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plasminogen activator (tisokinase / tisokinase, Kowa / Hapase)

✓ Approved

Asahi Kasei · 治疗药物

什么是 plasminogen activator？

plasminogen activator 是一种治疗药物，由Asahi Kasei研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名tisokinase, tisokinase, Kowa, Hapase
公司Asahi Kasei
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Asahi Kasei

治疗适应症

plasminogen activator 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Cardiac disordersMyocardial infarction✓ Approved

相关研究文献

PubMedPhlebology2026-08-06

Periprocedural coagulation and fibrinolytic changes after sclerotherapy for venous malformations.

Zhu Yingjie Y, Wang Chaonan C, Wang Weixin W, Jiang Fengli F et al.

PurposeTo prospectively characterize peri-procedural changes in thrombin-antithrombin complex (TAT), plasmin-α2-plasmin inhibitor complex (PIC), fibrin/fibrinogen degradation products (FDP), D-dimer, thrombomodulin (TM), and tissue plasminogen activator-inhibitor complex (t-PAIC) in patients with venous malformations (VMs) undergoing percutaneous sclerotherapy.MethodsThis prospective single-center observational study included 68 patients with VMs and 48 healthy controls. Peripheral venous blood was collected 24 h before treatment, immediately after treatment, and on postoperative days 1-3. Local lesional blood was aspirated through the access needle before contrast or sclerosant injection. Biomarker concentrations were compared using paired and repeated-measures analyses. Receiver operating characteristic (ROC) analyses were used only to explore discrimination between VM-associated hemostatic activation and healthy-control values.ResultsLocal lesional samples showed higher TAT, PIC, FDP, and D-dimer concentrations than paired preoperative peripheral samples, whereas TM and t-PAIC did not differ significantly. After sclerotherapy, TAT increased immediately, while D-dimer showed a more prolonged postoperative elevation. At the immediately post-procedure time point, exploratory ROC analysis showed an AUC of 0.9517 for TAT and 0.8931 for D-dimer. The TAT/PIC ratio also increased immediately after treatment, suggesting a transient laboratory shift toward coagulation predominance. No symptomatic venous thromboembolism, pulmonary embolism, overt disseminated intravascular coagulation, or major bleeding was observed during 30-day follow-up.ConclusionIn patients with venous malformations undergoing sclerotherapy, TAT showed an immediate post-procedural increase consistent with acute thrombin generation, whereas D-dimer showed a more sustained postoperative pattern. These findings describe peri-procedural hemostatic activation and support further outcome-based evaluation of TAT and TAT/PIC.

PMID 42557218
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PubMedQatar medical journal2026-08-06

Parinaud's syndrome in posterior stroke treated with intravenous thrombolysis: A case report.

Benetti Mauricio M, Gonzalez Fabio F, Caiza-Zambrano Francisco F, Neme-Segura Yemina Y et al.

Parinaud's syndrome, or dorsal midbrain syndrome, is characterized by vertical gaze palsy, light-near dissociation, convergence-retraction nystagmus, and bilateral eyelid retraction. The majority of cases are caused by pineal region tumors, whereas vascular etiologies are less frequent. Early recognition of this neuro-ophthalmological syndrome can be crucial for diagnosing brainstem strokes, particularly when initial neuroimaging findings are normal. A 66-year-old man presented to the Emergency Department with sudden-onset vertical diplopia, dysarthria, and gait instability, consistent with an acute neurological event. Neuro-ophthalmological examination revealed the complete classical triad of Parinaud's syndrome. Brain magnetic resonance imaging (MRI) and computed tomography angiography (CTA) showed no acute ischemic lesions or vascular abnormalities. Given the disabling oculomotor findings and the strong suspicion of posterior circulation ischemia, intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) was administered within 3.5 h of symptom onset. The patient achieved complete neurological and oculomotor recovery within 24 h, and follow-up brain MRI confirmed the absence of structural damage. The present case illustrates Parinaud's syndrome, a rare neuro-ophthalmological manifestation of acute posterior circulation ischemia, treated with intravenous thrombolysis. Although its global prevalence remains unknown, published series show that the syndrome is exceptionally uncommon, with vascular etiologies representing approximately 25% of cases-making stroke the second most common cause after pineal region tumors.In contrast to pineal region tumors, which typically produce a slowly progressive clinical course, vascular etiologies are characterized by abrupt symptom onset. This case underscores the importance of recognizing Parinaud's syndrome as a possible manifestation of posterior circulation ischemia, particularly when early neuroimaging findings appear normal. Its rarity and atypical presentation can make therapeutic decision-making challenging in the acute setting, highlighting the diagnostic value of a meticulous ocular examination.

PMID 42558928
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PubMedNature chemical biology2026-08-06

A covalent PFKL activator suppresses tumor growth.

Jiang Xiaoding X, Lynch Eric M EM, Lyu Congcong C, Wilson Crystal N CN et al.

Glycolysis fuels vital cellular functions, and its dysregulation has been implicated in cancer, neurodegeneration, antibiotic resistance and diabetes. The glycolytic dependency of cancer, known as the Warburg effect, represents a key vulnerability for development of targeted anticancer agents; however, the development of such agents remains challenging owing to metabolic heterogeneity and resistance. Here we developed a covalent phosphofructokinase-1 liver type (PFKL) activator that couples glycolytic activation with delivery of a cytotoxic carnitine palmitoyltransferase 2 (CPT2)-targeting payload to cancer cells in vitro and in vivo. The electrophile-drug conjugate site-specifically and proteome-wide selectively modifies K677 in the allosteric effector site to stabilize the R-state tetramer of PFKL, while concomitantly releasing a CPT2-selective inhibitor to destabilize cell metabolism. The delivery mechanism of electrophile-drug conjugates is analogous to that of antibody-drug conjugates, but differentiated by their selective covalent targeting of intracellular proteins.

PMID 42557312
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PubMedExpert opinion on therapeutic patents2026-08-06

An updated patent review of STAT6 inhibitors and modulators (2020 - present).

Khan Muhammad Zafar Irshad MZI, Du Bo-Qun BQ, Xue Mei M, Yu Meng-Qian MQ et al.

Signal Transducer and Activator of Transcription 6 (STAT6) is a critical transcription factor in the interleukin-4 (IL-4) and IL-13 signaling pathways and serves as a key pathogenic driver of type 2 (TH2) immune responses. Dysregulated STAT6 activity is implicated in asthma, atopic dermatitis, autoimmune diseases, eosinophilic disorders, and certain cancers. As such, targeting STAT6 presents a promising therapeutic strategy for these diseases. This review provides a comprehensive analysis of patent strategies for targeting STAT6 from 2020 to the present. We categorize and evaluate chemical entities based on their core structural features, highlighting key motifs, major patent assignees, and the progression of lead candidates through preclinical and clinical development. Recent advances reflect a clear evolution from broad JAK/STAT pathway inhibitors toward highly selective STAT6-targeted agents. Although research and development in this area are progressing rapidly with significant achievements, key challenges remain - including optimizing pharmacokinetic properties, achieving tissue specificity, and mitigating off-target effects. The emergence of bifunctional degraders, such as PROTACs, represents a promising frontier for achieving complete and sustained pathway suppression. Future success will likely depend on combining innovative chemistry with sophisticated patient stratification biomarkers to translate potent STAT6 inhibition into safe, effective therapies.

PMID 42557044
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PubMedBlood science (Baltimore, Md.)2026-08-06

STAT3 inhibition eradicates multiple myeloma stem-like cells and induces immunogenic cell death.

Sha Yuqian Y, Li Wenyu W, Zhang Yan Y, Liu Tengyuan T et al.

Signal transducer and activator of transcription 3 (STAT3) is a pivotal oncogenic driver in multiple myeloma (MM), and its constitutive activation promotes malignant plasma cell proliferation, survival, and drug resistance in the bone marrow microenvironment. Despite therapeutic advances, MM remains incurable due to persistent STAT3-driven tumorigenesis and the resilience of MM stem cells. We investigated the therapeutic potential of napabucasin (BBI608), a novel STAT3 inhibitor, in MM. Our data demonstrated that BBI608 potently suppressed MM cell proliferation in vitro and in vivo, while significantly impairing the clonogenic potential and inducing robust apoptosis. Mechanistically, BBI608 exhibited dual efficacy by targeting bulk tumor cells and eradicating the stem-like compartment of MM cells, thereby addressing a critical therapeutic challenge. Moreover, we revealed that BBI608 triggered immunogenic cell death (ICD) via the activation of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), which subsequently enhanced T-cell-mediated anti-tumor immunity. Our findings highlight STAT3 inhibition as a promising strategy to simultaneously eradicate MM cells, target stem cell reservoirs, and harness anti-tumor immunity, providing a robust rationale for the clinical translation of BBI608 in MM therapy.

PMID 42559484
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PubMedNagoya journal of medical science2026-08-06

IKAROS isoforms differentially control gene expression and differentiation of a B-cell acute lymphoblastic leukemia cell line.

Ogimoto Yuya Y, Kawachi-Nakamura Mariko M, Hashimoto Kazunori K, Yanagisawa Kiyoshi K

B-cell acute lymphoblastic leukemia (B-ALL) is the most common malignancy occurring in children and a leading cause of cancer-related mortality, thus there is an urgent need for development of novel therapeutic strategies for high risk B-ALL patients. The significance of IKZF1 gene alterations in B-ALL cases is controversial, as some studies have shown those to be associated with poor prognosis, while others have reported that deletion of exons 4-7 of the IKZF1 gene, which results in generation of IKAROS isoform 6, is related favorable prognosis. For the present study, clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 was employed for knockout of the IKZF1 gene and various IKAROS knockout lines were established, which allowed for investigation of precise functions of the gene by comparing four lines with different IKAROS isoform 1 and 6 statuses. The results clearly showed induction of significant differentiation and cell cycle progression in IKAROS isoform 6 knockout clones. Furthermore, knockout of IKAROS isoform 6 resulted in significant upregulation of the expression of IKAROS isoform 1 as well as signal transducer and activator of transcription 5 (STAT5) activity, which are considered to be related to the observed features. Further investigations are warranted to provide greater mechanistic insight regarding IKAROS-mediating pathways, which will lead to development of novel therapy for human B-ALL.

PMID 42558870
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