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4-

4-factor prothrombin complex

✓ Approved

Intas Pharmaceuticals · F2 · Cell-based Therapies

What is 4-factor prothrombin complex?

4-factor prothrombin complex is a cell-based therapies developed by Intas Pharmaceuticals. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyIntas Pharmaceuticals
Drug ClassCell-based Therapies
Molecular TargetF2, F7, F9, F10
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Intas Pharmaceuticals

Mechanism of Action

Molecular Targets

4-factor prothrombin complex acts on 4 molecular targets:

F2coagulation factor II, thrombin (THPH1, PT)
F7coagulation factor VII (SPCA)
F9coagulation factor IX (P19, F9 p22)
F10coagulation factor X (FXA, FX)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

4-factor prothrombin complex is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersExtravasation blood✓ Approved
Vascular disordersHaemorrhage✓ Approved

Related Research Articles

PubMedInternational journal of molecular sciences2026-10-16

Glutaminolysis and mTOR-C/EBPβ Signaling Drives the Differentiation of Novel IL-10-Producing Regulatory T Cells.

Tajima Masaki M, Fuss Ivan J IJ, Ikuta Naoko N, Mao Liming L et al.

Here we report that Dectin-1-stimulated dendritic cells (DCs) induce unique IL-10-producing T cells with strong regulatory function during fungal infection or experimental asthma. These T cells, which we call Dect-10 T cells, are induced by DC-initiated signaling that sets in motion two complementary mechanisms of IL-10-producing T cell differentiation. The first involves induction of nascent Dect-10 T cell IL-4 synthesis and attendant GATA3 production, the latter being a factor that exerts canonical and epigenetic transcriptional function at separate IL-10 promoter sites. The second involves TGFβ superfamily signaling associated with induction of glutaminolysis and generation of alpha-ketoglutarate, a factor that induces rapamycin-sensitive TORC1 activation; in turn, such activation causes the translation of the LIP isoform of C/EBPβ and the formation of a CREB1-LIP complex that binds to adjacent sites on the IL-10 promoter to facilitate the transactivation of the IL10 gene. Dect-10 T cell regulatory function is manifested through its capacity to down-regulate normally protective immune responses to hyphal C. albicans renal infection. In addition, Dect-10 T cells, in accord with their IL-4-dependent genesis, suppress dust mite-induced experimental asthma.

PMID 42883696
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PubMedInternational journal of molecular sciences2026-10-16

Reduced Schiff Base Copper(II) Complexes Derived from 2-, 3-, and 4-Methoxybenzylamine: DNA Binding and Cleavage, BSA Binding, Cytotoxic and SOD Mimetic Properties.

Lintnerová Lucia L, Herich Peter P, Korec Jana J, Svitková Barbora B et al.

A series of reduced Schiff base ligands derived from salicylaldehyde (1) and methoxybenzylamines (2a-c) were prepared and used to prepare three copper(II) complexes, 5a (2-methoxyderivative), 5b (3-methoxyderivative), and 5c (4-methoxyderivative). They were characterized by spectral methods and X-ray crystallography. The complexes showed DNA cleavage activity, with 30% cleavage at 3 × 10-3 M and up to 94.5% at 5 × 10-3 M. Absorption titration studies with ct-DNA and EB-DNA displacement methods revealed strong binding of the prepared complexes, with complexes 5b and 5c favored. Viscosity measurements and thermal degradation of DNA studies indicate DNA groove binding. All complexes exhibit a moderately strong binding affinity to serum albumin. The complexes performed very well in the resazurin assay monitoring mitochondrial activity, with significant cytotoxic effects (around 95% already at 1 × 10-4 M). The MTT assay confirmed the complexes' cytotoxicity against cancer cell lines (A549, HepG2) compared with HEL fibroblasts. All complexes showed remarkable selectivity for HepG2 cells, with selectivity indices (HEL vs. HepG2) up to 3.05 for complex 5a, and complex 5b achieved the lowest IC50 (33.0 ± 5.3 μM) against HepG2 cells. From a regioisomerism perspective, complex 5a outperformed the others in DNA cleavage; complex 5b, with the 3-methoxy group, showed the most interesting cytotoxicity results, and both complexes 5b and 5c showed good DNA-binding properties.

PMID 42883897
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PubMedNutrients2026-10-16

Preoperative Zinc Deficiency as a Novel Prognostic Predictor for Postoperative Recurrence in Hepatocellular Carcinoma.

Adachi Yuki Y, Shimada Shingo S, Mizukami Shoichiro S, Takizawa Tomoki T et al.

Background/Objectives: The impact of preoperative zinc (Zn) status on the survival and recurrence of patients with hepatocellular carcinoma (HCC) after hepatectomy remains unclear. This study aimed to clarify whether preoperative Zn deficiency affects the prognosis of patients with HCC undergoing initial curative hepatectomy. Methods: We retrospectively reviewed 105 patients who underwent initial curative hepatectomy for HCC at our institution (2011-2018). Preoperative Zn deficiency was defined as serum Zn < 70 µg/dL. Clinical and tumor parameters were compared between patients with and without Zn deficiency. Disease-free and overall survival were evaluated using the Kaplan-Meier method, and prognostic factors were identified via univariate and multivariate Cox proportional hazards analyses. Subgroup analyses were conducted based on age, gender, and etiology. Results: Among 105 patients, 46 (43.8%) showed Zn deficiency (Zn deficiency group), whereas 59 (56.2%) showed normal Zn (normal Zn group). Compared with the normal-Zn group, the Zn deficiency group showed significantly lower hemoglobin, prothrombin activity, serum albumin, and smaller tumor size (all p < 0.05). The Zn deficiency group experienced significantly worse disease-free survival (p = 0.015) but no difference in overall survival (p = 0.63). On multivariate analysis, zinc deficiency (hazard ratio [HR] 1.83, p = 0.040) and prothrombin activity (HR 0.98, p = 0.042) were independent predictors of worse disease-free survival. Subgroup analysis revealed that Zn deficiency was significantly associated with elevated recurrence risk in patients with HCV-related liver disease (HR 3.67, p = 0.013). Conclusions: Preoperative Zn deficiency is an independent predictor of worse DFS after curative hepatectomy. Although further large-scale studies are required to confirm these findings, evaluating preoperative Zn status may help identify patients at high risk of HCC recurrence.

PMID 42884598
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PubMedAnalytical methods : advancing methods and applications2026-10-16

Selective and sensitive colorimetric detection of copper(II) using methylthiazole-quinolinol based sensor: application in real samples and its experimental and DFT studies.

Abolghasemi Sareh Sadat SS, Fallah Moafi Hadi H, Mousavi Seyed Hossein SH

A novel methylthiazole-quinolinol-based sensor (MTAMQ) named (E)-2-methyl-5-((4-methylthiazol-2-yl)diazenyl)quinolin-8-ol was synthesized. In the presence of copper(II) ions (Cu2+), the MTAMQ sensor exhibits a stable color change from yellow to red. The MTAMQ sensor displayed a linear response toward Cu2+ ions over the concentration range of 0.10 to 55 µM (0.006 to 3.5 mg L-1), with a detection limit of 103.93 nM (6.60 µg L-1). The binding constant of the MTAMQ-Cu2+ complex was 1.41 × 104 M-1, and the stoichiometric ratio of complex formation was 1 : 1. Using EDTA, the MTAMQ sensor can be recycled and reused up to 4 times. Density functional theory (DFT) calculations were conducted for the MTAMQ sensor and the MTAMQ-Cu2+ complex. The MTAMQ sensor was successfully used to detect and quantify Cu2+ ions in various foodstuff and water samples, and the results were very close to those of the atomic absorption spectroscopy (AAS) method. To enable the detection of Cu2+ ions without the need for a complex device, paper test strips were prepared using the MTAMQ sensor and offered successful results. The unique features of the MTAMQ sensor, including naked-eye detection of copper ions in environmental samples without the need for specialized equipment, real-time analysis, cost-effectiveness, simple operation, rapid response, high stability under different conditions, and excellent selectivity and sensitivity, make it a promising alternative to previously reported colorimetric sensors.

PMID 42885444
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PubMedInternational journal of molecular sciences2026-10-16

Mitophagy and Ferroptosis in Diabetic Kidney Disease: A Hypothesis of Their Synergistic Interplay in Renal Tubular Injury-A Narrative Review.

Gong Yanyu Y, Liu Qiuping Q, Dai Hanyuan H, Li Jialing J et al.

Tubular injury induced by mitophagy or ferroptosis serves as a critical pathological basis for the progression of diabetic kidney disease (DKD). Mitophagy constitutes a critical process of mitigating tubular injury by eliminating damaged organelles to maintain cellular equilibrium and homeostasis. Ferroptosis, a form of programmed cell death characterized by lipid peroxidation, serves as a pivotal factor in the progression of DKD. While numerous studies have elucidated the complex relationship between mitophagy and ferroptosis, there is a scarcity of literature addressing the relationship between these two processes in the context of tubular damage in DKD. We reviewed recent literatures exploring the associations among mitophagy, ferroptosis, and renal tubular injury in DKD, and tried to summarize the complex crosstalk between ferroptosis and autophagy in DKD. We hope to offer some new ideas for the treatment of DKD.

PMID 42883999
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PubMedClinical and experimental immunology2026-10-16

Dysregulated complement activation in COVID-19: The Role of Soluble Complement Inhibitors.

van der Meulen Stef S, Wang Haiyu H, Nugteren Saskia S, Ponchel Frederique F et al.

In viral infections, complement activation can contribute to viral clearance, but excessive activation, as observed in severe COVID-19, may drive immunopathology. While much is known about complement-activating factors in COVID-19, insight into the role of endogenous complement inhibitors remains limited. We performed a longitudinal analysis within the BEAT-COVID cohort, comprising hospitalized patients with SARS-CoV-2 infection admitted to the intensive care unit (ICU) or ward, and age-matched healthy controls. Serum levels of the complement activation marker soluble membrane attack complex (sC5b-9) and soluble inhibitors C1-Inhibitor (C1-INH), C4b-Binding Protein (C4BP), Factor H, and Factor I were measured by ELISA. In vitro endothelial complement sensitivity was assessed by flow cytometry. Soluble inhibitors were also measured in a cohort of patients with long COVID. Patients admitted to the ICU showed elevated sC5b-9 levels compared to patients admitted to the ward and controls, correlating with disease severity, length of hospitalization, and need for mechanical ventilation, but not mortality. Unexpectedly, levels of all soluble complement inhibitors were elevated, particularly in patients admitted to the ICU. Factor H levels positively correlated with sC5b-9. Endothelial cells pre-incubated with serum from patients admitted to the ICU became more susceptible to complement attack. In patients with long COVID, Factor H and C4BP levels remained elevated compared to pre-pandemic healthy controls. Severe COVID-19 is characterized by extensive complement activation despite elevated circulating inhibitor levels, suggesting impaired local complement regulation at the cell surface, potentially amplified by overwhelming systemic activation, rather than inhibitor deficiency.

PMID 42885872
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