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AD

AD-206 (AD 206 / AD206)

✓ Approved

Addpharma · Small Molecule · Small Molecule

What is AD-206?

AD-206 is a small molecule developed by Addpharma. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesAD 206, AD206
CompanyAddpharma
Drug ClassSmall Molecule
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Addpharma

Therapeutic Indications

AD-206 is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Gastrointestinal disordersGastrooesophageal reflux disease✓ Approved
Gastrointestinal disordersGastrointestinal disorderPhase I

Related Research Articles

PubMedNature reviews. Neurology2026-09-19

Atypical Alzheimer disease: a multi-axis framework toward defining heterogeneity.

Grinberg Lea T LT, Murray Melissa E ME

Alzheimer disease (AD) is defined biologically by the presence of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain; however, these pathologies do not affect all brain regions equally. Typical AD usually presents with memory impairment, whereas atypical forms of AD, including posterior cortical atrophy, logopenic variant primary progressive aphasia, behavioural and dysexecutive AD, and corticobasal syndrome, manifest with prominent non-memory symptoms. Aβ biomarkers usually confirm that AD pathology is present, whereas regional tau, neurodegeneration and dysfunction more closely track the affected network and the presenting symptoms. The atypical variants, which tend to present at a younger age than typical AD, provide human models to study selective vulnerability of neurons and circuits. They also help us to test whether immune-glial, vascular, protein-handling, synaptic or genetic factors shape regional vulnerability and rate of progression beyond total Aβ and tau burden. In this Review, we integrate clinical, neuropathological, imaging, genetic and molecular evidence to describe atypical AD within the broader AD spectrum. We propose a practical multi-axis framework comprising clinical phenotype, AD biological context (AD pathology plus co-pathologies and molecular modifiers), network topography (regional patterns) and tempo (rate of clinical and biomarker progression). This framework could reduce diagnostic mismatches, make cohorts more comparable and support trials that include outcomes tailored to the affected brain networks.

PMID 42760345
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PubMedMolecular neurodegeneration advances2026-09-19

CSF proteomic quantitative trait loci mapping reveals genetic insights into Alzheimer's disease.

Reus Lianne M LM, Jiang Chenyang C, Vilor-Tejedor Natalia N, Boltz Toni T et al.

Despite the identification of numerous genetic risk variants for Alzheimer's disease (AD), mechanisms through which these variants act remain unclear. Identifying specific proteins levels affected by genetic variation can provide valuable insights into the underlying biological pathways implicated in AD. To gain more insight into effects of genetic variation on AD-related processes, we conducted a genome-wide protein pQTL study using untargeted TMT mass spectrometry in cerebrospinal fluid (CSF) of 2,215 proteins across 487 individuals. Replication was assessed in the independent EMIF-AD MBD cohort of 242 individuals. We identified 399 independent CSF pQTL signals (P Bonferroni < 2.26 × 10⁻11) associated with 222 proteins, 69% of which were novel. Findings included gene-protein links such as RPS23P10/HSPA6 with CSF FCGR2A, BIN2 with CSF GALNT6, APOE with CSF HS3ST1, and the HLA-region with CSF HLA-DPB1 and PLXDC2. We replicated 230 of 270 gene-protein associations. A proteome-wide association study identified genetically predicted CSF protein levels to be associated with AD, including SIRPA, PLXDC2, and GALNT6. Many AD pQTLs in CSF were enriched in neuroimmune activation, suggesting a genetic basis for neuroimmune dysregulation in AD. This study highlights how genetic variation shapes protein expression in the central nervous system, offering mechanistic insight into AD. The online version contains supplementary material available at https://doi.org/10.1186/s44477-026-00048-7.

PMID 42761049
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PubMedBritish journal of pharmacology2026-09-19

Bioengineered microbiotic levodopa therapy improves cognition and reduces pathology in a rat model of Alzheimer's disease.

Abdelhamid Mona M, Padhi Piyush P, Gifani Mahsa M, Beck John S JS et al.

Degeneration of the pontine noradrenergic and midbrain dopaminergic systems contributes to cognitive-behavioural disturbances during the prodromal stages of Alzheimer's disease (AD). We developed a genetically engineered, programmable probiotic Escherichia coli Nissle 1917 strain (EcNrha L-DOPA) capable of producing L-3,4-dihydroxyphenylalanine (L-DOPA) in a sustained and titratable manner, thus offering a novel gut-brain delivery mechanism to increase brain levels of noradrenaline and dopamine during the early stages of AD. We replicated locus coeruleus (LC) projection system degeneration in AD by administering dopamine-β-hydroxylase IgG-saporin immunotoxin into the prefrontal cortex of 6-months-old Tg344-19 AD rats. The animals then received EcNrha L-DOPA/benserazide or placebo by daily gavage for 6 weeks. We assessed cognitive-behavioural function prior to postmortem assessments of amyloid-β plaque load, glial cell activation and neuronal and synaptic markers. Gut colonization, along with plasma and brain L-DOPA, dopamine, noradrenaline and metabolite levels, were also measured. EcNrha L-DOPA displayed stable gut colonization and resulted in sustained therapeutic levels of L-DOPA in plasma and brain, resulting in increased cortical and hippocampal noradrenaline levels. EcNrha L-DOPA reduced anxiety-like behaviour improved spatial and working memory. The treatment reduced forebrain Aβ plaque and MHC-II antigen-presenting microglial load. Additionally, EcNrha L-DOPA increased protein levels of the dendritic spine marker PSD95. This translational study suggests that EcNrha L-DOPA modifies AD by boosting brain catecholamine production, reducing Aβ accumulation and neuroinflammation, promoting synaptic health, and enhancing cognitive function. Collectively, these results highlight EcNrha L-DOPA as a promising preclinical engineered gut microbiome-based therapeutic strategy for early-stage AD.

PMID 42760588
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PubMedGeroScience2026-09-19

Alzheimer's disease biomarkers in relation to non-cognitive domains within the intrinsic capacity framework: a narrative review.

Wei Xiaoxia X, Shao Ruitai R, Rolland Yves Y, Vellas Bruno B et al.

Alzheimer's disease (AD) biomarkers may be associated with decline in non-cognitive domains of intrinsic capacity (IC), but such evidence has not been synthesized. This narrative review, based on a structured PubMed search (last search: December 31, 2025), included 119 human studies examining associations of core AD biomarkers (e.g., amyloid-beta (Aβ) and tau protein) and biomarkers of non-specific processes involved in AD pathophysiology (including neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), structural magnetic resonance imaging (MRI), and fluorodeoxyglucose positron emission tomography (FDG-PET)) with composite IC scores and non-cognitive IC domains. Among included studies, 2 investigated composite IC scores, 49 depressive symptoms, 30 locomotion, 29 hearing impairment, 19 vitality, and 1 vision impairment. The very limited longitudinal evidence on composite IC scores suggests that lower IC was associated with increased p-tau181 levels and that higher baseline NfL predicted steeper IC decline, whereas plasma Aβ42/Aβ40 showed no clear association. At the IC domains' level, higher cerebral Aβ deposition was associated with poorer locomotion, especially slower gait, more consistently than other biomarker modalities. Higher levels of tau biomarkers and NfL were more often associated with lower or declining handgrip strength. Depressive symptoms represented the most investigated non-cognitive IC domain, showing consistent longitudinal associations with lower fluid Aβ42, greater cerebral amyloid deposition, and subsequent brain atrophy. Hearing impairment was linked mainly to higher tau and NfL, reduced glucose metabolism, and brain atrophy; evidence for vision impairment was almost totally absent. Overall, the pattern of associations varied by biomarker modality, IC domain, and study design, suggesting that AD-related pathology and neurodegeneration have functional correlates beyond cognition. Methodological quality, formally appraised with the Newcastle-Ottawa Scale and the JBI checklist, was acceptable for most included studies.

PMID 42760484
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PubMedMedicine2026-09-19

Association between COVID-19 and exacerbation of allergic skin diseases: A retrospective questionnaire-based cross-sectional study in Western China.

Liu Yu-Ling YL, Zhang Zeng-Yun-Ou ZY, Chen Xiao-Mei XM

Coronavirus disease 2019 (COVID-19) has been linked to systemic immune dysregulation and various cutaneous manifestations, but its association with chronic allergic skin diseases, including atopic dermatitis (AD) and chronic urticaria (CU), remains unclear. This retrospective questionnaire-based cross-sectional study enrolled patients with AD and/or CU from a tertiary dermatology outpatient center in Western China. Self-administered questionnaires collected data on COVID-19 infection status, clinical characteristics, medication use, and self-reported changes in disease status within 14 days of COVID-19 symptom onset or diagnosis. Outcomes were self-reported rather than based on validated severity scores, and no prospective longitudinal follow-up was performed. Multivariable logistic regression analyses were conducted to identify factors associated with self-reported exacerbation. Covariates were selected a priori based on clinical relevance, and no missing data were present. A total of 509 patients with AD and/or CU were included. Compared with the non-COVID-19 group, participants with COVID-19 more frequently reported current alcohol consumption, pre-COVID-19 antihistamine use, insomnia, allergic rhinitis, and discontinuation of dermatological medications. COVID-19 infection was associated with self-reported exacerbation of allergic skin diseases in both the baseline-adjusted model (odds ratio [OR] = 4.611, 95% confidence interval [CI] = 2.268-9.377) and the fully adjusted model (OR = 4.445, 95% CI = 2.159-9.151). Among participants with COVID-19, fever, headache, fatigue, taste loss, reported use of antipyretics and antibiotics, and nervousness differed between the exacerbation and non-exacerbation groups. After multivariable adjustment, fatigue (OR = 1.601, 95% CI = 1.049-2.443), taste loss (OR = 1.654, 95% CI = 1.004-2.723), and the reported use of antibiotics (OR = 1.609, 95% CI = 1.036-2.499) and antipyretics (OR = 1.575, 95% CI = 1.037-2.392) were associated with self-reported exacerbation, although the medication-related associations likely reflected confounding by indication. Sensitivity analyses yielded consistent results. In this retrospective questionnaire-based cross-sectional study conducted during the omicron wave, COVID-19 infection was associated with self-reported exacerbation of AD and CU within 14 days of symptom onset or diagnosis. Because the outcome was based on participants' recall of symptom change rather than objective clinical assessment, the findings should be interpreted with caution, and their generalizability is limited by the single-center, omicron-period design. Associations with antipyretics and antibiotics likely reflect confounding by indication rather than direct pharmacological effects. Prospective multicenter studies with standardized outcome measures are needed to validate these findings.

PMID 42760740
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PubMedJournal of imaging informatics in medicine2026-09-19

An Explainable Multimodal Model for Assessing Mucosal Healing in Small Bowel Crohn's Disease: A Multicenter Study with Prospective Validation.

Cheng Ting T, Rong Chang C, Hao Jiancheng J, Zhang Yu Y et al.

Accurate assessment of mucosal healing (MH) in small bowel Crohn's disease (SBCD) remains challenging because double-balloon enteroscopy (DBE), the reference standard, is invasive and unsuitable for repeated monitoring. This study was aimed at developing and validating an explainable multimodal model integrating CT enterography (CTE)-based radiomics with clinical data for post-biologic MH assessment in SBCD. This multicenter study included 206 retrospective patients (training: n = 114; internal validation: n = 50; external test: n = 42) and 20 prospective patients. Clinical predictors were identified by logistic regression, with C-reactive protein (CRP) as the only independent predictor. CTE radiomics features were processed by Pearson correlation and SelectKBest, then compared across six feature-selection methods and nine classifiers to determine the optimal radiomics pipeline. Clinical models used CRP alone, while multimodal models combined CRP with selected radiomics features. Performance was evaluated using AUC, calibration, DCA, and DeLong testing. The SHapley Additive exPlanations (SHAP) provided interpretability. MH was achieved in 52.6%, 54.0%, and 21.4% of patients across cohorts. The LASSO-XGBoost radiomics model achieved AUCs of 0.854, 0.821, and 0.808 across retrospective cohorts and 0.824 in the prospective cohort. The XGBoost multimodal model achieved AUCs of 0.860 and 0.842 in internal and external validation, significantly outperforming the clinical model (P < 0.05). SHAP identified CRP and two radiomics features as top predictors. The explainable multimodal model integrating CTE radiomics and CRP enables accurate, non-invasive MH assessment with prospective-validated generalizability, supporting its potential as a clinical decision-support tool.

PMID 42760455
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