
Read full article →
PubMedbioRxiv : the preprint server for biology2026-07-17

Medin-Induced Pro-inflammatory and Prothrombotic Activation of Coronary Artery Endothelial Cells: A Potential Novel Mediator Linking Aging and Atherosclerosis.

Morrow Kaleb K, Karamanova Nina N, Woltjer Randy R, Krajbich Victoria V et al.

Age is the most important risk factor for coronary artery disease (CAD) independent of traditional risk factors. Aging induces classic pro-inflammatory and prothrombotic vascular phenotypic changes whose molecular mediators remain poorly understood. Medin is a common cleavage product protein that accumulates in vasculature with aging and shown to cause endothelial dysfunction. Its role in CAD is unknown. The study aimed to evaluate the effects of medin on human coronary artery endothelial cell (HCAEC) pro-inflammatory and prothrombotic activation and establish the relationship between medin and coronary atherosclerosis in human decedents. HCAECs were exposed to physiologic dose of medin (5 µM) for 20 hours and ribonucleic acid sequencing (RNAseq) with signaling pathway analyses and reverse transcription polymerase chain reaction of select pro-inflammatory and prothrombotic genes performed. Corresponding protein expression was measured by Western blot or enzyme linked immunosorbent assay in HCAECs exposed to medin (5 µM) without or with nuclear factor-κB (NFκB) inhibitor RO106-9920 (10 µM). Coronary arteries from 40 deceased individuals underwent immunohistochemistry and medin and plaque burden were quantified and their relationship evaluated. RNAseq showed predominant pro-inflammatory gene expression changes induced by medin. HCAECs treated with medin showed increased phosphorylated NFκB, elevated protein expression of interleukin (IL)-6, IL-8, monocyte chemotactic protein (MCP)-1, intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and plasminogen activator inhibitor (PAI)-1 and reduced protein expression of thrombomodulin; these changes were reversed by RO106-9920 co-treatment. In human tissues, coronary artery medin strongly correlated with plaque burden (R=0.76, p<0.0001) and coronary macrophage content (R=0.72, p<0.0001). Coronary arteries from decedents with myocardial infarction had higher medin than those without (5.53±2.67% versus 0.02±0.02%, p=0.0005). Medin induced NFκB-mediated endothelial cell pro-inflammatory and prothrombotic activation and was strongly associated with coronary plaque burden and inflammation. Medin is a novel candidate mediator linking aging and coronary atherosclerosis.

PMID 42465488
Read full article →
PubMedScientific reports2026-07-17

Evaluation of the properties of gel, film and paper coated with nanocellulose and nanochitin.

Dehghani Firouzabadi Mohammadreza M, Bousfield Douglas D, Tajvidi Mehdi M

Bio-based nano-materials have great potential as films and as paper coatings to produce materials that are suitable for food packaging. However, more needs to be understood about the characteristics of the starting materials and how they influence the final film properties. The objective of this study was to comparatively investigate the structural, thermal, mechanical, rheological, and functional properties of nanocellulose and nanochitin films or gels and their application as bio-coatings for paper. The thermal behavior of nanocellulose and nanochitin samples was similar. The tensile strength and strain of the nanocellulose films were significantly higher than those of the nanochitin films. The viscosity of both nanocellulose and nanochitin gels decreased uniformly with increasing shear rate. The coating process was carried out at a speed of 5 cm/s for single-layer and double-layer coatings. Bio-coating of the paper with nanochitin significantly improved the barrier properties (resistance to water, air, and oil penetration). At similar coat weights, the nanochitin-coated papers always consistently exhibited a lower thickness than the nanocellulose-coated papers. The brightness of nanocellulose-coated papers was higher than that of nanochitin-coated papers. This study demonstrates the potential of these bio-based nanomaterials for sustainable and effective paper bio-coatings.

PMID 42463733
Read full article →
PubMedBioresource technology2026-07-17

Structural evolution and reaction pathways of hematite reduction by biomass-lignin derived bio-coke.

Wu Kefeng K, Ge Lichao L, Yao Lei L, Yang Chunxia C et al.

In this study, bio-cokes with different mass ratios were prepared by co-pyrolysis of pine sawdust and lignin, and their hematite reduction behavior, gas release characteristics, and carbon structural evolution at 600-1000 °C were systematically investigated. The results show that hematite reduction follows a stepwise pathway of Fe2O3 → Fe3O4 → FeO → Fe, with the FeO-to-Fe transition identified as the key rate-controlling step because it becomes thermodynamically favorable only above 800 °C. Increasing the lignin proportion improved the fixed carbon content of bio-coke, leading to higher reduction efficiency at all tested temperatures, with a maximum reduction rate of 96.8% at 1000 °C. TG-FTIR and kinetic analyses revealed that the P2-L1 sample released CO and CO2 more intensely and concentratively in the high-temperature region, thereby enhancing gas-phase reduction through the Boudouard reaction. Raman spectroscopy and microscopic observations further confirmed that higher lignin content promoted ordered carbon structural reorganization during high-temperature treatment, forming a more stable and graphitized carbon structure. This facilitated deeper deoxygenation and higher metallic iron yield. This work investigates the influence of lignin content variation in the blended feedstock on bio-coke structure and reduction performance, providing guidance for the development of biomass-derived reducing agents in low-carbon metallurgy.

PMID 42462832
Read full article →
PubMedBiochemical pharmacology2026-07-17

Apigenin restores macrophage homeostasis and angiogenesis via Fgr/IL10 axis in recurrent spontaneous abortion.

Li Meng-Ying MY, Cao Xiao-Yan XY, Chen Si-Man SM, Yang Yi-Xing YX et al.

Recurrent spontaneous abortion (RSA) is closely associated with disruption of both immune homeostasis and vascular development at the maternal-fetal interface. To decode the underlying cellular defects, we performed single-cell RNA sequencing (scRNA-seq) on human decidual tissues, revealing a profound imbalance in macrophage polarization and impaired efferocytosis in RSA patients. Through transcriptomic screening and clinical validation, we pinpointed the Fgr proto-oncogene, Src family tyrosine kinase (Fgr) as a key pathological driver overexpressed in RSA macrophages, acting as a molecular brake on the pro-healing M2 phenotype. Seeking a targeted intervention, we demonstrated that the natural flavonoid Apigenin (Api) directly binds and inhibits the Fgr kinase domain, which essentially triggers robust Interleukin 10 (IL10) secretion. Crucially, this Api-mediated Fgr/IL10 signaling axis not only restores M2 polarization and enhances apoptotic cell clearance, but also rescues pro-angiogenic crosstalk with endothelial cells in a vascular endothelial growth factor (VEGF) -dependent manner. Furthermore, in a lipopolysaccharide (LPS)-induced murine miscarriage model, Api administration effectively reduced embryo resorption and rescued pregnancy loss. Collectively, our study highlights the Fgr/IL10 axis as a critical determinant of decidual homeostasis and establishes Api as a promising therapeutic strategy for RSA.

PMID 42462890
Read full article →
PubMedAmerican journal of cancer research2026-07-17

IGF2BP1 orchestrates glycolytic reprogramming via HK2 to accelerate hepatocellular carcinoma malignancy.

Wang Qing Q, Miao Hui H, Wang Yizhou Y, Zeng Jianhong J et al.

Dysregulated glucose metabolism is a hallmark of hepatocellular carcinoma (HCC), yet the upstream regulators driving this metabolic reprogramming remain incompletely understood. In this study, insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) was identified as a critical oncogenic driver in HCC. Clinically, IGF2BP1 is markedly overexpressed in HCC tissues and cell lines, with expression levels correlating strongly with tumor aggressiveness. Functionally, silencing IGF2BP1 significantly attenuated HCC cell proliferation, migration, and invasion, concomitant with a profound suppression of glycolytic flux. Mechanistically, we demonstrate that IGF2BP1 directly binds to and stabilizes HK2 mRNA, thereby upregulating Hexokinase 2 (HK2) protein expression. This stabilization triggers a metabolic cascade characterized by increased glucose uptake, lactate production, pyruvate accumulation, and elevated lactate dehydrogenase A (LDHA) levels. Crucially, HK2 knockdown completely abrogated the pro-glycolytic and pro-tumorigenic effects induced by IGF2BP1, confirming HK2 as a critical downstream effector. In vivo xenograft models further corroborated these findings, showing that IGF2BP1 depletion drastically inhibited tumor growth while downregulating the HK2/LDHA axis and reducing pyruvate levels. Collectively, our study elucidates a novel IGF2BP1/HK2 axis that drives HCC malignancy via glycolytic reprogramming, highlighting IGF2BP1 as a promising prognostic biomarker and therapeutic target.

PMID 42465019
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about Factor VIIIa