Drug Database
PL

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

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

PubMedTherapeutic advances in hematology2026-07-27

Plain language summary: How safe and effective is long-term treatment with intravenous plasminogen concentrate for people with type 1 plasminogen deficiency?

Shapiro Amy D AD, McDaniel Heather H, Decker Robert W RW, Nakar Charles C et al.

What is this study about? Type 1 plasminogen deficiency (PLGD-1 for short) is a long-term, ultra-rare condition where the body does not make enough of a protein called plasminogen. This can cause thick layers made of a fibrous, insoluble protein called fibrin (known as lesions) to develop in different parts of the body. Intravenous plasminogen concentrate (IV PLG concentrate for short, also known as RYPLAZIM®) is the first medicine approved to treat this condition. It works by replacing plasminogen in the body. In this study, adults and children with PLGD-1 received long-term treatment with IV PLG concentrate. They had already received IV PLG concentrate before, as part of the clinical trial that led to the approval of the treatment, or through the expanded access programs. The researchers wanted to know how safe and effective long-term treatment with IV PLG concentrate was. They also wanted to explore whether giving IV PLG concentrate more or less often would affect how well the treatment worked. What were the results? Study participants had no new lesions associated with PLGD-1 or return of previous lesions when they received the treatment as prescribed. Some participants had previous lesions come back when they received the treatment less often than prescribed. These lesions rapidly improved or went away again when they started more frequent treatment, as originally prescribed. Most of the adverse events that participants experienced were classified as mild, and none were related to the study treatment. What do the results mean? Overall, long-term treatment with IV PLG concentrate is effective for people living with PLGD-1 and is well tolerated. Treatment with IV PLG concentrate can be personalized to meet people's individual needs. What is the purpose of this plain language summary? The purpose of this plain language summary is to help you understand the findings from recent research. Where can I find the original article on which this summary is based? You can read the original article titled 'Safety and efficacy of long-term treatment of type 1 plasminogen deficient patients with intravenous plasminogen replacement therapy' published in the journal Haemophilia for free at: https://doi.org/10.1111/hae.70019 Who sponsored the study and this summary? The study was sponsored by Prometic Biotherapeutics Inc., currently Kedrion Biopharma Inc. This summary was sponsored by Kedrion Biopharma Inc. Who is this summary for? This summary may be of interest to people living with PLGD-1, their families, and caregivers. Patient advocates, patient organizations, healthcare professionals, and funders of healthcare services may also find this summary useful.

PMID 42504189
阅读全文 →
PubMedCranio : the journal of craniomandibular practice2026-07-27

Cytokines and biomarkers of bone resorption and cartilage degeneration in synovial fluid of patients with temporomandibular joint osteoarthritis: A scoping review.

Torres Catalina C, Vera Darco D, Solar Melissa M, Fuentes Del Campo Aler A

Osteoarthritis of the temporomandibular joint is characterized by joint tissue degeneration. However, the synthesized and categorized information regarding biomarkers present in synovial fluid samples from patients who have not been treated for this disease is scarce. This review aims to provide an overview of inflammatory cytokines, bone, and cartilage degeneration biomarkers relevant to this temporomandibular disorder (TMD). Following JBI and PRISMA-ScR guidelines, 26 studies from five databases were analyzed, identifying 45 biomarkers. Inflammatory cytokines (interleukin 1 beta, interleukin 6, tumor necrosis factor alpha), cartilage degeneration markers (matrix metalloproteinases), and bone resorption markers (receptor activator of nuclear factor kappa-B ligand, osteoprotegerin) were most frequently reported. Vascular endothelial growth factor was associated with cartilage degeneration and bone resorption. These biomarkers may aid in disease characterization; however, further standardized clinical studies are required for validation and comparison with other TMDs.

PMID 42504100
阅读全文 →
PubMedProtein & cell2026-07-27

CRISPR screening identifies GNPTAB as a noncanonical STING activator driving cellular senescence.

Yin Jian J, Gao Yizhou Y, Jing Yaobin Y, Jiang Xiaoyu X et al.

Cellular senescence is accompanied by profound lysosomal alterations, yet whether lysosome-associated factors actively drive aging remains unclear. Through a focused CRISPR/Cas9 screen in human mesenchymal progenitor cells (hMPCs), we identified N-acetylglucosamine-1-phosphotransferase subunits alpha and beta (GNPTAB), an enzyme responsible for lysosomal hydrolase targeting, as a potent regulator of cellular senescence. Genetic ablation of GNPTAB attenuated senescence, whereas its overexpression accelerated senescence. This pro-senescent function occurred independently of GNPTAB's canonical enzymatic role. Instead, GNPTAB binds to the innate immune adaptor stimulator of interferon genes (STING) via a specific interface (E1119), leading to activation of STING and its downstream TANK-binding kinase 1 (TBK1), as well as pro-inflammatory gene expression. A STING-binding-deficient GNPTAB mutant (E1119A) preserved canonical lysosomal functions but failed to induce senescence, while STING depletion abolished GNPTAB-driven senescence. Together, these findings uncover a new signaling pathway wherein GNPTAB engages STING to facilitate its activation, nominating this interface as a potential target for mitigating age-related cellular dysfunction.

PMID 42505080
阅读全文 →
PubMedSmall (Weinheim an der Bergstrasse, Germany)2026-07-27

MoN/Au/cTAT Boosted Sonochemotherapy Post-Intravesical Instillation in Bladder Cancer.

Zhang Yunhua Y, Shi Xin X, Yuan Ye Y, Gao Xincheng X et al.

Intravesical chemotherapy is effective for non-muscle-invasive bladder cancer (NMIBC) but limited in muscle-invasive bladder cancer (MIBC) due to poor tissue penetration, underscoring the need for alternative dynamic treatment strategies. Sonochemotherapy (SCT), which combines ultrasound-triggered reactive oxygen species (ROS) generation with controlled drug release, presents a promising approach. Given the superficial anatomical location of the bladder, SCT's deep tissue penetration and favorable safety profile make it particularly suitable for bladder cancer treatment. However, SCT efficacy is frequently constrained by insufficient ROS production and sonosensitizer instability. To overcome these challenges, a MoN/Au/cTAT nanocomposite was developed by conjugating cisplatin and human immunodeficiency virus-1 transcription activator (cTAT) onto MoN/Au nanosheets to enhance the stability and the effect of SCT. As a result, MoN/Au/cTAT demonstrates potent cytotoxicity against bladder cancer cells under ultrasound irradiation. In vivo, it effectively suppresses muscle-invasive orthotopic bladder tumors while maintaining a high safety margin. In summary, the nanosonosensitizer-chemodrug platform combines cTAT for improved transmucosal delivery and tumor penetration with MoN/Au to efficiently generate ROS under ultrasound irradiation, offering a transformative strategy for muscle-invasive bladder cancer therapy.

PMID 42504482
阅读全文 →
PubMedAnalytical chemistry2026-07-27

DNA Nanowire-Assisted CRISPR/Cas12a Triple Cascade Amplification for Sensitive Detection of Myeloperoxidase Activity.

Shi Jia-Yi JY, Wu Shun-Li SL, Tan Yan Y, Jiang Hong-Xin HX et al.

Myeloperoxidase (MPO) is an inflammation-associated heme enzyme implicated in cardiovascular oxidative stress, but sensitive activity-based detection in complex clinical samples remains challenging. Herein, we report a CRISPR/Cas12a-based triple-cascade amplification platform for rapid and sensitive MPO activity detection. The core sensing element consists of DNA nanowires containing multiple Cas12a activator strands, tethered to magnetic beads via biotin-labeled and phosphorothioate-modified linkers. In the chloride-containing assay system, MPO-catalyzed generation of HOCl oxidatively cleaves these linkers, releasing the nanowires and activating Cas12a, which, in turn, cleaves fluorescent reporters. This design integrates three amplification stages (MPO catalysis, multiactivator release, and Cas12a trans-cleavage), achieving ultrasensitive detection without additional nucleic acid amplification. Under the optimized chloride-containing conditions, the assay achieved a detection limit of 10.20 pg/mL for MPO. A preliminary pilot analysis using human serum samples from acute coronary syndrome patients and healthy individuals showed different signal distributions, supporting the feasibility of applying the platform to complex serum matrices, although contributions from eosinophil peroxidase/HOBr-mediated probe activation cannot be excluded. The platform is readily adaptable to lateral flow assays and portable fluorescence readouts, offering versatile formats for point-of-care-compatible analysis. This work provides a sensitive CRISPR/Cas12a-based strategy for MPO activity-related hypohalous oxidant assessment under defined assay conditions and demonstrates its preliminary applicability in complex serum matrices.

PMID 42503780
阅读全文 →
PubMedImmunology2026-07-27

4-1BBL Suppresses Anti-Inflammatory Responses by Regulating Metabolic Reprogramming of Macrophages.

Kang Young Jun YJ

Integration of intracellular signalling and metabolic reprogramming is critical for macrophage polarisation and the induction of pro- or anti-inflammatory responses. However, the molecular switches that govern these processes remain incompletely defined. While 4-1BB ligand (4-1BBL), a member of the TNF superfamily, is known to promote sustained pro-inflammatory responses in macrophages, its role in anti-inflammatory macrophage responses has not been fully elucidated. This study identifies that 4-1BBL serves as a negative regulator of anti-inflammatory macrophage polarisation. Genetic deletion or pharmacological inhibition of 4-1BBL significantly enhanced the expression of anti-inflammatory cytokines and markers in mouse macrophages. In IL-4R signalling, 4-1BBL restrained Janus kinase 1 (JAK1) and signal transducer and activator of transcription 6 (STAT6) phosphorylation, thereby modulating transcriptional programmes associated with anti-inflammatory macrophage activation. Consistently, 4-1BBL deficiency elevated mitochondrial oxidative phosphorylation and fatty acid oxidation, accompanied by increased expression of metabolic genes in anti-inflammatory macrophages. Transcriptomic analysis further revealed a shift towards anti-inflammatory and oxidative metabolic gene signatures in IL-4-treated 4-1BBL-deficient macrophages. Importantly, the inhibition of 4-1BBL signalling also augmented anti-inflammatory responses in human monocytes and facilitated the transition from pro-inflammatory to anti-inflammatory phenotypes. Collectively, these findings establish 4-1BBL as a crucial molecular switch that regulates macrophage polarisation by integrating inflammatory signalling with metabolic reprogramming, highlighting 4-1BBL as a potential therapeutic target for promoting inflammation resolution.

PMID 42504467
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多plasminogen activator