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donepezil (E 2022 / TK023 / TK 023)

✓ Approved

Eisai Co., Ltd. · ACHE · 小分子

什么是 donepezil？

donepezil 是一种小分子，由Eisai Co., Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Transdermal。

药物档案

商品名E 2022, TK023, TK 023
公司Eisai Co., Ltd.
药物类别小分子
分子靶点ACHE
给药途径Transdermal
状态Approved
来源： ClinicalTrials.gov, Eisai Co., Ltd.

作用机制

分子靶点

donepezil 作用于 1 个分子靶点：

ACHEacetylcholinesterase (Cartwright blood group) (N-ACHE, ACEE)
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

donepezil 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
Nervous system disordersDementia Alzheimer's typePhase I

相关研究文献

PubMedThe Analyst2026-10-26

Agricultural waste-derived sweat sensor integrated into wettability-tunable microfluidics for noninvasive metabolic evaluation.

Guo Shuyi S, Wang Haixu H, Bo Xiangjie X

Wearable sweat patches allow real-time and noninvasive monitoring of metabolism through sweat biomarker analysis. However, challenges related to sweat collection efficiency and the lack of sustainable sweat sensors impede the widespread adoption of sweat analysis. Here, we report the design of a wearable sweat patch integrating an agricultural waste-derived sweat sensor for sensitive sweat uric acid (UA) and glucose (Glu) analysis and surface wettability-controlled microfluidics for efficient sweat collection. We evaluate the performance of the wearable patch for the noninvasive monitoring of UA and Glu in sweat. We also validate the usability of the wearable patch in assessing metabolic status in metabolic disorders including gout and diabetes.

PMID 42929105
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PubMedJournal of applied biomaterials & functional materials2026-10-26

Arbutin/kojic acid-loaded MHA hydrogel array patches attenuate UVB-induced epidermal hyperplasia and remodeling-associated responses.

Lee Seung-Min SM, Cha Sangryul S, Jeon DooLee D, Choi Wooseok W et al.

Acute ultraviolet B (UVB) exposure induces epidermal hyperplasia, pigmentation-related responses, and early extracellular matrix remodeling. Topical tyrosinase inhibitors, including arbutin and kojic acid, can have limited residence on damaged skin. Here, we evaluated a skin-conformal composite patch comprising aligned polyurethane nanofiber membranes integrated with methacrylated hyaluronic acid (MHA) hydrogel arrays loaded with arbutin or kojic acid. Seven-week-old Hairless Mouse, Strain 2 (HRM2) mice were assigned to six groups: control (CTL), UVB only (UV), UVB plus topical arbutin (UVA), UVB plus topical kojic acid (UVK), UVB plus arbutin-loaded MHA patch (UV-A-MHA), and UVB plus kojic acid-loaded MHA patch (UV-K-MHA). Dorsal skin received a single UVB dose (200 mJ/cm2), was treated immediately, and was analyzed on Day 4. Drug-loaded MHA patch treatment attenuated UVB-induced epidermal thickening and was associated with qualitative differences in dermal matrix organization, while direct comparisons with the corresponding freely applied formulations varied across endpoints. These histological findings were evaluated using hematoxylin and eosin, Masson's trichrome, Picro-Sirius Red, and Fontana-Masson staining. GFP-loaded MHA hydrogels remained detectable in the epidermis and upper dermis through Day 4, supporting local cargo retention under skin-contact conditions. Preliminary HPLC-UV analysis detected arbutin and kojic acid parent peaks in MHA formulations before and after 60 s of UV exposure. Patch treatment was associated with significant reductions in α-smooth muscle actin and vimentin, whereas effects on SMAD phosphorylation differed between the two drug formulations, without detectable changes in body weight or serum TNF-α and IL-6. Because the main experiment lacked drug-free MHA patch and bandage-only controls, scaffold-, occlusion-, and drug-specific effects could not be fully separated. These findings support aligned nanofiber-supported MHA hydrogel arrays as functional biomaterial patches for localized cutaneous delivery and modulation of acute UVB-induced remodeling-associated responses.

PMID 42929246
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PubMedGels (Basel, Switzerland)2026-10-26

Engineering Smart Hydrogels Through Dynamic Polymer Networks for Controlled Drug Delivery.

Choi Chanju C, Seo Dongseong D, Kim Taeho T, Park Jonghyun J et al.

Smart hydrogels are increasingly explored as adaptive platforms for controlled drug delivery because their polymer networks can respond dynamically to chemical, biological, and physical cues. Among these systems, dynamic polymer networks formed through reversible covalent and noncovalent interactions provide a unique means of coupling molecular-scale bond exchange with time-dependent changes in hydrogel structure, mechanics, degradation, and therapeutic transport. This review presents an integrated framework linking dynamic crosslink chemistry, exchange kinetics, network properties, and drug-release behavior. Dynamic covalent, supramolecular, metal-ligand, and hybrid network strategies are compared with particular emphasis on how crosslink lifetime, mesh accessibility, swelling, viscoelasticity, stress relaxation, and degradation govern therapeutic cargo loading, retention, diffusion, and release. Representative release mechanisms and kinetic models are discussed together with cargo-specific design considerations for small molecules, proteins and peptides, nucleic acids, and nanoparticle-based therapeutics. Biomedical applications are further considered according to therapeutic requirements and administration routes, including injectable local depots, topical and transdermal delivery, and regenerative systems. Finally, key translational challenges involving physiological complexity, biocompatibility, reproducibility, scale-up, sterilization, and storage stability are critically assessed. By connecting molecular interaction dynamics with network-level behavior and therapeutic performance, this review provides design principles for developing more predictable, programmable, and clinically translatable dynamic hydrogel drug-delivery systems.

PMID 42929917
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PubMedJournal of tropical medicine2026-10-26

Green-Synthesized Silver Nanoparticles Improve Cognitive Function and Modulate Nrf2/HO-1-BDNF-Related Gene Expression in Experimental Chronic Toxoplasmosis.

Khaksarian Mojtaba M, Khalaf Amal Khudair AK, Shojaee Saeedeh S, Shakib Pegah P et al.

This study aimed to evaluate the neuroprotective effects of silver nanoparticles (AgNPs) green-synthesized using the ethanolic extract of Muscari neglectum against Toxoplasma gondii-induced cognitive impairment and to explore the underlying Nrf2/BDNF and oxidative stress-related mechanisms. Chronic toxoplasmosis was experimentally induced in mice using the Tehran strain of T. gondii. Forty-eight mice were randomly allocated into six experimental groups, including a noninfected control group, an infected untreated control group, and four treatment groups receiving pyrimethamine (PYM, 20 mg/kg), donepezil (DON, 2 mg/kg), AgNPs (10 mg/kg), or AgNPs (20 mg/kg). Spatial learning and memory capabilities were assessed using the Morris water maze test. Post-treatment, brain cyst number and size were determined via microscopic examination. Additionally, quantitative real-time PCR was employed to evaluate the expression levels of genes associated with oxidative stress and neuroprotection, including brain-derived neurotrophic factor (Bdnf), NADPH oxidase 2 (Nox2), superoxide dismutase 2 (Sod2), catalase (Cat), glutathione peroxidase 1 (Gpx1), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (Hmox1). Treatment with AgNP resulted in a significant, dose-dependent improvement in behavioral performance, evidenced by reduced escape latency and enhanced exploration of the target quadrant (p < 0.001). Moreover, AgNP administration markedly decreased both the number and size of brain Toxoplasma cysts, with the 20 mg/kg dose demonstrating superior efficacy compared to PYM (p < 0.01). Molecular analyses indicated significant upregulation of Nrf2, Hmox1, Bdnf, Sod2, Cat, and Gpx1, accompanied by downregulation of Nox2 expression in mice treated with AgNP (p < 0.001). These findings suggest that green-synthesized AgNP exert significant, dose-dependent antiparasitic and neuroprotective effects in the context of chronic toxoplasmosis. AgNP notably reduced brain cyst burden, enhanced spatial learning and memory, and normalized oxidative stress-related gene expression. Importantly, AgNP exhibited greater efficacy than both PYM and DON, indicating their potential as a promising therapeutic approach for neurotoxoplasmosis.

PMID 42928771
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PubMedBiosensors2026-10-26

Spectral Optimization of Programmable LED Illumination for Smartphone-Based Colorimetric Biosensor Readout.

Serea Elena E, Donciu Codrin C, Temneanu Marinel Costel MC

Smartphone-based colorimetric biosensor readout is strongly influenced by illumination, yet lighting conditions are often characterized mainly by illuminance rather than by their spectral composition. This study investigates the spectral, photometric, colorimetric, and energetic effects of programmable LED illumination on smartphone colorimetric readout under controlled acquisition conditions. Twenty lighting scenarios were generated using three independently controlled color-capable LED luminaires and characterized by spectral irradiance, illuminance, chromaticity, color rendering, and electrical power. A Samsung Galaxy S20 FE was used to acquire JPEG and RAW images of a standardized 24-patch ColorChecker target used as a controlled colorimetric reference for evaluating the optical readout methodology, and colorimetric deviation was quantified using CIEDE2000. Mean ΔE00 ranged from 11.73 to 42.33 across the investigated scenarios. Two conditions differing by less than 1% in illuminance produced a 37% difference in mean colorimetric error, demonstrating that illuminance alone does not determine readout accuracy. An illuminance-only regression model yielded R2 = 0.819, whereas inclusion of a relative spectral descriptor increased R2 to 0.919. High-output conditions also revealed substantial JPEG clipping despite negligible RAW saturation. These results show that reliable smartphone colorimetric readout requires joint consideration of illumination intensity, spectral composition, electrical demand and image-saturation constraints.

PMID 42930106
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PubMedCardiovascular research2026-10-26

NOR-1 is an upstream regulator of Ca2+ homeostasis and calmodulin kinase II-dependent arrhythmogenesis.

Vázquez-Sufuentes Paula P, Jiménez-Sábado Verónica V, Ballester-Servera Carme C, Casabella-Ramón Sergi S et al.

Dysregulation of NOR-1 has been reported in cardiovascular diseases associated with altered calcium handling. We therefore investigated how NOR-1 affects calcium homeostasis and arrhythmogenesis to identify the underlying mechanisms. We assessed the expression of NOR-1 and calcium regulatory proteins in myocardial samples from humans and mice that overexpress human NOR-1 in the heart (TgNOR-1). Gene promoter activity was determined by transient co-transfection assays. Calcium imaging, patch-clamp recordings and immunofluorescent labeling was performed in mouse cardiomyocytes. Experimental data were used for mathematical modeling. Arrhythmias were induced in vivo by an epinephrine/caffeine challenge. In human cardiac samples, mRNA levels of genes coding for SERCA2a, CASQ2, TN-C1 and PLB correlated with those of NOR-1, while TgNOR-1 mice exhibited higher cardiac levels of these calcium regulatory proteins than wild-type animals (WT). NOR-1 increased luciferase activity driven by the proximal promoter of both human and mouse genes. Calcium transients were smaller in TgNOR-1 cardiomyocytes while L-type calcium current and SR calcium content were unchanged. Mathematical modeling revealed that more calcium binds to CASQ2 and is released from the SR in TgNOR-1 cardiomyocytes, but the resulting calcium transient is smaller because more calcium is buffered by TN-C1. Furthermore, NOR-1 transgenesis increased the level of reactive oxygen species and CAMKII oxidation, as well as RyR2 phosphorylation at Ser-2814, which led to a higher incidence of calcium waves and afterdepolarizations in resting TgNOR-1 cardiomyocytes. In electrically paced myocytes, NOR-1 transgenesis promoted extra-transients at low frequencies and calcium alternans at high frequencies. Importantly, these derangements in intracellular calcium handling concurred with a dramatic increase in epinephrine/caffeine-induced bidirectional ventricular tachycardia in TgNOR-1 mice. Moreover, the antioxidant N-acetylcysteine and the CAMKII inhibitor KN-93 attenuated arrythmia in TgNOR-1 mice and arrhythmogenic calcium release in isolated myocytes. Our findings highlight NOR-1 as an upstream regulator of CAMKII-oxidation underlying arrhythmia induced by defective calcium homeostasis, pointing to therapies targeting CAMKII as a means to attenuate arrhythmia triggered by pathological upregulation of NOR-1.

PMID 42929040
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