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Adenosine (adenosine, Sanofi / Adenoscan inj / Adenosine, Pfizer)

✓ Approved

Astellas Pharma · 小分子 · 小分子

什么是 Adenosine？

Adenosine 是一种小分子，由Astellas Pharma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adenosine, Sanofi, Adenoscan inj, Adenosine, Pfizer
公司Astellas Pharma
药物类别小分子, 影像药物
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Astellas Pharma

治疗适应症

Adenosine 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
Cardiac disordersArteriosclerosis coronary artery✓ Approved
Hepatobiliary disordersHepatic ischaemia✓ Approved

相关研究文献

PubMedCells2026-10-26

Adenosine-A2 Receptor Signaling in Astrocytes Mitigates Cerebral Ischemic Injury via Suppressing Glutamate-Induced Excitotoxicity.

Yuan Cheng C, Chen Jixin J, Chen Yazhi Y, Cui Liyuan L et al.

Excitotoxicity constitutes a core pathological mechanism in cerebral ischemia and other central nervous system disorders. Astrocytes serve as pivotal regulators of glutamate-glutamine cycle homeostasis and thereby play a critical role in mitigating excitotoxicity. This study established a rat thromboembolic stroke model via autologous thrombus induction and systematically investigated the mechanisms underlying adenosine-mediated neuroprotection through pharmacological modulation of the adenosine pathway using adenosine, dipyridamole, and selective adenosine receptor antagonists. Subsequently, light-sensitive opsin expression in astrocytes was driven by the GFAP promoter, enabling cell-type-specific optogenetic modulation of astrocyte activity. Our findings demonstrate that adenosine significantly attenuates cerebral injury in a rat model of thromboembolic stroke, with astrocytes identified as the primary cellular target. Adenosine elicits an anti-excitotoxic effect by coordinately upregulating GLT-1 protein expression and downregulating Cx43 protein expression in astrocytes, thereby regulating glutamate transport and diffusion. Moreover, our findings demonstrate that adenosine-mediated neuroprotection is significantly attenuated by SCH58261 but not by PSB1115. We conclude that the adenosine-A2A receptor system plays a critical role in the regulation of glutamate homeostasis.

PMID 42929887
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PubMedDiseases (Basel, Switzerland)2026-10-26

Elevated Adenosine Kinase and Decreased ENTPD1 mRNA Levels in Peripheral Blood Leukocytes of Patients with MASLD Differentiate Metabolic Dysfunction-Associated Steatohepatitis from Hepatic Steatosis.

Kurbatova Irina I, Zhulai Galina G, Dudanova Olga O, Topchieva Lyudmila L

Background: Adenosine kinase (ADK) and the ectonucleotidases CD39 and CD73 regulate adenosine metabolism and play important roles in the pathogenesis of liver diseases. Their involvement in metabolic dysfunction-associated steatotic liver disease (MASLD) remains insufficiently characterized, particularly in humans. This study aimed to comparatively analyze ADK levels, the mRNA levels of the long and short ADK isoforms and the ENTPD1, NT5E, and ADORA2A genes in peripheral blood leukocytes (PBLs), and the proportion of CD39- and CD73-expressing cells in the blood of healthy individuals and patients with different forms of MASLD (hepatic steatosis (HS) and metabolic dysfunction-associated steatohepatitis (MASH)). Methods: Blood samples were obtained from 42 healthy individuals and 98 patients with MASLD. ADK and cytokine levels were measured by ELISA. mRNA levels were determined by RT-PCR. The proportions of CD39- and CD73-expressing cells were determined by flow cytometry. Results: Patients with HS and MASH differed in ADK concentration and relative ENTPD1 gene expression in PBL. Compared with HS, MASH was characterized by higher ADK concentrations and lower ENTPD1 mRNA levels, both of which showed potential for distinguishing MASH from HS: ADK, AUC = 0.764 (95% CI, 0.637-0.892; p = 0.001); ENTPD1 mRNA, AUC = 0.649 (95% CI, 0.546-0.752; p = 0.007). Patients with MASLD, including those with HS and MASH, had lower proportions of CD39+ monocytes than controls, whereas the proportions of CD4+CD39+ T helper cells did not differ significantly between the groups. Conclusions: ADK levels in PBLs may be associated with the presence and activity of inflammation in MASLD. Compared with patients with HS and healthy controls, patients with MASH had elevated ADK levels and lower relative levels of ENTPD1 transcripts in PBLs. The latter finding may be related to the reduced proportion of CD39+ monocytes.

PMID 42929999
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PubMedJournal of medical case reports2026-10-26

High-dose regular insulin as a potential rescue therapy in severe aluminum phosphide poisoning: a case report.

Sedaghattalab Moslem M, Akbari Ghaidafeh G

Aluminum phosphide (rice tablet) can cause cardiocirculatory collapse and has negative cardiac inotropic effect. Positive inotropic effect of insulin on the cardiac myocytes is through calcium flux. Insulin increases the intramyocytes calcium concentration by increasing conductance of calcium through the L-type calcium channels and by increasing intramyocytes concentration of cyclic adenosine monophosphate. In addition to increasing the intramyocytes calcium level, insulin also enhances the responsiveness of the cardiac cells to calcium. High-dose insulin is a potential therapy for hypodynamic and hypotensive septic shock due to its positive inotropic qualities. In this paper, a critical aluminum phosphide poisoning patient (a 25-year-old Iranian young woman), presented with mixed severe metabolic acidosis and respiratory alkalosis, tachypnea, tachycardia, and hypotension. In contrast to our previous experiences that ingestion of aluminum phosphide tablets associated with multiple organ failure and severe shock in approximately all critical poisoning patients, early initiation of high-dose intravenous regular insulin for this patient prevented multiorgan dysfunction and death. Treatment with high-dose intravenous insulin associated with IV fluids, sodium bicarbonate, hydrocortisone, potassium, dextrose therapy and supportive care resolved completely signs and symptoms of patient after 3 days in ICU. High-dose intravenous regular insulin may be act as a rescue therapy for aluminum phosphide poisoning patients. While this single case suggests a potential benefit, further studies are required to confirm these findings.

PMID 42928247
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PubMedCureus2026-10-26

Ticagrelor-Induced Bradyarrhythmias in Acute Coronary Syndrome: A Case Series of Three Patients.

Molleti Ashish A, Sankaran Ramesh R, Vinod Kumar Balakrishnan B, Arul Judah N JN

Ticagrelor is a reversible oral P2Y12 receptor inhibitor recommended in preference to clopidogrel for most patients with acute coronary syndrome. In addition to inhibiting platelets, it raises extracellular adenosine, which is thought to explain its underappreciated capacity to cause bradyarrhythmia. We report three consecutive patients with acute coronary syndrome who developed serious bradyarrhythmias after ticagrelor administration. The first, a 58-year-old woman treated with a drug-eluting stent to the left anterior descending artery, developed high-grade atrioventricular block with asystolic pauses that required a temporary pacing wire, after which ticagrelor was stopped, prasugrel was substituted, and she recovered. The second, a 48-year-old woman with an anterior myocardial infarction, had a cardiac arrest with complete heart block after ticagrelor loading, was resuscitated, paced temporarily, switched to prasugrel, and recovered. The third, a 77-year-old man with an inferoposterior and right ventricular myocardial infarction, had recurrent asystole and ventricular arrhythmia that persisted despite switching to prasugrel and required a permanent pacemaker. None of the patients were receiving an atrioventricular nodal blocking drug, and in every patient the treated coronary lesion was patent on a repeat angiogram, which made ongoing ischemia from stent failure an unlikely sole explanation. A formal Naranjo assessment rated the association as possible in each case. A ticagrelor-induced adverse effect should be considered in any patient who develops unexplained bradycardia or syncope after its administration. Early rhythm monitoring and prompt withdrawal are the key steps, and although the rhythm usually recovers, permanent pacing may be needed when conduction disease is superimposed on ischemic injury to the conduction system.

PMID 42928934
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PubMedACS sensors2026-10-26

Bivalent Ligand-Aptamer Binding-Cooperated Hybridization Assembly for Illuminating Ratiometric Fluorescence Biosensing of Convertible Ag Nanoclusters.

Long Min M, Chen Xiaoyu X, He Maolan M, Fu Yuchen Y et al.

To address low affinity and reaction rate in monovalent ligand-aptamer binding, herein, we propose a bivalent binding-cooperated hybridization assembly (bbHA) strategy to light up the ratiometric fluorescence of convertible Ag nanoclusters (cAgNC) for detecting adenosine triphosphate (ATP). Two identical repeats of ATP-recognizable aptamer splits (a1 and a2) are separately programmed in an aptamer templating strand (aT) and an aptamer converter strand (aC), while two pairs of cAgNC-clustering and emission-converting segments are tethered in aT (template-a1-a1-template) and aC (converter-a2-a2-converter), respectively. Two tandem red cAgNC emitters are preferably developed in aT. Upon presenting ATP, the affinity recognition by a specific aptamer (a1/a2) entity enables cooperative binding events for triggering rapid complementary hybridization of aT and aC. The other proximal a1/a2 pair is bulged and merged to speed up the second ATP affinity binding. The structurally stable aT·2ATP·aC complex is formed to orient two ended converters and clusters together, thereby modulating its red fluorescence into green through electronic interactions between Ag0 and particular nucleobases. The resulting signal ratio of dual-emissive cAgNC exhibits a linear dependence on ATP, achieving sensitive and accurate quantification via inherent built-in correction. In contrast to the monovalent mechanism, the bbHA-based strategy features superior assay performances such as higher target responsiveness, faster reaction kinetics, and more efficient transduction. Thus, this label-free method would offer a new paradigm to construct simplified, specific, robust, and cost-effective sensing platforms for applicable assay of various small-molecule analytes.

PMID 42928640
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PubMedFood & function2026-10-26

AMPK-dependent mechanisms mediate the protective effects of grape pomace extract in obesity-associated chronic renal disease in mice.

Figueras Tatiana S TS, Cacciamani Valeria E VE, Gil Lorenzo Andrea F AF, Suhaiman Laila L et al.

Obesity-associated kidney disease involves metabolic dysfunction accompanied by lipotoxicity, inflammation, and fibrosis. We previously showed that grape pomace extract (GPE), a polyphenol-rich byproduct of winemaking, exerts renoprotective effects in obese mice; however, the underlying mechanisms remain incompletely understood. This study aims to investigate whether adenosine monophosphate-activated protein kinase (AMPK) mediates the protective effects of dietary GPE supplementation in high-fat diet (HF)-induced obese mice. Male C57BL/6J mice were fed a standard diet (16% calories from fat) or a HF (60% calories from fat) with or without GPE (300 mg per kg body weight per day) for 16 weeks. A subset of animals was treated with compound C (CC), a widely used AMPK inhibitor, during the last 4 weeks. GPE attenuated HF-induced body weight gain, visceral adiposity, dyslipidemia, glucose intolerance, and renal dysfunction, while improving histopathological alterations. Mechanistically, GPE restored renal AMPK phosphorylation, increased autophagy markers (increased LC3-II/LC3-I ratio and Beclin-1 levels) and reduced renal lipid accumulation. In addition, GPE enhanced levels of the mitochondrial biogenesis regulator PGC-1α, while attenuating oxidative stress (Nox4, 4-HNE, and oxidant species production), inflammatory signaling (NF-κB-NLRP3 pathway), and renal fibrosis. Notably, pharmacological AMPK inhibition reversed the GPE effect, leading to worsening of renal injury, autophagy impairment, increased lipid deposition, and exacerbation of fibrotic and inflammatory markers. These findings demonstrate that AMPK activation is a mediator of the metabolic and renoprotective effects of GPE, positioning GPE as a promising functional food ingredient for attenuation of obesity-associated kidney disease.

PMID 42929130
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