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AD-214 (AD 214, Addpharma / AD214, Addpharma)

✓ Approved

Addpharma · 小分子 · 小分子

什么是 AD-214？

AD-214 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：Oral (PO)。

药物档案

商品名AD 214, Addpharma, AD214, Addpharma
公司Addpharma
药物类别小分子
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Addpharma

治疗适应症

AD-214 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
Gastrointestinal disordersGastrooesophageal reflux disease✓ Approved

相关研究文献

PubMedAlzheimer's & dementia : the journal of the Alzheimer's Association2026-10-26

Neuropathologic features of cognitively defined Alzheimer's disease subgroups in the Adult Changes in Thought study.

Latimer Caitlin S CS, Walker Rod L RL, Bogdani Marika M, Keene C Dirk CD et al.

Individuals with Alzheimer's disease (AD) dementia can be subgrouped based on cognitive performance at diagnosis. We compared neuropathology across cognitively defined AD subgroups in the Adult Changes in Thought study. Scores for memory, executive functioning, language, and visuospatial abilities were derived from the Cognitive Abilities Screening Instrument and a neurocognitive battery. Subgroups were defined by relative performance within domains. Standardized neuropathologic evaluation was performed post mortem. Associations were estimated using ordinal logistic regression, with odds ratios (OR) and 95% confidence intervals (CIs) comparing neuropathology between the AD subgroups and relative to individuals without dementia. Of 885 participants with post mortem neuropathology, 370 had AD dementia: 54% AD-no domain, 15% AD-memory, 15% AD-visuospatial, 8% AD-language, and 7% AD-executive. Among AD subgroups, associations were detected for limbic-predominant age-related transactive response DNA binding protein 43 kDa encephalopathy neuropathologic change (LATE-NC; P = 0.019) and hippocampal sclerosis (HS; P = 0.006), with highest levels in AD-language (LATE-NC OR 2.37, 95% CI 1.03-5.46 and HS OR 2.19, 95% CI 0.88-5.50) and AD-memory (LATE-NC OR 1.88, 95% CI 1.02-3.46 and HS OR 3.11, 95% CI 1.56-6.20) relative to AD-no domain, and lowest levels in AD-visuospatial. AD-visuospatial tended to have lowest estimated Alzheimer's disease neuropathologic change (ADNC) burden across AD subgroups. Relative to participants without dementia, all AD subgroups expectedly had higher ADNC burden, and several AD subgroups had higher odds of Lewy body pathology (P = 0.017) and gross infarcts (P = 0.004), with broadly similar estimates across multiple AD subgroups. Neuropathologic patterns of ADNC and co-pathologies across AD dementia subgroups suggest cognitive phenotyping may inform clinicopathologic studies of AD dementia.

PMID 42928437
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PubMedCells2026-10-26

TDP-43 Coincides with Noradrenergic Neurons in Alzheimer's Disease (AD) and Primary Age-Related Tauopathy (PART).

Uruk Gokhan G, Youssef Hossam H, Gatto Rodolfo G RG, Hossain Nadia N et al.

TAR DNA-binding protein 43 (TDP-43) pathology is a major contributor to cognitive decline in Alzheimer's disease (AD), yet the cellular substrates and circuit-level consequences of its limbic accumulation remain poorly defined. Here, we combined multiplex immunofluorescence with 3D Artificial Intelligence (AI)-based object detection and quantitative colocalization to map phosphorylated TDP-43 (pTDP-43) across neuronal subtypes in the amygdala, hippocampal subfields, and entorhinal cortex (ERC) in human AD, AD with Lewy body disease (AD-LBD), and primary age-related tauopathy (PART). Across 15 deeply phenotyped cases, pTDP-43 showed preferential accumulation in neuromodulatory noradrenergic neurons, with more limited involvement of glutamatergic terminals and cholinergic populations. Noradrenergic neurons marked by dopamine β-hydroxylase (DβH) demonstrated extensive colocalization with pTDP-43 across regions, correlating with APOE genotype, amyloid burden, and tau staging in this cross-sectional cohort, suggesting that neuromodulatory circuits might represent a major convergence point for AD-related molecular stressors. Dopaminergic (tyrosine hydroxylase (TH)) and cholinergic (choline acetyltransferase (ChAT)) neurons showed more restricted but pathology-dependent involvement, with LBD consistently showing lower pTDP-43 burden across multiple transmitter systems. Glutamatergic vesicular glutamate transporter-1 (VGLUT1)-positive neurons and terminals exhibited minimal colocalization except in PART. Principal component (PCA) and hierarchical clustering analyses (HCA) integrating pTDP-43 colocalization with neuropathologic staging metrics (A, B, C, Thal, Braak, LBD) reliably separated PART, AD-TDP, and AD-TDP-LBD groups, with LBD emerging as a dominant modifier of cellular vulnerability. Together, these findings point out that TDP-43 pathology in AD preferentially targets neuromodulatory circuits, is strongly shaped by coexisting synucleinopathy, and provides a cell-type-resolved framework for understanding how TDP-43 contributes to limbic network dysfunction in neurodegeneration.

PMID 42929824
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PubMedDrug design, development and therapy2026-10-26

Metabolic Insights into Coumarins from Angelica Dahurica Radix: Underlying Mechanisms of Herb-Drug Interactions.

Rao Jinqiu J, Qin Shasha S, Yang Yafei Y, Zhao Jiaying J et al.

Angelica dahurica Radix (AD), a traditional Chinese medicine, is widely used and has a diverse array of pharmacological activities. The main chemical components of AD are coumarins. AD and its main components are often used in combination with other drugs and have anti-inflammatory, antibacterial, antitumor, and whitening effects. With the increasing use of AD-containing formulations in clinical applications, herb-drug interactions (HDIs) have increased. A comprehensive narrative review is performed based on multiple databases, including Web of Science, ScienceDirect, PubMed, Elsevier, CNKI, and Scopus, from 1988 to 2026, using the keywords "Angelica dahurica Radix", "coumarins", "cytochrome P450 enzymes (CYPs)", UDP-glucuronosyltransferases (UGTs), and "transporter". Only fully published peer-reviewed articles satisfying our predefined inclusion criteria were ultimately included. This study aimed to explore whether AD, a key regulator of pharmacokinetic drug interactions, affects the expression and activity of CYPs, UGTs, and P-glycoprotein (P-gp). This study mainly included drug-metabolizing enzymes (DMEs) and transport proteins. Recent studies have indicated that AD and its main components (linear and angular furanocoumarins) exert multiple regulatory effects on CYP1A2, CYP2D6, CYP3A4, and P-gp. Collectively, the results of clinical trials of human volunteers, in vitro liver microsome assays, and rodent pharmacokinetic experiments collectively demonstrate that AD and its main coumarin constituents lead to complex inhibitory and inductive regulation of key DMEs and transporters, altering the absorption, metabolism and elimination of coadministered drugs and triggering HDIs. This study may provide a comprehensive reference for safe and rational clinical combined medication with AD preparations.

PMID 42928897
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PubMedAmerican journal of clinical dermatology2026-10-26

Prevalence of Atopic Dermatitis in the United States, 2019-2023: National, State, and County-Level Estimates from Administrative Claims Data.

Abuabara Katrina K, Capozza Korey K, Muthuri Stella S, Florea Ana A et al.

The prevalence of diagnosed atopic dermatitis (AD) and associated patient and treatment characteristics have not been comprehensively investigated in the United States of America (USA), especially at the state and county levels. Evaluating geographic distribution, treatment utilization, and disease characteristics at a more granular level can enhance the understanding of disease burden and aid in the identification of areas with unmet needs. The aims of the study were to describe the prevalence of AD, the associated medical conditions, and filled prescription medications for patients with diagnosed AD in the USA at the national, state, and county levels. Using the open-claims IQVIA® Longitudinal Access and Adjudicated Data database, individuals with ≥ 1 ICD-10-CM AD diagnosis code between 1 January 2019 and 31 December 2023 (index period) were identified. Age- and sex-standardized prevalences were calculated at national, state, and county levels. Geographic location was inferred from the healthcare provider's zip code. Demographics and treatments were assessed during the 365-day baseline period. A total of 5,573,454 patients were identified with an AD diagnosis during the index period. Median age of patients with diagnosed AD was 18 years (interquartile range, 6-49); 57.1% of patients were female, 38.3% were children (0-11 years old), 11.4% were adolescents (12-17 years old), and 50.2% were adults (≥ 18 years old). Nationally, the prevalence of diagnosed AD was 2.4%; age-standardized prevalence was 2.2% in males and 2.6% in females. Prevalence was highest in children (7.2%), followed by adolescents (3.6%) and adults (1.4%). State-level prevalence ranged from 1.3% (Missouri) to 4.5% (Washington, DC). At the county level, AD prevalence ranged from 0 to 19.6%. Prescriptions filled during the baseline period included topical (56.3%) and oral (22.6%) corticosteroids, biologics (2.8%), and oral JAKis (0.2%). During the 6-month postindex period, topical (27.6%) and oral (11.6%) corticosteroids remained the most frequently filled prescriptions; biologics (2.8%) and oral JAKis (0.2%) were less frequently filled. Using a large open-claims database, distinct variations in AD prevalence between age groups and geographies were identified. Differences in the low use of biologics and oral JAKis with high corticosteroid use were observed nationally.

PMID 42928407
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PubMedMolecular neurobiology2026-10-26

Evaluating the Impacts of Inflammatory Proteins on the Risk of Alzheimer's Disease.

Zhang Ziyao Z, Cao Hongbao H, Baranova Ancha A, Zhang Fuquan F

Accumulating evidence suggests that inflammation contributes to the pathogenesis of Alzheimer's disease (AD). However, the relationship between circulating inflammatory proteins and AD remains incompletely understood. Two-sample Mendelian randomization (MR) was used to assess the associations of 91 circulating inflammatory proteins with AD. The discovery stage protein GWAS included 14,824 participants, and the validation stage analysis used UK Biobank data from 54,219 participants. The AD dataset comprised 85,934 cases and 401,577 controls. The inverse variance weighted (IVW) method was the primary approach, complemented by weighted median, MR-Egger, heterogeneity, and pleiotropy analyses. MR estimates from both stages were subsequently combined by meta-analysis, followed by drug-gene interaction analyses. In the discovery stage, four proteins showed nominal associations with AD: AXIN1 (OR = 1.082, P = 0.026), NGF (OR = 1.061, P = 0.048), CXCL11 (OR = 0.952, P = 0.017), and TNFRSF9 (OR = 0.946, P = 0.048). However, none survived FDR correction (FDR = 0.799). In the validation stage, only TNFRSF9 reached nominal significance (OR = 0.870, P = 0.031), which did not survive FDR correction (FDR = 0.125); AXIN1 showed an opposite direction. Meta-analysis provided suggestive pooled estimates for CXCL11 (OR = 0.956, P = 9.34 × 10⁻3), TNFRSF9 (OR = 0.926, P = 0.034), and NGF (OR = 1.061, P = 0.034), but these should not be regarded as independent confirmation. DGIdb analysis identified interactions between the genes of interest and various drugs or compounds. These findings provide exploratory genetic evidence linking circulating inflammatory proteins to AD, but robust replication was not established after multiple testing correction and requires further validation.

PMID 42928319
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PubMedMedComm2026-10-26

Impact of Dupilumab Therapy on Skin Barrier Function in Patients With Moderate-to-Severe Atopic Dermatitis: A Phase IV, Non-Randomized, Open-Label, Parallel-Group Clinical Study.

Liu Taoming T, Chen Shuting S, Zhao Weijia W, Di Dake D et al.

Dupilumab improves skin barrier function in patients with atopic dermatitis (AD), but data for Chinese patients are limited. This 16-week, prospective, exploratory study investigated the impact of dupilumab on skin barrier function in Chinese patients with moderate-to-severe AD. Forty-four participants (24 patients with AD and 20 healthy volunteers) were enrolled. Patients with AD received dupilumab treatment every 2 weeks and were followed up to Week 16. Tape-stripped stratum corneum samples were collected from participants at seven specific time points for proteomic and lipidomic profiling, together with transepidermal water loss (TEWL) measurement. At Week 16, TEWL after five tape strips was significantly reduced versus baseline (adjusted p = 0.0006). Proteomics revealed significant upregulation of sphingolipid and other lipid metabolism pathways within the first 2 weeks, coinciding with early TEWL improvement; keratinocyte differentiation and keratinization pathways were enriched from Week 8 through Week 16. Lipidomics revealed that specific dysregulated ceramides-CER(d16:0/16:0), CER(d16:0/20:3), CER(t20:1/23:0), and CER(t20:1/24:1)-showed significant changes by Weeks 2-8 and completely normalized by Week 16. Dupilumab improved skin barrier function in Chinese patients with moderate-to-severe AD, accompanied by dynamic molecular changes; these correlative findings require functional validation to establish causality. Trial Registration: ClinicalTrials.gov NCT05624112.

PMID 42928785
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