Drug Database
AD

AD-201 (AD 201 / AD201)

✓ Approved

Addpharma · Small Molecule · Small Molecule

What is AD-201?

AD-201 is a small molecule developed by Addpharma. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesAD 201, AD201
CompanyAddpharma
Drug ClassSmall Molecule
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Addpharma

Therapeutic Indications

AD-201 is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

Related Research Articles

PubMedFrontiers in aging neuroscience2026-07-25

Relationship between executive function and activities of daily living in Alzheimer's disease: a study based on the stop-signal task.

Gao Manman M, Yan Yibing Y, Wu Yue Y, Geng Zhi Z et al.

Early clinical manifestations of Alzheimer's disease (AD) include an apparent decline in memory and executive function. Executive function is closely related to activities of daily living (ADL) and is important for maintaining an independent, high-quality lifestyle. This study aimed to explore the executive control ability and neuromechanisms of AD patients through stop-signal task (SST) elicited event-related potentials (ERPs) and their relationship with ADL. Thirty-six patients with AD and 36 sex and age matched healthy controls (HCs) were recruited. Electroencephalography (EEG) data recorded during the SST was compared between groups, and SST-related indicators were determined to assess executive control ability in AD patients. The relationship between ADL and SST-related indicators was explored. We performed Receiver Operating Characteristic (ROC) analysis on SST- and EEG-related indices. Differences in the following indices were found between the two groups: Go accuracy (P< 0.001), Go omissions (P< 0.001), Go errors (P< 0.001), Go error reaction time (RT) (P< 0.001), failed stop RT (P = 0.021), all accuracies (P = 0.005), mean amplitude of N300 (P = 0.043), peak amplitude of N300 (P = 0.043), and peak latency of N300 (P< 0.001). And Go accuracy (r = -0.603, P = 0.005) and all accuracy (r = -0.624, P = 0.003) in the AD group were negatively partially correlated with ADL. These SST- and EEG-related indicators had an Area Under the Curve of 0.771 and 0.831, both of which could be used to jointly diagnose AD (both P< 0.001). This study suggests that the worse the executive function of AD patients, the more serious the ADL impairment. AD patients have electrical abnormalities associated with executive control. Different SST- and EEG-related indicators can be used to diagnose AD. This provides a new avenue for further elucidation of the pathological mechanisms of AD.

PMID 42499555
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PubMedNeuroprotection (Chichester, England)2026-07-25

Circadian rhythms and chronotherapy in Alzheimer's disease: Mechanisms and therapeutic implications.

Singh Bivek B, Pigazzani Filippo F, Manfredini Roberto R

Alzheimer's disease (AD), the most prevalent form of dementia, has been increasingly associated with disruptions in circadian rhythms and sleep-wake regulation. This narrative review synthesizes recent literature on how circadian dysfunction may contribute to AD pathogenesis, biomarker profiles, and treatment response. Mechanistic studies suggest important interactions between core clock genes and neurodegenerative cascades involving oxidative stress, neuroinflammation, glial reactivity, and proteostasis. Disruptions in circadian-regulated molecular pathways, including brain and muscle ARNT-like 1 (BMAL1)-sirtuin 1 (SIRT1), nuclear factor kappa B (NF-κB)-NOD-like receptor family pyrin domain containing 3 (NLRP3), and period circadian regulator 2 (PER2)-antioxidant signaling pathways, may compromise neuronal resilience and worsen AD-related pathology. Emerging evidence also suggests distinct circadian patterns in AD-relevant biomarkers, including melatonin, cortisol, orexin, core body temperature, blood-brain barrier permeability, and glial marker oscillations. These rhythmic patterns may have diagnostic and prognostic relevance and support the need for time-aware biomarker interpretation. Chronotherapeutic strategies targeting circadian biology, including melatonin receptor agonists, light therapy, time-restricted feeding, and circadian-aligned drug delivery systems, may help improve targeted clinical endpoints in AD. This review also discusses chronoepigenetics as an emerging area in which clock-regulated epigenetic modifications may influence neurodegenerative trajectories. Future directions include next-generation chronotherapeutic targets, such as glial clocks, clock-gated inflammatory mechanisms, and systemic comorbidities with circadian modulation, including diabetes and hypertension. Overall, the available evidence supports a close association between circadian disruption and both AD pathology and therapeutic response, while also highlighting important gaps in large-scale clinical trials. This time-oriented perspective may support the development of personalized, biomarker-guided, and rhythm-informed approaches to AD care. By bridging chronobiology and neurodegeneration, this review highlights how circadian precision medicine may refine future approaches to understanding and managing AD.

PMID 42499341
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PubMedFrontiers in cardiovascular medicine2026-07-25

Mechanistic study of ARHGAP27 promoting the progression of aortic dissection by regulating the RhoA/ROCK/YAP pathway.

Wang Zijie Z, Tao Jing J, Yang Yining Y

Aortic dissection (AD) is a life-threatening cardiovascular disease. ARHGAP27 can regulate cytoskeleton and cellular functions, which may be related to the phenotypic switching of vascular smooth muscle cells (VSMCs) in AD. However, the role of ARHGAP27 in AD has not been reported yet. The AD-related data sets were downloaded from GEO database to screen differential genes. HE and IHC staining was used to detect the pathological changes and the expression level of ARHGAP27 in AD tissue. AD cell models were constructed in vitro by inducing HAVSMCs with PDGF-BB to evaluate the effects of ARHGAP27 overexpression or knockdown on cell survival, migration, invasion and phenotypic switching. Rescue experiments were performed using the ROCK activator LPA to test pathway specificity. ARHGAP27 was significantly upregulated in the dataset and the tissue. In vitro experiments have shown that overexpression of ARHGAP27 can further promote the survival, migration and invasion of VSMCs, and the expression of synthetic phenotypic proteins MMP2 and MMP9, and inhibit the expression of contraction phenotypes α-SMA and SM22α. Knockdown of ARHGAP27-2 can obtain the opposite result. In terms of mechanism, PDGF-BB down-regulates the expression levels of RhoA, ROCK1/2, and up-regulates the phosphorylation levels of YAP in VSMCs. Overexpression of ARHGAP27 further enhances the effect of PDGF-BB, while knockdown of ARHGAP27-1 and ARHGAP27-2 inhibits the effect of PDGF-BB. Treatment with LPA would reverse the effects produced by ARHGAP27 overexpression. ARHGAP27 is upregulated in AD and accelerates its pathological progression by regulating the RhoA/ROCK/YAP pathway.

PMID 42499796
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PubMedFrontiers in immunology2026-07-25

Association between Alzheimer's disease and MHC-I antigen processing and presentation pathway: a narrative review.

Wang Caixian C, Yun Qilin Q, Zhang Zuoming Z, Zhao Han H et al.

Alzheimer's disease (AD) is the most common cause of dementia worldwide and remains a major public health burden. Although amyloid-beta deposition and tau pathology are the defining pathological features of AD, increasing evidence indicates that immune dysregulation and chronic neuroinflammation also contribute to disease onset and progression. However, the specific immune pathways involved in AD and their mechanistic relevance remain incompletely understood. The major histocompatibility complex class I (MHC-I) antigen processing and presentation pathway has attracted growing attention because of its classical role in adaptive immunity and its potential functions within the central nervous system. In this narrative review, we summarize current evidence linking AD to the MHC-I, or human leukocyte antigen class I (HLA-I), pathway from genetic, molecular, cellular, and immunological perspectives. Available studies implicate the broader HLA region in AD susceptibility and suggest that alterations in HLA-I-related loci, antigen-processing machinery, MHC-I-associated molecules, and downstream immune responses may contribute to disease heterogeneity. At the molecular and cellular levels, changes in MHC-I molecules, antigen-processing machinery, and associated signaling pathways have been reported in microglia, neurons, astrocytes, and oligodendroglial lineage cells. In parallel, changes involving β2-microglobulin and the presence of expanded or cytotoxic like CD8+ T cells suggest that adaptive immune mechanisms may participate in AD pathology. Nevertheless, direct evidence demonstrating immune responses specific to particular antigens and restricted by HLA-I in human AD remains limited. Overall, current findings indicate that the MHC-I/HLA-I pathway may represent an important component of AD pathophysiology and contribute to disease progression by influencing immune homeostasis and cellular interactions within the central nervous system. Further studies integrating human tissue analysis, immunopeptidomics, spatial profiling, and paired T cell receptor approaches are needed to clarify its mechanistic, biomarker, and therapeutic significance.

PMID 42500646
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PubMedThe Journal of biological chemistry2026-07-25

The Src family kinase YES regulates DNAJB6b chaperone activity to modulate tau aggregation in Alzheimer's disease.

Lin Meng-Chieh MC, Chen Huan-Yun HY, Lin Te-Sheng TS, Lin Sue-Jane SJ et al.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a gradual deterioration of memory. While its prevalence increases with age, the underlying mechanisms remain incompletely understood. Here, we examine the biological consequences of phosphorylation-mediated chaperone activity in AD-associated tau aggregates. Increased phosphorylation of DNAJB6b at Y53 is observed in the brain lysates of AD patients. Our research found that an activated Src family kinase, YES, phosphorylates Y53 in the J-domain of DNAJB6b and enhances the binding between DNAJB6b and Hsp70. The strengthened association between DNAJB6b and Hsp70 may lead to the accumulation of tau aggregates. These findings suggest that up-regulation of YES kinase modifies DNAJB6b and that the resulting alteration in DNAJB6b-dependent tau disaggregation may contribute to an increased risk of AD.

PMID 42497989
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PubMedFood science & nutrition2026-07-25

Zizybeoside II From Jujube Fructus Prolongs Lifespan and Mitigates Alzheimer's Disease Progression in Caenorhabditis elegans Through HSF-1/HSP-16.2 Pathway.

Li Pu-Sen PS, Liu Yang Y, Zhao Meng-Rui MR, Zhu Ya-Qiong YQ et al.

Jujube (Ziziphus jujuba Mill.) has been consumed as a nutraceutical and medicinal food in China for millennia. Recent studies have highlighted the nutritional and bioactive properties of jujube fruit extracts, with potential to mitigate Alzheimer's disease (AD) progression through longevity-enhancing effects. Our previous study explored the lifespan-extending mechanisms of Jujube Fructus extract (JE) in Caenorhabditis elegans (C. elegans). Here, we evaluated the efficacy of zizybeoside II (ZB), separated from JE through HPLC, in extending lifespan and ameliorating AD pathology in C. elegans. The results showed that ZB treatment significantly prolonged C. elegans lifespan while maintaining reproductive capacity, with concurrent enhancements in normal activity and stress resistance during aging. Additionally, we found that ZB effectively alleviated various β-Amyloid (Aβ)-induced neurotoxic phenotypes in AD worms, including paralysis and behavioral deficits. Mechanistic investigations in N2a/APP695 cells demonstrated that ZB reduced the accumulation of Aβ and phosphorylated tau (p-Tau) proteins, diminished oxidative stress levels through the HSF-1/HSP16.2 pathway, and thereby slowed the progression of AD. This study provides a theoretical basis for the subsequent clinical trials of ZB in delaying AD.

PMID 42499619
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