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acetylsalicylic acid + dipyridamole (Asasantin / Asasantin Retard / Asasantine LP)

✓ Approved

Boehringer Ingelheim International GmbH · PTGS1 · 小分子

什么是 acetylsalicylic acid + dipyridamole?

acetylsalicylic acid + dipyridamole 是一种小分子,由Boehringer Ingelheim International GmbH研发。该药已获批,用于治疗相关适应症,给药途径:Oral (PO)。

药物档案

商品名Asasantin, Asasantin Retard, Asasantine LP
公司Boehringer Ingelheim International GmbH
药物类别小分子
分子靶点PTGS1
给药途径Oral (PO)
状态Approved

作用机制

分子靶点

acetylsalicylic acid + dipyridamole 作用于 1 个分子靶点:

PTGS1prostaglandin-endoperoxide synthase 1 (COX3, PCOX1)
需要更深入的分析?Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

acetylsalicylic acid + dipyridamole 针对 2 个适应症,涉及 2 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersDelayed ischaemic neurological deficit✓ Approved
Infections and infestationsCOVID-19Phase III

相关研究文献

PubMedInternational journal of pharmaceutics2026-08-04

Multimodal convolutional neural network for tablet-level dissolution prediction using compression force and UV fluorescent imaging.

Honti Barbara B, Mészáros Lilla Alexandra LA, Szabó-Szőcs Bence B, Nagy Zsombor Kristóf ZK et al.

The prediction of tablet dissolution from in-process data remains a key challenge in pharmaceutical manufacturing, as in vitro dissolution is a critical quality attribute that cannot be measured inline. In this study, a multimodal convolutional neural network (MI-CNN) was developed to predict tablet-level dissolution profiles for immediate-release tablets, combining images taken under UV illumination and compression force. To evaluate the contribution of input selection and feature representation, the MI-CNN was compared with a single-input CNN (SI-CNN) using images only, and a multilayer perceptron (MLP) based on hand-crafted image descriptors and compression force. All models were evaluated on a dataset generated using a Design of Experiments approach, covering multiple compression forces, disintegrant concentrations, and acetylsalicylic acid particle size fractions. The MI-CNN achieved the most consistent performance, with comparable training and validation errors (RMSE: 13.09% and 12.54%, respectively), and demonstrated robust generalization across formulation conditions, including an unseen particle size range. The SI-CNN showed reduced accuracy (RMSEval: 25.41%), particularly in cases where dissolution differences were governed by tablet compaction. The MLP model exhibited excellent training performance (RMSEtrain: 2.94%) but poor generalization (RMSEval: 27.15%), indicating overfitting due to the limited ability of histogram-based features to adequately represent the complexity of the dataset. Model explanation using SHapley Additive exPlanations (SHAP) revealed that both compression force and image-derived features contributed to the predictions. Overall, the results demonstrate that combining process variables with image-based information enables accurate and robust dissolution prediction at the tablet level, supporting data-driven approaches for real-time release testing.

PMID 42546994
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PubMedDrug design, development and therapy2026-08-04

Emerging Roles and Possible Therapeutic Applications of Arachidonic Acid Metabolites in Sepsis and Sepsis-Associated Organ Dysfunction.

Wang Chengpeng C, Jiang Xiaoqing X, Chen Yanke Y, Nan Wenbin W et al.

Sepsis is a life-threatening syndrome characterized by dysregulated immune responses, frequently complicated by multiple organ dysfunction. Despite advances in supportive care, targeted therapies remain lacking, and sepsis remains a considerable global health burden. Increasing evidence indicates that arachidonic acid and its metabolites are critical regulators of inflammation, immune responses, and apoptosis in the pathophysiology of sepsis. Arachidonic acid is metabolized through cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP) pathways, generating diverse eicosanoids with distinct effects. Pro-inflammatory mediators such as prostaglandin E2 (PGE2), leukotriene B4 (LTB4), and, in certain contexts, 20-hydroxyeicosatetraenoic acid (20-HETE) may exacerbate vascular leakage, oxidative stress, and organ dysfunction. Recent studies have revealed that dynamic alterations in arachidonic acid metabolism contribute to cardiac, pulmonary, hepatic, and renal injury in sepsis. This review consolidates current understanding of arachidonic acid metabolic pathways and their role in sepsis-induced organ injury. Targeting arachidonic acid metabolism-particularly inhibition of COX/LOX-derived eicosanoids or stabilization of protective epoxyeicosatrienoic acids (EETs)-may offer promising therapeutic strategies. Understanding the context-dependent roles of arachidonic acid metabolites may support future biomarker development, patient stratification, and targeted therapeutic strategies for sepsis and sepsis-associated organ dysfunction.

PMID 42548996
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PubMedMicrobial cell factories2026-08-04

Adaptive laboratory evolution of Saccharomyces cerevisiae enhances butyric acid tolerance and enables co-cultivation with Clostridium tyrobutyricum.

Oehlenschläger K K, Bauschatz S S, Schepp E E, Holtmann D D et al.

Adaptive laboratory evolution (ALE) was successfully applied to improve the tolerance of Saccharomyces cerevisiae toward butyric acid, enabling its use in co-culture with Clostridium tyrobutyricum for the simultaneous production of ethanol and butyric acid as ester precursors. S. cerevisiae was adapted through serial transfer at progressively increasing butyric acid concentrations up to 20 g L⁻1. The evolved yeast population exhibited significantly enhanced butyric acid tolerance and maintained ethanol production under acid-stress conditions. Interestingly, the evolved population also displayed increased maximum glucose consumption rate and ethanol productivity under non-stress conditions. Whole-genome variant analysis was performed by comparing the wild-type strain, an intermediate evolved population and the final evolved population obtained during ALE. The results suggest that adaptation may be associated with changes in regulatory processes, cellular homeostasis, and membrane and cell wall remodeling. The co-culture with the acid producer C. tyrobutyricum demonstrated efficient and balanced substrate utilization, indicating a stable division of labor between the two organisms. Fed-batch cultivation yielded 20.31 ± 2.43 g L⁻1 butyric acid and 28.18 ± 3.37 g L⁻1 ethanol. With the evolved yeast, ethanol concentrations increased fourfold compared to those achieved with the wild-type strain in previous studies, underscoring the potential of ALE to overcome limitations in co-culture systems.

PMID 42547894
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PubMedLife sciences2026-08-04

Ascorbic acid attenuates obesity induced myogenic impairment in C2C12 cells.

Pinto Joel Rimson JR, K Deepika Bhat DB, Bose Bipasha B, Sudheer Shenoy P P

Obesity is commonly associated with skeletal muscle atrophy and is attributed to chronic inflammation, oxidative stress, and impaired adipose-muscle cross talk. Ascorbic acid, a potent antioxidant and its role in obesity induced muscle atrophy is not clearly understood. Hence, the aim of the study was to rescue obesity induced skeletal muscle atrophy with ascorbic acid in vitro. C3H10T1/2 mesenchymal stem cells were developed into obesogenic adipocytes by palmitic acid treatment to generate obesogenic adipocyte-conditioned media (ObCM). C2C12 myoblasts and differentiated myotubes were treated with ObCM in the presence or absence of ascorbic acid (AsA). Cell viability and reactive oxygen species generation were evaluated by MTT assay and DCFDA staining. Gene and protein expression analyses were performed using quantitative real-time PCR and western blotting. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test. In the present study, we have established a palmitic acid induced hypertrophic adipocyte model using C3H10T1/2 mesenchymal stem cells and generated obese conditioned medium to replicate obese microenvironment. Differentiated C2C12 myotubes when exposed to obese conditioned media resulted in reduced myotube diameter, increased expression in ROS, inflammatory cytokines, activation of ubiquitin proteasome system and upregulated muscle atrophy genes. Treatment with Ascorbic acid significantly mitigated ROS generation, reduced inflammatory cytokines, and restored myogenic protein expression associated with modulation of NF-κB signalling. Our findings suggest that ascorbic acid alleviates adipocyte-derived inflammatory stress and protects against myotube atrophy, highlighting its therapeutic potential in obesity-associated muscle wasting.

PMID 42547010
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PubMedFood chemistry2026-08-04

Multi-omics analysis provides mechanistic insights into tanninase-assisted flavor evolution in Phyllanthus emblica L. wine.

Chen Jie J, Zhang Xinyong X, Liu Ni N, Chen Xujie X et al.

Winemaking from Phyllanthus emblica L. is limited by astringency and tannin-associated instability. This study evaluated tanninase pretreatment followed by Saccharomyces cerevisiae fermentation for improving tannin-rich P. emblica L. wine. Metagenomics, LC-MS, and HS-SPME-GC-MS were used to characterize microbial succession and metabolite profiles. A total of 231 non-volatile metabolite features and 183 volatile flavor compounds were putatively annotated. Tanninase pretreatment reduced tannin content from 0.23% to 0.15% before inoculation and was associated with increased ellagic acid, suggesting partial hydrolysis of hydrolysable tannins. The NF group showed higher S. cerevisiae abundance, reaching 77.64%, and altered phenolic, organic acid, fatty acid, amino acid-related, and aroma-related metabolite profiles. Microbial-metabolite analysis suggested that aromatic amino acid metabolism may contribute to floral and fruity ester formation through the Ehrlich pathway. Sensory evaluation showed reduced bitterness/astringency, clearer appearance, and improved overall quality in NF wine.

PMID 42546623
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PubMedPhysiological reports2026-08-04

Amino acid homeostasis in the kidney: Physiological roles and pathological dysregulation.

Liu Shuo S, Shi Caifeng C, Zhou Yang Y, Dai Chunsun C

Amino acids are fundamental to life as protein building blocks and key regulators of metabolism and signaling. The kidney plays a critical, yet underappreciated, role in amino acid homeostasis through three interconnected pillars: selective glomerular filtration, efficient tubular reabsorption, and metabolic processing, which includes de novo synthesis and interconversion of amino acids, as well as their catabolism for energy production and gluconeogenesis. These processes are tightly coupled to systemic acid-base regulation, gluconeogenesis, and whole-body nitrogen clearance. When kidney function declines, the resulting alterations in amino acid profiles are not merely passive markers of reduced filtration but are increasingly recognized as potential mediators that may actively contribute to disease progression, as supported by a growing body of preclinical and clinical evidence. This Review synthesizes current knowledge on renal amino acid homeostasis and proposes four dysregulation patterns in kidney disease: metabolic rewiring, branched-chain amino acids paradox, uremic toxin accumulation, and organelle dysfunction. We further discuss emerging therapeutic strategies aimed at restoring amino acid homeostasis, including dietary modulation, pharmacological targeting of metabolic enzymes and transporters, and microbiome-directed interventions. Finally, we identify key unanswered questions that should guide future research in this rapidly evolving field.

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