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AD

AD-201 (AD 201 / AD201)

✓ Approved

Addpharma · 小分子 · 小分子

什么是 AD-201？

AD-201 是一种小分子，由Addpharma研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名AD 201, AD201
公司Addpharma
药物类别小分子
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, Addpharma

治疗适应症

AD-201 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
Vascular disordersHypertension✓ Approved
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

相关研究文献

PubMedPediatric dermatology2026-08-05

Association Between Infantile Atopic Dermatitis and Mother-to-Infant Bonding Disorder: A Cross-Sectional Study.

Kamo Sawako S, Tabuchi Takahiro T, Nishi Daisuke D

Mother-to-infant bonding disorder (MIBD) can hugely impact the relationship between mothers and infants, maternal mental health, and child development. Although infantile atopic dermatitis (AD) is known to influence caregivers' quality of life and mental health, its effect on MIBD is not fully understood. This study examined the association between MIBD and infantile AD using data from 4236 postpartum women from a cross-sectional nationwide survey: the Japan COVID-19 and Society Internet Survey (JACSIS). We assessed MIBD using the Japanese version of the Mother-to-Infant Bonding Scale (MIBS-J), the presence of infantile AD based on maternal perception (reported AD: R-AD) and physician's diagnosis (diagnosed-AD: D-AD), and participants' demographics. To assess the association between MIBD and infantile AD, we conducted a modified Poisson regression with robust error variance that provided relative risks (RRs) and 95% confidence intervals (CIs). The prevalence of MIBD was about 24.2% (n = 1024). Whether infantile AD was R-AD (RR = 1.22, 95% CI: 1.07-1.40) or D-AD (RR = 1.41, 95% CI: 1.18-1.69), its presence was significantly associated with a higher RR for MIBD. Furthermore, we found that infantile AD was associated with a higher RR for Anger and Rejection, a subscale of the MIBS-J. This study showed that infantile AD is a potential risk factor for MIBD. Further studies should investigate the link between infantile AD and MIBD and determine effective support for mothers and infants with AD.

PMID 42552592
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PubMedGlia2026-08-05

Predicting Relevant Microglia-Associated Cell-Cell Communication Pathways in Alzheimer's Disease: A Role for SPP1.

Kotah Janssen M JM, Lima Marina Trombetta MT, Dragt Esmée C EC, Voulgaroglou Asimenia A et al.

Microglia play a key role in the pathophysiology of Alzheimer's Disease (AD) and their increased heterogeneity likely affects disease progression. We previously identified distinct microglial signatures that were enriched in AD donors and associated with amyloid and tau, respectively. Here we generated a snRNAseq dataset from postmortem control and AD cases and analyzed alterations in cell-cell communication pathways that might be relevant to AD pathophysiology. One signaling pathway perturbed in AD cases involved SPP1, and while this pathway was also present in control samples, microglia-microglia SPP1 signaling was restricted to AD donors. Further analyses within microglia-microglia signaling predict AD-specific induction of GAS6-AXL signaling (from inflammatory and ribosomal microglia), and SPP1-ITGAV/ITGB5 signaling (from disease-associated and inflammatory microglia, among others). Together, these findings might in part explain the increased microglia phagocytic profile described in AD. RNAscope confirmed enrichment of SPP1 expressing microglia near amyloid plaques in AD brain tissue samples. These data indicate altered cellular communications between microglia in the AD brain.

PMID 42552722
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PubMedAlzheimer's & dementia : the journal of the Alzheimer's Association2026-08-05

Plasma p-tau217 detects Alzheimer's disease co-pathology in cerebral amyloid angiopathy: Comparison to CSF biomarkers in the ANGMAR cohort.

Fernández-Lebrero Aida A, Jiménez-Balado Joan J, García-Escobar Greta G, Contador José J et al.

Cerebral amyloid angiopathy (CAA) frequently co-occurs with Alzheimer's disease (AD), generating mixed vascular-neurodegenerative phenotypes. Plasma phosphorylated tau (p-tau)217 is a robust biomarker of AD, but its performance in CAA remains unclear. We studied 231 participants, including 50 patients with CAA (Boston v2.0), 154 with AD, and 27 cognitively unimpaired controls. Plasma p-tau217 was measured on an automated platform and compared to cerebrospinal fluid (CSF)-defined AD status. Associations with magnetic resonance imaging (MRI) markers of CAA burden were evaluated. Among CAA participants, 29 met CSF criteria for AD co-pathology. Plasma p-tau217 discriminated CAA patients with and without AD co-pathology (area under the curve = 0.920) and showed no association with MRI markers of CAA burden. Predefined cut-offs (≥ 0.27 pg/mL and ≥ 0.34 pg/mL) yielded high accuracy for identifying AD co-pathology within CAA. Plasma p-tau217 shows high diagnostic accuracy for identifying AD co-pathology in CAA and is not associated with MRI markers of CAA burden, supporting its specificity for AD-related pathology.

PMID 42552750
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PubMedLymphatic research and biology2026-08-05

Lymphedema and Alzheimer's Disease: Connecting Through the "Peripheral-Central Lymphatic System".

Wang Xinxin X, Li Yilan Y, Ye Jianping J, Lian HongKai H et al.

The connection between the peripheral lymphatic system (PLS) and the central lymphatic system (CLS) plays a crucial role for the overall circulatory system. Notably, there are several similarities between lymphedema and Alzheimer's disease (AD). Accumulating evidence suggests that lymphedema might be associated with AD, potentially influencing its progression through mechanisms related to the peripheral-central lymphatic circulation. This review summarizes the lymphatic system's structure, function, and drainage pathways, emphasizing how aging and blockage of the CLS can exacerbate the progression of AD. Additionally, we discuss the relationship between lymphedema and AD, highlighting the significance of the PLS-CLS and exploring lymphaticovenous anastomosis as a promising treatment for both lymphedema and AD.

PMID 42552845
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PubMedJournal of the European Academy of Dermatology and Venereology : JEADV2026-08-05

Multi-omics analyses reveal host-microbe interactions in atopic dermatitis and psoriasis.

Yang Ying Y, Olah Peter P, Salava Alexander A, Barker Jonathan J et al.

Atopic dermatitis (AD) and psoriasis (PSO) are chronic inflammatory skin diseases that impose substantial physical and psychological burdens. Although fungal-bacterial balance is important for skin immune homeostasis, the role of the skin mycobiome and its interaction with bacterial communities and host immunity in these diseases remains poorly understood. To characterize alterations in the skin mycobiome and its interactions with bacterial communities and host immune responses in AD and PSO. Adult patients with chronic AD, plaque-type PSO and healthy volunteers were included in this study. Skin microbiota samples and biopsies were collected from lesional and non-lesional skin areas, including the posterior thigh for AD and the lower back for PSO. Whole-metagenome shotgun sequencing was used to profile microbial communities. SparCC was used to construct fungal-bacterial co-occurrence networks, and integration of host transcriptomic and microbial features was performed using O2PLS. Both AD and PSO showed disease-associated restructuring of Malassezia species and reduced fungal-bacterial ecological connectivity in lesional skin. In AD, Malassezia arunalokei was inversely associated with Staphylococcus aureus and linked to antimicrobial peptide-centred host gene modules enriched for IL-17 signalling. Its abundance decreased with increasing disease severity and inversely correlated with inflammatory immune cell signatures. In PSO, altered Malassezia composition was associated with IL-17-driven transcriptional programmes and lipid metabolic pathways, suggesting interactions between fungal imbalance and inflammatory-metabolic processes. Our findings expand current models of skin dysbiosis beyond bacteria and suggest that disrupted fungal-bacterial interactions are linked to immune activation in AD and PSO and, in AD, to disease severity. Although further validation is required, skin microbiome features may provide clinically relevant information for disease monitoring, patient stratification and future microbiome-informed therapeutic strategies. Our study lays the groundwork for microbiome modulation as a potential therapeutic strategy for AD and PSO.

PMID 42554585
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PubMedRSC advances2026-08-05

Design, synthesis, and evaluation of pyrano[3,2-c]coumarin derivatives for simultaneous targeting of amyloid-β42 and acetylcholinesterase in transgenic AD model of Drosophila.

Sharma Saurabh S, Sharma Shalini S, Raghuvanshi Vaishali V, Kumari Sandhya S et al.

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder involving amyloid-β (Aβ) aggregation, cholinergic dysfunction, oxidative stress, mitochondrial impairment, and progressive neuronal loss. Consequently, the development of multi-target-directed ligands (MTDLs) capable of modulating multiple pathological pathways simultaneously has emerged as a promising therapeutic strategy. In this context, the present study describes the design, synthesis, and biological evaluation of a novel series of pyrano[3,2-c]coumarin derivatives 4a-n as dual Aβ42 and acetylcholinesterase (AChE) targeting anti-AD agents. Compounds 4a-n showed significant protection by inhibiting tissue specific Aβ42 aggregation in a transgenic AD model of Drosophila. In particular, compounds 4g and 4i were identified as potential lead compounds for targeting AD. These compounds inhibited endogenous Aβ42 aggregation and exhibited a significant rescue of eye phenotypes at respective effective concentrations (ECs) (4g, 46% rescue at EC = 250 µM and 4i, 65% rescue at EC = 50 µM). Furthermore, compounds 4g and 4i effectively reduced lipid-peroxidation, which was determined by assessing thiobarbituric acid reactive substances (TBARS) levels, at 25 and 50 µM, respectively, and reactive oxygen species (ROS). Compounds 4g and 4i also exhibited AChE inhibitory activity, with IC50 values of 0.02652 and 0.0268 µM, respectively. In silico molecular docking studies of 4i with Aβ42 (PDB ID: 1IYT) and AChE (PDB ID: 4EY4) also corroborated their anti-AD activity. Therefore, the present study indicated these compounds, especially 4i, could be promising lead candidates for AD drug development.

PMID 42553843
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