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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
来源： ClinicalTrials.gov, Boehringer Ingelheim International GmbH

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

PubMedJournal of fungi (Basel, Switzerland)2026-07-27

Transporter Engineering for Enhancing Citric Acid Production in Aspergillus niger.

Li Jie J, Li Mingyang M, Song Yan Y, Xu Zeyu Z et al.

The efficient industrial production of citric acid by A. niger requires overcoming the limitations of substrate uptake and citrate export on the citrate synthesis efficiency. This study addresses these obstacles using a transporter engineering strategy, modifying the endogenous high-affinity glucose transporter MstF and citrate exporter CexA. The "push-pull" strategy was used to improve citric acid production by increasing glucose import and citrate export. A single overexpression of mstF improved citric acid production, reaching 179.35 g/L in the H7 strain. However, cexA high expression impaired dense mycelium pellet formation and affected the expression of key genes, resulting in reduced citric acid production. For balancing intracellular accumulation and secretion of citrate, simultaneous overexpression of mstF and cexA increased citric acid production and efficiency. In a 30 L fermenter, strain A5 achieved a citric acid titer of 185.91 g/L, a productivity of 3.21 g/h/L, and a shortened fermentation cycle. Collectively, these results provide a reference for the industrial production of citric acid and other organic acids.

PMID 42506234
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PubMedAnatolian journal of cardiology2026-07-27

Composite Uric Acid Index for Prediction of Significant Coronary Stenosis on Computed Tomography Angiography.

Çamkıran Volkan V, Us Gediz Doğay GD, Aksoy Eray E, Kılıç Şahhan Ş et al.

A recently proposed uric acid index combining fasting glucose, triglycerides, and uric acid has shown promise in cardiovascular risk stratification. It was assessed whether the index could predict significant coronary artery stenosis (≥50%) on coronary computed tomography (CT) angiography and compared its diagnostic performance with serum uric acid. In this retrospective, single-center study, 258 adults who underwent coronary CT angiography between January 2023 and December 2024 were included. Coronary calcification was scored using the Agatston method by 2 cardiologists. Clinical, demographic, and laboratory data were collected. The uric acid index was calculated as Ln [triglycerides × uric acid × glucose/2]. Univariable and hierarchical multiple logistic regression analyses were performed. Seventy-one patients (27.5%) showed ≥50% stenosis. Those with stenosis were older and had higher Agatston scores, creatinine, uric acid, glucose, HbA1c, and lower high-density lipoprotein cholestrol (HDL-C). In the final multiple models adjusted for age, sex, creatinine and Agatston score, the uric acid index remained a strong independent predictor of ≥50% stenosis (odds ratio [OR] = 1.988, P = .019, 95% confidence interval [CI] = 1.117-3.538). The index demonstrated significant incremental predictive value over the base model, with a Net Reclassification Improvement (NRI) of 0.500 (P < .05) and an Integrated Discrimination Improvement (IDI) of 0.029. The area under the curve for the uric acid index (0.688) exceeded that of uric acid (0.664). In a real-world coronary CT angiography cohort, the composite uric acid index independently predicted significant coronary stenosis. Its incremental predictive value requires validation in larger, prospective studies.

PMID 42505007
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PubMedAIDS (London, England)2026-07-27

Altered bile acid metabolism in people with HIV correlates with systemic and intestinal inflammation.

Irwin Sophie S, Elliott Julie J, Li Fan F, Ruiz Paola P et al.

To examine associations between plasma bile acids, systemic and gut inflammation, and intestinal bile acid receptor expression in people with HIV (PWH). Retrospective case-control study using paired plasma and colorectal biopsy samples from adults with and without HIV. Samples from 31 PWH and 21 people without HIV (PWOH) were analyzed. Plasma bile acids were quantified by targeted liquid chromatography-mass spectrometry (LC-MS) and cytokines by multiplex assays. Bile acid receptors farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) were quantified in gut tissue by quantitative reverse-transcriptase (qRT)-PCR, and immunohistochemistry with digital image analysis to localize receptor expression. Intestinal inflammation was assessed by histopathology. Group comparisons, multivariable regression, and Pearson correlations were used to evaluate relationships among bile acids, inflammation, and receptor expression. Decreased levels of the primary bile acid chenodeoxycholic acid [P < 0.001, false discovery rate (FDR) = 0.002] as well as decreased levels of conjugated secondary bile acids glycochenodeoxycholic acid (P < 0.001, FDR=0.001), and taurochenodeoxycholic acid (P = 0.007, FDR = 0.02), and glycoursodeoxycholic acid (P = 0.008, FDR = 0.02) were observed in PWH. Antiretroviral therapy may also be a contributor to bile acid alterations with decreased glycodeoxycholic acid (P = 0.02, FDR = 0.19). There was no difference in FXR expression in the gut, but PWH had higher TGR5 expression (P < 0.001), which correlated with intestinal inflammation histopathology scores (r = 0.56, P = 0.004). PWH had decreased plasma primary and secondary bile acids. In addition, PWH had higher TGR5 expression in the gut, which correlated with intestinal inflammation. Reduced anti-inflammatory bile acid signaling may be one potential mechanism contributing to ongoing inflammation in HIV.

PMID 42504576
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PubMedGels (Basel, Switzerland)2026-07-27

A Coupled Model of Acid Transport, Gel Cleanup, and Fracture Propagation in Prepad Acid Fracturing.

Zhang Weiyou W, Sun Yongpeng Y, Meng Xianghua X, Dou Rutong R

In conventional hydraulic fracturing of low-permeability sandstone reservoirs, polymer-gel leak-off creates low-permeability filter cakes that impair productivity. This study proposes a prepad acid fracturing technique using a fluoroboric acid (HBF4) pre-flush to dissolve gel residues and mineral fines. A fully coupled mathematical model integrates HBF4 hydrolysis kinetics, multi-mineral surface reactions, porosity-permeability evolution via the Panda-Lake model, and dynamic leak-off coefficient feedback. Simulations show HBF4 decreases monotonically along the fracture while HF peaks at 40-60 m from wellbore. Acid concentration in the leak-off zone decays exponentially, defining a gel-dissolution zone within 0.5 m of the fracture wall. Acid dissolution increases near-wall porosity to 12-15% and permeability to 2.5-3.5 mD (3- to 4-fold). The leak-off coefficient varies dynamically: high in the acid-dominated zone (1.5-2.2 × 10-3 m/√min) favoring gel dissolution, and low in the gel-dominated zone (≈0.8 × 10-3 m/√min) promoting fracture extension. Compared with conventional polymer gel fracturing, the proposed method achieves a 15.9% higher stimulation ratio and 22.5% higher productivity after 100 days, despite slightly shorter fractures. The core advantage is restoring leak-off zone permeability from 0.45 mD to 0.85 mD and increasing gel filter cake permeability from 8 × 10-4 mD to 0.1 mD, with an average relative error of 8.2% against experimental data. These findings provide theoretical guidance for optimizing prepad acid fracturing in gel-damaged low-permeability sandstones.

PMID 42505304
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PubMedMetabolites2026-07-27

Bile Acid Metabolism in Gout Pathogenesis from Gut-Liver-Joint Crosstalk to Therapeutic Opportunities.

Chen Beiyan B, Chen Xin X, Li Jing J, Gao Shuang S et al.

Beyond their established role in lipid digestion, bile acids function as key metabolic and immune signaling molecules. This review synthesizes recent advances in bile acid metabolism within the context of gout and hyperuricemia, proposing a gut-liver-joint crosstalk framework. Dysregulated bile acid metabolism-characterized by a reduced total bile acid pool, decreased hydrophobic secondary bile acids, elevated 12α-hydroxy bile acids, and impaired enterohepatic circulation-has been mechanistically linked to both hepatic urate overproduction via the PPAR-α/xanthine oxidase pathway and monosodium urate crystal-induced NLRP3 inflammasome activation, although human causal evidence remains to be established. The nuclear receptor FXR suppresses NLRP3 at the transcriptional level, while the membrane receptor TGR5 acts post-translationally through Cyclic adenosine monophosphate/Protein Kinase A (cAMP/PKA) and Glucagon-like peptide-1 (GLP-1) signaling. Gut microbiota dysbiosis amplifies these abnormalities through a vicious cycle of reduced bile acid signaling, increased intestinal permeability, and systemic endotoxemia. Based on these insights, we summarize five therapeutic strategies: FXR modulators, TGR5 agonists, microbiota-based interventions, natural products, and ursodeoxycholic acid replacement therapy. Future research should prioritize gout-specific preclinical models, clinical trials of TGR5 agonists, standardized microbiota-based therapies, dual-target molecules, and personalized patient stratification based on bile acid profiles.

PMID 42506417
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PubMedInsects2026-07-27

Regional Soil and Soybean-Associated Bacterial Communities Are Linked to Larval Nutritional Composition in the Edible Insect Clanis bilineata tsingtauica.

Li Zong-Nan ZN, Li Qing-Yi QY, Wu Qiu-Lin QL, Cui Su-Fen SF et al.

Regional soil conditions may affect edible insect nutrients through associated changes in host plants and bacterial communities, but these relationships remain poorly understood. Here, we compared soils, soybean leaves, larval gut bacteria, and nutritional composition of Clanis bilineata tsingtauica across three sites. Soil nutrient parameters were measured before and after larval inoculation, bacterial communities were analyzed in soil, leaves, and larvae, and larval amino acid, protein, and fatty acid profiles were determined. Available potassium increased 1.17-fold in Lianyungang; several nutrients decreased in Huaian, whereas soil pH decreased by 4.0% in Nanjing. Larvae from Lianyungang contained higher levels of several amino acids (Serine, Glycine, etc.), whereas those from Huaian had higher saturated and unsaturated fatty acid contents (Stearic acid, Elaidic acid, etc.). Genus-level overlap analysis showed partial taxonomic overlap among soil, leaves, and larvae, and the number of shared genera generally declined from soil to leaves to larvae, consistent with compartment-specific filtering. Correlation analyses further indicated that soil nutrients, especially available phosphorus and available potassium, were significantly correlated with dominant bacterial genera and with specific larval amino acid and fatty acid traits. Overall, these findings suggest that regional soil background is associated with coordinated variation in soybean-associated bacteria, larval gut bacteria, and the nutritional composition of C. bilineata tsingtauica larvae.

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