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

PubMedEuropean journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V2026-05-24

Tuning lipid monolayer behavior with soluble surfactants: A pathway to enhanced ultradeformable drug carriers.

Dopierała Katarzyna K, Przybylska Alicja A, Kustrzyńska Karolina K, Michniak-Kohn Bożena B

Transferosomes are ultradeformable lipid vesicles used to enhance transdermal drug delivery. Their key component is the edge activator, which modulates membrane fluidity and deformability. In this study, we propose an integrated approach to evaluate the surfactants-Tween® 20, Tween® 60, Tween® 80 (Croda International), and sodium cholate (SC)-as edge activators in transferosomal formulations with 1,2-dioleoyl-3-trimethylammonium propane (DOTAP). Monolayer and bilayer investigations were combined to identify the most suitable surfactant. Among the investigated surfactants, SC exhibited the most favorable overall performance, leading to transferosomes with enhanced membrane fluidity and desirable viscoelastic properties. The results also revealed a strong influence of surfactant concentration on the interfacial behavior of the lipid bilayer, attributed to electrostatic interactions between SC and DOTAP. Atomic force microscopy confirmed increased vesicle deformability from 4.10 to 8.83 nm and reduced Young's modulus from 167.29 to 88.22 MPa for SC-containing systems compared to pure DOTAP. DLS measurements further demonstrated appropriate colloidal properties, with vesicle size of 216-345 nm. Within a simplified Quality by Design framework, SC emerged as the most promising edge activator, although adhesion-related parameters did not clearly indicate dominance of this formulation. Overall, the proposed integrated strategy provides a rational approach for the rational design of transferosomal formulations.

PMID 42176870
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PubMedCell reports2026-05-24

FOXA1-mediated CEPT1 deficiency in airway epithelium drives asthma via an ER stress-mitochondrial dysfunction axis.

Chen Qile Q, Huang Yuyi Y, Wen Junjie J, Liang Canyang C et al.

Asthma is associated with disordered glycerophospholipid metabolism and decreased phosphatidylcholine (PC), but the molecular basis remains incompletely defined. Through integrative data mining, we identify CEPT1, a key enzyme in glycerophospholipid biosynthesis, to be significantly downregulated in the airway epithelium of asthma. CEPT1 deficiency causes PC/PE reduction and phospholipid imbalance, activates all three endoplasmic reticulum (ER) stress pathways, disturbs ER Ca2+ stores, and drives mitochondrial Ca2+ overload, which in turn triggers mitochondrial oxidative stress. Notably, administration of polyenylphosphatidylcholine (PPC) restores ER and mitochondrial homeostasis and reduces apoptosis, cytokine release, and mucus overproduction. FOXA1 is identified as a direct transcriptional activator of CEPT1. In vivo, CEPT1 overexpression alleviates airway inflammation and mucus hypersecretion. Collectively, our study elucidates an axis wherein FOXA1-mediated CEPT1 repression induces ER stress and mitochondrial dysfunction through disrupted calcium handling, driving mucin hypersecretion and airway inflammation-identifying CEPT1 restoration or PPC as potential mechanism-based interventions for asthma.

PMID 42176270
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PubMedInsect biochemistry and molecular biology2026-05-24

Homothorax Regulates BarH1 Expression and Olfactory Perception in Monochamus alternatus Hope.

Li Qi-Cheng QC, Wu Sheng-Xin SX, Yang Mei-Jiao MJ, Zhang Pu-Yuan PY et al.

Odorant-binding proteins (OBPs) play a crucial role in the host location of the Japanese pine sawyer beetle, Monochamus alternatus, a significant forest pest responsible for the transmission of pine wilt disease. We previously identified BarH1 as a direct regulator of the odorant-binding protein Obp19; however, its upstream regulation remains unclear. In this study, we delineate a sexually dimorphic transcriptional network that governs BarH1 expression and olfactory plasticity. We identified critical cis-regulatory elements in the MaltBarH1 promoter, including an enhancer (-3035 to -2677 bp) and a repressor (-2677 to -2560 bp) that finely modulate its transcription. Yeast one-hybrid screening revealed Homothorax (Hth) as a key upstream activator that specifically binds to the MaltBarH1 promoter. Notably, this network exhibits marked sexual dimorphism: females display sustained upregulation of BarH1-Obp19 following exposure to camphene, whereas males exhibit suppression. Behaviorally, Hth knockdown specifically transformed male attraction to camphene into repulsion, while females remained unaffected. Our findings establish MaltBarH1 as an integrative hub within a sex-specific regulatory circuit that processes olfactory information distinctly between the sexes. This work provides novel insights into insect chemosensory plasticity and identifies potential targets for pest management strategies.

PMID 42176996
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PubMedAngewandte Chemie (International ed. in English)2026-05-24

Direct Synthesis of Polar Polyolefin Elastomers Enabled by Neutral Nickel-Catalyzed High Temperature Solution Copolymerization.

Hu Xiaoqiang X, Chen Jingmin J, Wang Lei L, Mu Hongliang H et al.

Copolymerization of olefin and polar monomer to produce the desired polar polyolefin materials is a longstanding challenge, which becomes much more difficult when carried out at industrially preferred high temperatures due to both catalyst deactivation and rapid chain transfer reactions. Here, we report for the first time the direct synthesis of high-molecular-weight polar polyolefin elastomers (P-POEs) from high-temperature solution copolymerization of ethylene and biomass-derived polar monomer at above 130°C. The key lies in the discovery of highly thermostable α-ketocarboxamide nickel catalysts, which are not only neutral catalysts that do not require excess alkyl aluminum as an activator/scavenge/protecting agent but also in situ generate desired branches (36.8-70.6/1000C) through chain walking reaction that circumvents the need of α-olefins. Molecular weights of P-POEs with ester incorporations of 0.6-8.7 mol% produced at 130°C-170°C, which is also the preferred temperature for the synthesis of commercially non-polar polyolefin elastomer (POE), reach 59-276 kDa that are 2-9 times higher than those obtained previously at high temperatures. Both high-molecular-weights and polar functional characteristics enable P-POE as attractive materials, endowing them with desired properties, including tensile strength, strain recovery, melt flowability, hydrophilicity, dyeability, adhesion, and compatibilization properties.

PMID 42175829
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PubMedAging cell2026-05-24

Tubular Omega-3 Fatty Acid Receptor FFAR4 Deficiency Aggravated Renal Aging and Chronic Kidney Disease.

Yang Letian L, Tang Lei L, Li Jian J, Liu Dekai D et al.

Aging leads to renal function decline and increases the risk of chronic kidney disease (CKD). Omega-3 polyunsaturated fatty acids (PUFAs) are essential fatty acids for humans, exerting their functions via free fatty acid receptor 4 (FFAR4). Clinical studies indicate that omega-3 PUFAs supplementation shows benefits for the elderly population and CKD patients, but these results remain controversial. Herein, we found that omega-3 PUFAs alleviated renal fibrosis and tubular senescence in aged mice, adenine diet-induced CKD mice, and unilateral ureteral obstruction (UUO) mice. Meanwhile, omega-3 fatty acid receptor FFAR4 expression in tubular epithelial cells (TECs) were down-regulated in the old population and CKD patients, positively correlated with renal dysfunction. Systemic or TEC-specific knockout of FFAR4 aggravated renal aging and CKD in mice. Mechanically, FFAR4 agonism increases the production of endogenous PPARγ activator 15-deoxy-∆12,14-Prostaglandin J2 (15d-PGJ2), and improves PPARγ-dependent tubular epithelial cell senescence, which was indicated by anti-aging marker Klotho expression, senescence-associated β-galactosidase (SA-β-gal) activity, and profibrotic factor TGF-β1 secretion. The study demonstrated a novel role of FFAR4 from senescent TECs on fibroblast activation via paracrine effects and highlighted the therapeutic effects of omega-3 PUFAs with their receptor FFAR4 as an attractive drug target against renal aging and CKD.

PMID 42175992
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PubMedSignal transduction and targeted therapy2026-05-24

An oncostatin M receptor and chloride intracellular channel 1 crosstalk drives key oncogenic pathways in glioblastoma.

Mansourabadi Amir Hossein AH, Qu Dianbo D, Cianci Francesca F, Snider Jamie J et al.

Oncostatin M receptor (OSMR) plays diverse roles in several human malignancies, including brain, breast, and pancreatic cancer. In glioblastoma (GB), OSMR orchestrates a feedforward signaling mechanism with the truncated active mutant of epidermal growth factor receptor (EGFR), the EGFRvIII, and signal transducer and activator of transcription 3 (STAT3) to drive GB progression. Beyond EGFRvIII, OSMR promotes brain tumor stem cell (BTSC) respiration and therapy resistance. The molecular mechanisms underlying OSMR's multifaceted roles remain largely unclear. Here, we systematically mapped the OSMR interactome using Mammalian Membrane Two-Hybrid High-Throughput Screening (MaMTH-HTS). We identified OSMR-specific and OSMR/EGFRvIII-specific high-confidence candidate binding proteins, highlighting OSMR context-dependent functions. Among a subset of common interactors, we uncovered chloride intracellular channel 1 (CLIC1) as a critical regulator of OSMR-STAT3 signaling and the OSMR/EGFRvIII complex. CLIC1 physically associates with OSMR and EGFRvIII and facilitates EGFRvIII packaging into extracellular vesicles (EVs). Genetic deletion of CLIC1 disrupts the OSMR/EGFRvIII interaction, impairs STAT3 activation, reduces EGFRvIII EV content, and slows GB progression. Using whole-cell patch-clamp recordings and a monoclonal antibody that selectively targets transmembrane CLIC1 (tmCLIC1omab), we establish a distinct pharmacologically and biophysically tmCLIC1-mediated current in GB indispensable for sustaining EGFRvIII/STAT3 signaling. Importantly, we show that OSMR is required for maintaining CLIC1-mediated ionic balance at the plasma membrane (PM). Our study uncovers a bidirectional crosstalk between OSMR and tmCLIC1 in GB, essential for fueling its malignant growth.

PMID 42177207
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