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

✓ Approved

Astellas Pharma · Small Molecule · Small Molecule

What is Adenosine?

Adenosine is a small molecule developed by Astellas Pharma. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand Namesadenosine, Sanofi, Adenoscan inj, Adenosine, Pfizer
CompanyAstellas Pharma
Drug ClassSmall Molecule, Imaging Agents
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Astellas Pharma

Therapeutic Indications

Adenosine is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Cardiac disordersArteriosclerosis coronary artery✓ Approved
Hepatobiliary disordersHepatic ischaemia✓ Approved

Related Research Articles

PubMedFrontiers in pharmacology2026-09-19

Effects of adenosine triphosphate and reduced glutathione on biochemical, histopathological and immunofluorescence alterations associated with atezolizumab-induced cardiac tissue injury.

Yasar Yesim Kaya YK, Sezgin Esra Tuba ET, Suleyman Bahadir B, Mammadov Renad R et al.

In this study, the potential protective effects of adenosine triphosphate (ATP) and glutathione (GSH) against atezolizumab-induced cardiac injury in rat heart tissue were investigated. A total of 24 male albino Wistar rats were used in the experiment. The animals were divided into four groups: healthy group adenosine triphosphate + atezolizumab (ATAZ), GSH + atezolizumab (GHAZ), and atezolizumab alone (ATZ). ATP was administered intraperitoneally at a dose of 4 mg/kg, while GSH was administered orally at a dose of 200 mg/kg for 7 days. Atezolizumab was administered intraperitoneally to the experimental groups at a dose of 10 mg/kg twice weekly. At the end of the experiment, malondialdehyde total glutathione (tGSH), superoxide dismutase catalase, interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels in heart tissues were measured using biochemical methods. In addition, histopathological and immunofluorescence examinations were performed. The results showed that oxidative stress and inflammation markers increased, whereas antioxidant parameters decreased in the atezolizumab-treated group. ATP and GSH administration significantly attenuated these changes and exerted protective effects on cardiac tissue. Overall, ATP and GSH ameliorated the biochemical, histopathological, and immunofluorescence changes associated with atezolizumab-induced cardiac injury in this experimental model.

PMID 42761064
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PubMedCardiovascular research2026-09-19

Lysosomal signaling pathways influence heart rhythm, and regulate atrial function.

Akerman Emily E, Capel Rebecca A RA, Rog-Zielinska Eva A EA, Winbo Annika A et al.

In the heart, endogenous nicotinic acid adenine dinucleotide phosphate (NAADP) triggers lysosomal calcium (Ca2+) release to augment sarcoplasmic reticulum (SR) Ca2+ sequestration, producing larger Ca2+ transients. However, the role of lysosomal Ca2+ signals in pacemaker activity, a distinct Ca2+-operated function of the sinoatrial node (SAN), or in the atrial myocardium has not been investigated. Pharmacological or genetic ablation of the NAADP pathway inhibits the spontaneous beating rate response to β-adrenergic stimulation in intact SAN. We found intracellular signaling microdomains between lysosomes and neighboring SR or mitochondria in mouse, and goat tissue. The spatial relationship between lysosomes and other Ca2+-handling organelles are altered in goat atrial fibrillation. Furthermore, we demonstrate atrial myocytes produce 3'-5'-cyclic adenosine monophosphate (cAMP) in response to lysosomal signaling, adding a novel trigger for cyclic nucleotide signaling. Our findings support the hypothesis that lysosomal Ca2+ signaling contributes to regulation of cardiomyocyte cAMP levels and pacemaker activity.

PMID 42760609
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PubMedFrontiers in pharmacology2026-09-19

A PBPK-VBE approach for bioequivalence extrapolation of senaparib capsule strengths in the context of nonlinear pharmacokinetics: bridging from the clinical starting dose to the linear pharmacokinetic range.

Wu Xiaofei X, Wang Ziyang Z, He Yanna Y, Wu Keheng K et al.

Senaparib (Sepalna®), a novel oral poly (adenosine diphosphate -ribose) polymerase (PARP) 1/2 inhibitor, was approved in China in 2025 as maintenance therapy for advanced ovarian cancer. The recommended starting dose is 100 mg once daily, which may be adjusted to 80 mg, 60 mg, or 40 mg to manage adverse events. While conventional bioequivalence (BE) clinical studies established equivalence between the 10 mg and 20 mg capsules strengths at the 100 mg dose level, these findings cannot be extrapolated to the lower dose range due to senaparib's nonlinear pharmacokinetics and the current absence of definitive regulatory guidance for such scenarios. This study aimed to evaluate the bioequivalence between the 10 mg and 20 mg capsule strengths of senaparib, a drug exhibiting nonlinear pharmacokinetics, across the 20-80 mg dose range. We developed and validated an integrated approach combining physiologically based pharmacokinetic (PBPK) modeling with in vitro dissolution data to evaluate virtual bioequivalence (VBE) between the two capsule strengths across the 20-80 mg dose range. Under all evaluated conditions including variations in sample size, intra-individual variability levels, and prandial states (fasted and fed), the geometric mean ratios (GMRs) of key pharmacokinetic (PK) parameters consistently approached 100%, thereby confirming bioequivalence across the specified dosing range. This PBPK-VBE framework provides supportive evidence for bioequivalence bridging of senaparib capsule strengths across the linear dose range, illustrating the potential utility of this approach for formulation bridging when direct clinical BE studies across all dose levels are impractical.

PMID 42761077
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PubMedBrain stimulation2026-09-18

Vagus Nerve Stimulation Exerts Disease-Modifying Effects in Epileptic Rats by Enhancing Hippocampal Adenosine Signalling.

Xiong Zhonghua Z, Zhang Jing J, Gao Ran R, Liu Siqi S et al.

Vagus nerve stimulation (VNS) is an established neuromodulatory therapy for refractory epilepsy, but its disease-modifying mechanisms remain unclear. Adenosine is an endogenous anticonvulsant and a key regulator of epileptogenesis, and adenosine kinase (ADK) controls extracellular adenosine availability. This study investigated whether VNS modifies epilepsy progression by regulating hippocampal adenosine signalling. A pilocarpine-induced rat model of temporal lobe epilepsy was used. Animals were assigned to control, pilocarpine, VNS-treated, VNS 4-4W (4 weeks of active VNS followed by 4 weeks without stimulation), and sham groups. Spontaneous recurrent seizures (SRS) were monitored using video-electroencephalography, and spatial learning and memory were assessed using the Morris water maze. Hippocampal extracellular adenosine dynamics were measured in vivo using the GRABAdo1.0 sensor combined with fibre photometry. ADK and adenosine A1 receptor (A1R) expression levels were evaluated by immunostaining and Western blotting. Acute VNS induced a rapid increase in hippocampal extracellular adenosine levels. In pilocarpine-treated rats, active VNS significantly reduced the frequency and duration of SRS and improved spatial learning and memory compared with time-matched epileptic rats that did not receive active stimulation. These beneficial effects persisted after a 4-week stimulation-free period. VNS also suppressed hippocampal ADK overexpression and restored A1R expression. Furthermore, pharmacological blockade of A1Rs with DPCPX reversed the antiseizure effect of VNS. VNS exerts disease-modifying effects in epileptic rats by enhancing hippocampal adenosine signalling. These effects are associated with VNS-evoked adenosine release, inhibition of ADK overexpression, and restoration of A1R-mediated anticonvulsant signalling.

PMID 42759876
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PubMedACS omega2026-09-18

Inosine Exerts Glioprotective Effects against Lipopolysaccharide-Induced Damage in Primary Astrocyte Cultures: Role of the Adenosinergic System.

Pedra Nathalia S NS, de Aguiar Mayara S S MSS, Teixeira Fernanda C FC, de Mello Julia E JE et al.

Inosine is a purine nucleoside derived from adenosine metabolism that has been associated with neuroprotective and anti-inflammatory properties. The present study investigated the effects of inosine against lipopolysaccharide (LPS)-induced damage in primary astrocyte cultures and explored the potential contribution of adenosinergic signaling to these responses. LPS exposure impaired astrocyte viability and proliferation, altered cholinergic and purinergic enzyme activities, disrupted redox homeostasis, and increased the level of IL-6 release. Inosine treatment attenuated these alterations, restoring cell viability and proliferation, modulating acetylcholinesterase and ectonucleotidase activities, reducing oxidative damage, and preventing the LPS-induced increase in IL-6 levels. Mechanistic studies using pharmacological modulation of the adenosinergic system revealed that blockade of adenosine receptors interfered with some of the antioxidant effects of inosine, particularly those related to antioxidant enzyme activity, whereas its effects on cytokine modulation remained unchanged. Additional experiments using selective A2A receptor antagonists provided preliminary evidence that A2A receptor signaling may be involved in the antioxidant-related effects observed under inosine-treated conditions. Collectively, these findings demonstrate that inosine exerts multitarget protective effects in astrocytes, modulating oxidative stress, neurotransmission-related pathways, and inflammatory responses. These results support its potential as a promising strategy for restoring astrocyte homeostasis under neuroinflammatory conditions.

PMID 42756832
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PubMedAnimal models and experimental medicine2026-09-18

Adenosine monophosphate-activated protein kinase activation is associated with suppression of NLRP3 inflammasome-mediated neuroinflammation in a weight-drop model of traumatic brain injury in Sprague-Dawley rats.

Kodi Triveni T, Kumar Paka Sravan PS, Nandakumar Krishnadas K, Kishore Anoop A

Traumatic brain injury (TBI) disrupts adenosine monophosphate-activated protein kinase (AMPK) signaling, impairs energy homeostasis, activates inflammatory pathways, and triggers neuroinflammation. AMPK activators such as metformin (MET), quercetin (QUE), resveratrol (RES), cinnamaldehyde (CIN), and berberine (BER) exhibit anti-inflammatory and neuroprotective properties. However, their role in modulating the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome in TBI-induced neuroinflammation remains unclear. This study investigated the neuroprotective effects of AMPK activators in the weight-drop model of TBI, focusing on suppression of the NLRP3 inflammasome. Rats received an intraperitoneal administration of AMPK activators-MET (100 mg/kg), QUE (15 mg/kg), RES (25 mg/kg), CIN (25 mg/kg), or BER (50 mg/kg)-from days -3 to 17. TBI was induced on day 1 using the weight-drop method (240 g from 1.5 m). Cognitive performance was evaluated using the novel object recognition test and Morris water maze. Neuroinflammatory markers, including nuclear factor kappa B (NF-κB), NLRP3, pro-caspase-1, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and microglial polarization markers (CD86 and CD206), were assessed using Western blotting and enzyme-linked immunosorbent assay (ELISA). Oxidative stress and histopathological changes were also examined. TBI resulted in cognitive impairment, oxidative stress, and neuronal damage; reduced p-AMPK/AMPK ratio; decreased CD206 levels; and elevated the levels of NF-κB, CD86, TNF-α, and NLRP3 inflammasome components (NLRP3, pro-caspase-1, and IL-1β). Pretreatment with AMPK activators significantly improved cognitive deficits, attenuated oxidative stress and neuroinflammation, restored p-AMPK/AMPK ratio, promoted anti-inflammatory effects, and suppressed NLRP3 inflammasome activation. AMPK activators exhibited neuroprotection in TBI by improving cognition and regulating oxidative stress, microglial activation, and NLRP3-mediated neuroinflammation.

PMID 42755401
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