Drug Database
PL

plasminogen activator (tisokinase / tisokinase, Kowa / Hapase)

✓ Approved

Asahi Kasei · therapeutic agent

What is plasminogen activator?

plasminogen activator is a therapeutic agent developed by Asahi Kasei. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand Namestisokinase, tisokinase, Kowa, Hapase
CompanyAsahi Kasei
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Asahi Kasei

Therapeutic Indications

plasminogen activator is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Cardiac disordersMyocardial infarction✓ Approved

Related Research Articles

PubMedBioresource technology2026-08-30

Synergistic effect of fungal pretreatment and chemical activation on the development of porous carbon from walnut shells for microplastic removal.

Diao Yajie Y, Liu Wenjian W, Cai Xianwei X, Liu Heng H et al.

The compact structure of lignocellulosic biomass often limits activator diffusion, restricting pore development in activated carbons. In this study, a synergistic strategy combining Aspergillus niger pretreatment and chemical activation was developed to modify walnut shell structures and enhance pore formation. After pretreatment, walnut shells were activated with ZnCl2 at 550 °C and K2C2O4 at 800 °C, respectively. Three repeated experiments were performed to ensure data reliability, with errors within 5%. Increasing Aspergillus niger inoculum dosage, the yield of ZnCl2-activated carbon decreased from 42.6% to 37.7%, and increased the pyrolysis gas yield from 22.8% to 25.7%. For the K2C2O4 activation system, the AC yield decreased from 28.6% to 24.8%, while the gas yield increased from 33.8% to 39.4%. The porous structure formed by fungal pretreatment improved activator penetration and diffusion into the biomass. Furthermore, fungal pretreatment increased the surface area of activated carbons. The surface area of ZnCl2-activated AC increased from 721.7 to 1555.9 m2/g (116% increase), while that of K2C2O4-activated AC increased from 999.6 to 1220.8 m2/g (22% increase). This strategy optimized pore structures, reduced carbon crystallinity, and enhanced the surface hydrophilicity of AC. The obtained activated carbons exhibited remarkably enhanced adsorption performance toward polystyrene microplastics. This study reveals the synergistic effects of fungal pretreatment and chemical activation in regulating pore structures and adsorption properties of biomass-derived activated carbon. However, the long pretreatment time and reduced solid yield remain challenges for large-scale application. Future studies should optimize microbial systems and process conditions to enhance the economic feasibility of this strategy.

PMID 42669368
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PubMedEMBO reports2026-08-30

An evolutionarily conserved N-terminal domain of RRF-3 governs GTSF-1 binding in nematodes.

Govind Shamitha S, Ruppert Sebastian S, Kirangwa Joseph J, Busetto Virginia V et al.

GTSF1 is an essential activating cofactor for PIWI proteins in many metazoans. In the nematode Caenorhabditis elegans, however, GTSF-1 does not bind PIWI, but is associated with the RNA-dependent RNA polymerase RRF-3, supporting endo-siRNA (26G-RNA) biogenesis. Here, we demonstrate that this rewiring is deeply conserved across nematodes. For C. briggsae and Pristionchus pacificus, we show that GTSF-1 interacts with RRF-3 and is essential for 26G-RNA production and fertility. We map this interaction to an N-terminal domain of RRF-3, termed the GTSF-1 interacting domain (GID), and show that the GTSF-1 zinc finger region alone is sufficient for binding. Mutagenesis identifies critical residues mediating this interaction and reveals that GTSF-1 stability depends on RRF-3. Other RdRPs possess GID-like domains, which we propose to bind GTSF-1-related proteins. Phylogenomic and structural analyses support GTSF-1-RRF-3 interactions across all major nematode lineages and map the shift in GTSF-1 activity to the last common nematode ancestor. We propose that binding of GTSF-1 induces conformational changes in RRF-3 that facilitate RdRP complex assembly and activate its function, paralleling its role as a PIWI activator.

PMID 42668316
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PubMedAging2026-08-30

Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging.

Labrada Beisy Laborit BL, Kumar Amit A, Kolnohuz Alona A, Pineault Marie M et al.

Src homology region 2-containing phosphatase 1 (SHP-1), encoded by the protein tyrosine phosphatase non-receptor type 6 (PTPN6), regulates immune and metabolic signaling pathways. Although its functions in immune cells and insulin-responsive tissues are separately established, its integrative function in immunometabolic regulation remains unclear. A damaging variant in the PTPN6 gene (Ala455Thr) was discovered in a French-Canadian family and found to be the cause of early-onset emphysema. Using mice carrying this whole-body human-relevant mutation, we studied immunometabolic phenotypes across aging. Old mutant mice showed decreased body, liver and adipose tissue weights, improved glucose tolerance, and enhanced hepatic insulin sensitivity. Despite improved metabolic parameters, aged mutant mice developed liver abnormalities, including increased fibrosis and aberrant immune cell infiltration. Transcriptomic and histological analyses revealed an age-associated accumulation of intrahepatic B lymphocytes and macrophages, accompanied by increased SHP-1 protein levels and activation of Signal transducer and activator of transcription 3 (STAT3) signaling. Experiments in primary hepatocytes and old hepatocyte-specific Ptpn6 knockout mice suggest that these alterations are driven by immune rather than intrinsic hepatocyte mechanisms. These findings identify SHP-1 as a critical modulator of liver immune homeostasis during aging and demonstrate that immune cell infiltration contributes to age-related hepatic remodeling under SHP-1 deficiency.

PMID 42669491
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PubMedJID innovations : skin science from molecules to population health2026-08-30

Immunopathogenesis of itch: an integrative framework for chronic pruritus.

Kaczmarska-Such Agnieszka A, Reich Adam A

Chronic pruritus is increasingly recognized as a complex neuroimmune disorder rather than a purely sensory symptom. Historically, itch research has progressed through successive mechanistic paradigms-from histamine and mast cells, through dedicated neuronal circuits, to cytokine-driven and intracellular signaling pathways. Yet, each advance revealed that chronic pruritus cannot be explained by a single mediator or pathway. In this review, we propose the immunopathogenic spiral of itch as an integrative framework that describes both the evolution of pruritus research and the interconnected biology of itch pathogenesis. It reflects not only the cumulative history of the field but also the biological progression within an individual patient: from acute, single-mediator itch to a self-sustaining neuroimmune network in which multiple mechanistic layers operate simultaneously. In contrast to the traditional itch-scratch cycle, the spiral model captures how barrier dysfunction, immune activation, and neuroimmune remodeling link successive mechanistic layers into self-reinforcing networks. We discuss how histaminergic signaling, sensory neuron specialization, type 2 immune polarization, IL-17-dependent pathways, and JAK-signal transducer and activator of transcription convergence represent interconnected rather than competing layers of itch biology. This framework may help explain why single-target therapies achieve meaningful but incomplete itch control, supporting the rationale for multi-target therapeutic strategies.

PMID 42668492
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PubMedFrontiers in stroke2026-08-29

Higher allostatic load at hospitalization is linked to worse outcome 90 days after stroke.

Aamodt Eva Birgitte EB, Borei Karim K, Potter Thomas T, Vahidy Farhaan F

Allostatic load (AL), a marker of cumulative stress-related physiologic burden, may influence acute ischemic stroke (AIS) outcome through multisystem dysregulation. A total of 4,103 AIS patients were recruited from Houston Methodist Registry of Neurological Endpoint Assessments among Patients with Ischemic and Hemorrhagic Stroke (REINAH). Clinical information was collected at initial hospital stay and AL was created using ten parameters representing the metabolic, inflammatory and vascular systems. No neuroendocrine parameters were available. Length of stay (LOS) at the hospital was collected upon departure from the initial hospitalization, and mortality and dependency (modified Rankin Scale) were collected at 90 days post stroke. Factors independently associated with high AL were examined using a multivariable logistic regression model. Associations between baseline AL and post-stroke outcomes (LOS, mortality, and dependency) were examined using unadjusted and adjusted regression models. High AL was associated with longer LOS, and higher mortality and dependency at 90 days. Factors independently associated with high AL included younger age, Black race, higher area deprivation index, being single, illegal drug use, diabetes mellitus, sepsis, higher Charlson comorbidity index, anticoagulation reversal therapy, antihypertensive therapy, and higher NIHSS at 6 and 24 h post stroke, whereas being a woman, hypercholesterolemia, atrial fibrillation, anticoagulant therapy, intravenous tissue plasminogen activator treatment, and endovascular thrombectomy were associated with moderate-low AL. High AL is associated with poorer functional and clinical outcomes after AIS and may support future risk stratification work.

PMID 42666190
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PubMedJournal of endocrinological investigation2026-08-29

Salivary hormones and adipokines are associated with glycemic control and early renal and cardiometabolic markers in children and young adults with type 1 diabetes.

Robino Antonietta A, Tornese Gianluca G, Aldegheri Luana L, Franceschi Roberto R et al.

Type 1 diabetes (T1D) is recognized as a complex metabolic condition associated with hormonal dysregulation and early complications. This study aimed to evaluate salivary metabolic hormones and adipokines in children and young adults with T1D, and to assess their association with early markers of metabolic and vascular complications. Demographic, anthropometric, and clinical data were collected from 349 children and young adults with T1D, classified according to weight status. Salivary concentrations of metabolic hormones and adipokines were measured using a multiplex immunoassay. Compared with normal weight (NW) individuals, overweight/obese (OW) showed worse clinical outcomes, including higher HbA1c, lower eGFR, higher blood pressure, lower high-density lipoprotein cholesterol (HDL-C), and higher triglycerides. No differences in salivary hormone concentrations were observed according to weight status, while several hormones were significantly associated with clinical outcomes. HbA1c results inversely associated with ghrelin and glucagon-like peptide-1 (GLP-1) (p-value = 0.009 and p-value = 0.027, respectively), and positively with plasminogen activator inhibitor-1 (PAI-1) (p-value = 0.022). Renal function showed associations with ghrelin (p-value = 0.024), leptin (p-value <0.001), and visfatin (p-value = 0.002). Blood pressure was associated with ghrelin (p-value = 0.025) and leptin (p-value = 0.039), while lipid profile parameters were associated with ghrelin (HDL-C, p-value = 0.019) and glucagon (triglycerides, p-value = 0.034). Salivary metabolic hormones and adipokines are associated with early markers of metabolic and vascular dysfunction in young individuals with T1D, independently of weight status. These findings suggest a potential role for these biomarkers in early diabetes-related complications.

PMID 42667348
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