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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

PubMedInorganic chemistry2026-10-26

Sb3+-Sensitized Self-Trapped Exciton Emission and Energy Transfer for Tunable Tricolor and Near-White Luminescence in Cs2NaScCl6 Double Perovskite Microcrystals.

Liu Xiaoming X, Li Yang Y, Yao Longhui L, You Jiale J et al.

Metal-ion doping in lead-free double perovskites is an effective strategy for tailoring lattice structures and enhancing photoluminescence. Herein, Sb3+/Mn2+/Tb3+ codoped Cs2NaScCl6 microcrystals with tunable blue-green-red tricolor emission were synthesized via a solvothermal method. Under ultraviolet excitation, Sb3+ incorporation partially relaxes parity-forbidden transitions, enhances light absorption, and significantly promotes self-trapped exciton (STE)-related blue emission centered at ∼450 nm, increasing the photoluminescence quantum yield from 3.75% to 49.86%. Further codoping with Mn2+ and Tb3+ introduces red and green emission centers, respectively, enabling multipeak visible emission through efficient STE-mediated energy transfer. The optimized Cs2NaScCl6:1%Sb3+/4%Mn2+/30%Tb3+ microcrystals exhibit near-white-light emission with CIE coordinates of (0.3152, 0.3036) and a correlated color temperature of 6570 K. Time-resolved photoluminescence analysis verifies energy transfer from STE states to Mn2+ and Tb3+ activator centers, while thermogravimetric analysis demonstrates excellent thermal stability. These results demonstrate the potential of Sb3+/Mn2+/Tb3+ codoped Cs2NaScCl6 as a lead-free platform for tunable multicolor and near-white luminescence.

PMID 42929615
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PubMedJournal of biochemical and molecular toxicology2026-10-26

Theranekron Attenuates Inflammation, Oxidative Stress Index, and Apoptosis in Lipopolysaccharide-Induced Cardiovascular Toxicity: Association With Hypoxia-Inducible Factor-1 Alpha-Related Gene Expression.

Savran Mehtap M, Asci Halil H, Imeci Orhan O, Oguzlar Furkan Cagri FC et al.

This study aimed to evaluate the possible protective effects of Theranekron, an extract derived from Tarantula cubensis venom, on cardiovascular damage induced by lipopolysaccharide (LPS) in an experimental rat model. A total of 32 male Wistar Albino rats were randomly divided into 4 groups: Control, Lipopolysaccharide, Lipopolysaccharide plus Theranekron, and Theranekron alone. Lipopolysaccharide administration caused pronounced histopathological changes in the heart and aorta, including endothelial sloughing, hyperemia, hemorrhage, and infiltration of inflammatory cells. These pathological findings were accompanied by elevated oxidative stress markers, increased tumor necrosis factor-alpha and inducible nitric oxide synthase immunoreactivity, and increased caspase-3 immunoreactivity. Additionally, genes associated with the hypoxia-inducible factor-1 alpha (HIF-1α) pathway-such as interleukin 6, signal transducer and activator of transcription 3 (STAT3), and vascular endothelial growth factor-were significantly upregulated in the lipopolysaccharide group. Theranekron pretreatment was associated with partial attenuation of oxidative stress imbalance, of inflammatory and apoptotic immunoreactivity, and of the upregulation of HIF-1α-related transcripts. Overall, these findings suggest that Theranekron may offer partial protection against early LPS-induced cardiovascular injury.

PMID 42929009
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PubMedDevelopment, growth & differentiation2026-10-26

Evidence for a Role of Hox2 in Atrial Siphon Fusion of the Ascidian Ciona.

Liu Yurong Y, Yoshida Keita K, Hozumi Akiko A, Itagaki Kosuke K et al.

The hallmark of sessile adult ascidians is a vase-like shape with a single oral and atrial siphon. Ciona, however, develops two atrial siphons after metamorphosis, which subsequently fuse into one. The mechanisms underlying this fusion are unknown. This study suggests that Hox2 controls this process. Hox2-knockout animals using Transcription-Activator-Like Effector Nuclease (TALEN) retain two atrial siphons throughout their lives. During normal fusion, epidermal cells between the siphons narrow along the anterior-posterior axis. This cellular narrowing does not occur in Hox2-knockout animals, suggesting that the shape change in the epidermal cells produces tension, allowing the atrial siphon openings to converge at the midline for fusion. Hox2-knockout animals lack cupular organs, which are suspected hydrodynamic sensors in the internal epithelium of the fused atrial siphon and on the sperm duct. Among several knockout attempts, atrial siphon fusion was reproduced by only one TALEN pair, suggesting that this phenotype is driven by a mutation having a broader effect than those abolishing protein function. Many ascidians, unlike Ciona, develop a single atrial siphon shortly after metamorphosis. Our findings suggest that a phylogenetically conserved gene, Hox2, establishes this group-specific atrial siphon formation mechanism in Ciona.

PMID 42929298
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PubMedCells2026-10-26

Hyperglycemia-Induced Loss of Astrocytic Kir4.1 Is Associated with Increased DNMT1 Activity and Altered AMPK/SIRT1 Signaling.

Colón-Vázquez Jadier J, Hernández-Santiago Yanitza Y, Malpica-Nieves Christian J CJ, Rosado-Rivera Nathaly M NM et al.

The effects of chronic hyperglycemia on CNS, glial homeostasis and Kir4.1 regulation is poorly understood. Elevated blood glucose levels affect polyamine-sensitive inwardly rectifying potassium channels, Kir4.1, in astrocytes and retinal Müller glial cells. These cells regulate extracellular potassium and clear glutamate, processes supported by Kir4.1. Dysregulation of Kir4.1 channels has been implicated in glutamate toxicity, epilepsy, ataxia, and diabetes-induced neurodegeneration. In this study, we used Tandem Mass Tag Proteomic analysis, Pyrosequencing, SDS-PAGE and Western blot analysis, in whole brain and astrocytic primary cultures in hyperglycemic conditions testing DNMT1 and AMPK activities with RG-108, compound C, and AICAR treatments to investigate how hyperglycemia alters Kir4.1 expression in astrocytes and explored two regulatory mechanisms: (i) DNA methylation mediated by DNA methyltransferase 1 (DNMT-1), which uses S-adenosylmethionine (SAM) as a methyl donor, and (ii) metabolic signaling via the AMPK/SIRT-1 cascade. We found that hyperglycemia (25 mM glucose) (i) increased DNMT-1 protein levels in astrocytes by 1.5-2-fold and (ii) decreased AMPK and (iii) SIRT-1 levels, accompanied by a reduction in Kir4.1 protein expression. Pharmacological inhibition of DNMT-1 with RG-108 decreased DNMT-1 levels and restored Kir4.1. Treatment with AICAR, a selective AMPK activator, rescued SIRT-1 and Kir4.1 expression. In summary, hyperglycemia engages dual regulatory pathways: (i) epigenetic via DNMT-1 and (ii) metabolic via AMPK/SIRT-1, which converge on Kir4.1 downregulation in astrocytes. Therefore, both DNMT-1 inhibition and AMPK activation rescued Kir4.1 expression, suggesting functional support for potassium and glutamate homeostasis and membrane potential stability in glia.

PMID 42929878
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PubMedDiabetes/metabolism research and reviews2026-10-26

Exercise Modulates the Osteoimmune Axis: Myokine-Mediated Mechanisms in Diabetic Bone Disease.

Wu Chao C, Zou Jun J, Yuan Yu Y

Patients with type 2 diabetes mellitus (T2DM) often present with normal or even elevated bone mineral density (BMD), yet exhibit a significantly increased fracture risk-a phenomenon referred to as the 'diabetic bone paradox'. This discrepancy underscores the inadequacy of conventional BMD-centred assessment systems in fully elucidating the mechanisms underlying bone fragility in T2DM. Current evidence suggests that T2DM-related skeletal fragility is multifactorial, involving alterations in bone quality, advanced glycation end-product (AGE) accumulation, low bone turnover, microarchitectural deterioration, diabetic complications, increased fall risk and chronic inflammation. Recent advances in osteoimmunology have revealed that immune cell polarization driven by chronic low-grade inflammation, along with an imbalanced receptor activator of nuclear factor-κB ligand/osteoprotegerin (RANKL/OPG) axis, may contribute to the dysregulation of bone remodelling in T2DM. As a cornerstone intervention in T2DM management, exercise not only acts directly on bone tissue via mechanical loading but also may exert systemic immunomodulatory effects through myokines secreted by skeletal muscle. Exercise-induced myokines, such as interleukin-6 (IL-6), irisin, β-aminoisobutyric acid (BAIBA) and interleukin-15 (IL-15), may modulate the osteoimmune microenvironment and restore the dynamic equilibrium between bone resorption and formation by modulating macrophage polarization, restoring the Th17/Treg balance, bone marrow adipose tissue metabolism, and chronic inflammatory signalling pathways. Moreover, exercise may further promote bone metabolic homoeostasis by suppressing negative regulatory signals, such as myostatin. Therefore, this narrative review summarises the aberrant features of the osteoimmune axis in T2DM, with a focus on the potential mechanisms by which exercise and its induced myokines may modulate the osteoimmune microenvironment to ameliorate diabetic bone disease, thereby providing a framework for understanding exercise as a potential non-pharmacological intervention and identifying areas requiring further translational investigation.

PMID 42929066
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PubMedCells2026-10-26

Forskolin-Induced Lipid-Droplet Remodeling Is Associated with Improved Redox Homeostasis and Cryotolerance of Vitrified Porcine Oocytes and Parthenogenetic Embryos.

Xu Jiehuan J, Chen Yongliang Y, Cai Shaoli S, Gao Jun J et al.

Cryopreservation of mammalian oocytes and embryos is essential for the long-term conservation of livestock germplasm resources. Porcine oocytes and embryos accumulate high levels of intracellular lipids. This heavy lipid load aggravates vitrification-related oxidative stress and mitochondrial redox disturbance, greatly reducing cellular cryotolerance and hindering reliable preservation of indigenous pig germplasm. This study aimed to develop a non-invasive metabolic intervention strategy to mitigate lipid-associated oxidative cryodamage and improve the post-thaw quality of porcine oocytes and parthenogenetic embryos. Porcine cumulus-oocyte complexes were treated with forskolin, an adenylate cyclase activator, throughout in vitro maturation. For embryo assays, parthenogenetic embryos received continuous forskolin supplementation during oocyte maturation and were vitrified at Day 2 (cleavage stage). Vitrification disrupted lipid-droplet structural integrity and perturbed multiple metabolic pathways. Enrichment of starch, sucrose and galactose metabolism should be interpreted with caution as computational outputs, alongside changes in glycine, serine and threonine metabolism. Cryoinjury further induced mitochondrial depolarization, excessive reactive oxygen species production, redox imbalance and early apoptosis, ultimately impairing cell viability and embryonic developmental competence. Continuous forskolin exposure during oocyte in vitro maturation (with matching treatment for embryo groups) triggered lipid-droplet remodeling. This remodeling was associated with restored mitochondrial redox homeostasis and suppressed oxidative stress and apoptosis in warmed oocytes and embryos. Forskolin treatment enhanced post-thaw survival and cleavage rates of vitrified oocytes, as well as survival of cryopreserved embryos. By contrast, blastocyst formation rate showed only a numerical, non-significant increase. In conclusion, non-invasive forskolin-driven lipid-droplet remodeling can mitigate vitrification-triggered oxidative damage to lipid droplets and mitochondria. This work provides a practical pre-cryopreservation optimization strategy based on redox protection. It supports improved oocyte experimental protocols and offers useful references for germplasm conservation of rare and endangered pig breeds.

PMID 42929881
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