Drug Database
AD

AD-220 (AD 220A / AD 220 / AD220)

✓ Approved

Addpharma · Small Molecule · Small Molecule

What is AD-220?

AD-220 is a small molecule developed by Addpharma. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesAD 220A, AD 220, AD220
CompanyAddpharma
Drug ClassSmall Molecule
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Addpharma

Therapeutic Indications

AD-220 is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHyperlipidaemia✓ Approved
Metabolism and nutrition disordersHypercholesterolaemiaPreclinical

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Mitochondria-derived extracellular vesicles mediate Alzheimer's disease pathology through transmitting microglial Ggt1.

Li Yun Y, Xia Xiaohuan X, Sun Yiyan Y, Jia Kailing K et al.

Extracellular vesicles (EVs) can modify pathological progression in Alzheimer's disease (AD), the most common neurodegenerative disease in older adults, by spreading pathogenic factors. However, the function of mitovesicles (mtVs)-a recently identified subset of EVs-in AD remain unknown. Here we show that release of mtVs is enriched in brain tissue from patients with AD and 5×FAD mice. Administration of 5×FAD mouse brain-derived mtVs (ADmtVs) induced AD-like behavioral and pathological changes in wild-type mice and accelerated disease progression of AD mice. Moreover, the release of mtVs was regulated by mitochondrial respiratory metabolism, and blocking the release of mtVs significantly alleviated AD-like phenotypes. Proteomic analysis identified Ggt1 as a highly enriched protein in ADmtVs. Inhibiting Ggt1 expression and activity mitigated AD-like phenotypes of 5×FAD mice and delayed ADmtV-induced disease progression, suggesting Ggt1 as a pathological cargo of ADmtVs. Our findings highlight the pathological roles of mtVs in AD and highlight mtVs and Ggt1 as potential therapeutic targets.

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PubMedActa neuropathologica communications2026-11-11

Raman spectroscopic identification of biochemical alterations in Alzheimer's disease brain tissue.

Ghazanfarpour Samaneh S, Das Rahul Kumar RK, Ihnatovych Ivanna I, Sule Norbert N et al.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by chronic inflammation, neuronal loss, and continuous decline in memory and cognitive function. Raman Spectroscopy (RS) offers a powerful, label‑free approach for detecting early biochemical alterations in AD by generating highly sensitive molecular fingerprints, which is valuable for identifying subtle changes associated with protein misfolding, lipid dysregulation, and oxidative stress, key processes underlying AD onset and progression. In our study, full‑spectrum RS revealed clear biochemical distinctions between control and AD brain tissues, as well as between Braak IV and Braak VI AD stages. Multivariate analytical methods, including Singular Value Decomposition (SVD) and Linear Discriminant Analysis (LDA), were applied to manage spectral complexity and highlight the principal biochemical contributors to AD pathology. Multiple Raman bands in the 1200-1800 cm-1 region showed increased intensity in AD tissue, including 1296 cm-1 (lipid CH₂ deformation), 1440 cm-1 (lipid/cholesterol deformation), 1554 cm-1 (Amide II), 1585 cm-1 (protein‑folding-related vibrations), and 1640-1680 cm-1 (Amide I). These changes indicate enhanced protein aggregation, loss of ordered secondary structure, and extensive lipid membrane disorganization. Complementary gene‑expression analysis further demonstrated dysregulation of lipid homeostasis in AD, with altered expression of ABCA1, LIPE, CPT1A, PPARA, and SREBP‑1, indicating broad metabolic reprogramming. Together, the coordinated spectral and transcriptional shifts underscore lipid‑metabolic dysfunction as a central feature of AD. By capturing these molecular signatures, RS provides a promising tool for early detection and monitoring of AD progression.

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PubMedFrontiers in aging neuroscience2026-11-11

Deciphering the effects of aging on Alzheimer's disease based on mitochondrial dysfunction and neuroinflammation.

Luo Yamei Y, Yu Haoli H, Zhang Jun J, Wu Zhihong Z et al.

Alzheimer's disease (AD), a neurological disorder characterized by progressive deterioration of cognitive function, has complex pathogenic mechanisms and lacks curative therapies with proven efficacy. Aging and inflammatory responses, which play indispensable roles in the onset and progression of AD, are closely intertwined with mitochondrial dysfunction. During aging, a series of degenerative alterations, including accumulated mitochondrial DNA (mtDNA) mutations, excessive mitochondrial reactive oxygen species (ROS) accumulation, disrupted mitochondrial quality control (MQC) and disturbed energy metabolism, further induce structural mitochondrial damage. This damage causes the leakage of damage-associated molecular patterns (DAMPs) and activates numerous downstream inflammatory signaling pathways. In brain tissue, inflammatory cytokines, which continuously facilitate blood-brain barrier (BBB) disruption, aberrant activation of microglial cells, tau protein hyperphosphorylation, as well as Aβ accumulation, drive an endlessly amplified neuroinflammatory cascade that leads to irreversible neuronal damage and fuels the initiation and progression of AD. In this review, we clarify the regulatory effects of aging on AD pathogenesis through the mitochondrial dysfunction-chronic inflammation axis and ultimately focus on mitochondrial-targeted therapies, with future outlooks for AD treatment provided.

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Isovitexin Attenuates Aβ-Induced Neurotoxicity by Activating SKN-1/Nrf2 Signaling and Suppressing Ferroptosis in Caenorhabditis elegans Models of Alzheimer's Disease.

Hao Mengjiao M, Wu Dongni D, Sun Lingli L, Lai Xingfei X et al.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) deposition, oxidative stress, ferroptosis, and mitochondrial dysfunction, while effective therapeutic interventions remain limited. Epidemiological evidence indicates that tea and flavonoids with antiaging properties lower AD risk. In this study, untargeted metabolomic profiling identified isovitexin as a differentially abundant flavonoid in postfermented dark tea (DT), and Caenorhabditis elegans (C. elegans) AD models were employed to evaluate its anti-AD potential and elucidate the underlying molecular mechanisms. The results showed that isovitexin significantly extended lifespan, reduced Aβ accumulation, and improved neuromuscular function, demonstrating marked neuroprotective effects. Mechanistically, isovitexin mitigated Aβ-triggered toxicity through SKN-1 signaling, accompanied by the attenuation of Aβ-evoked ferroptosis and mitochondrial dysfunction. Collectively, these results broaden the therapeutic potential of dark tea flavonoids and support further investigation of isovitexin as a candidate for mitigating Aβ-induced neurodegeneration.

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Dynamically Repairable Hydration-Lubricating Microspheres for Osteoarthritis Therapy.

Ma Penggang P, Ying Ting T, Wang Rui R, Zong Chenyu C et al.

Osteoarthritis (OA) progression is closely associated with the deterioration of joint lubrication. Although surface-grafted lubrication coatings can reduce friction, they are susceptible to mechanical damage under repetitive shear stress, resulting in rapid lubrication failure. Therefore, constructing a dynamically reconfigurable lubrication interface capable of continuous restoration under friction is critical for long-term joint protection. Herein, a dynamically self-repairing hydration lubrication microsphere system (HMs-CD@Ad-PMPC) is developed based on host-guest interactions. β-Cyclodextrin (β-CD)-functionalized silk fibroin microspheres dynamically recruit adamantane (Ad)-terminated poly(2-methacryloyloxyethyl phosphorylcholine) (PMPC) brushes through supramolecular host-guest recognition, thereby establishing a robust yet reversible hydration lubrication interface. Under shear stress during joint motion, partial dissociation of Ad-PMPC chains induces transient lubrication attenuation, while spontaneous molecular reassembly rapidly restores the lubrication interface upon stress release, thereby enabling dynamic self-repairing lubrication. In vitro, HMs-CD@Ad-PMPC maintains a stable low coefficient of friction (COF, 0.03-0.04) under cyclic shear conditions, exhibiting excellent wear resistance and long-term lubrication stability. In vivo, the system effectively reduces joint wear, preserves cartilage integrity, and significantly delays OA progression. This work establishes a dynamic lubrication strategy capable of restoring interfacial functionality under mechanical stress, providing a promising platform for long-term joint lubrication and OA therapy.

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PubMedMolecular neurodegeneration advances2026-11-11

The role of lactate in Alzheimer's disease: from controversies to therapeutic opportunities.

Ashley Clair C CC, Macauley Shannon L SL

Alzheimer's disease (AD) is increasingly recognized as a disorder of disrupted brain metabolism, yet the role of specific metabolic intermediates in disease pathogenesis remains incompletely defined. Lactate, long considered a byproduct of glycolysis, is now understood to function as both an energy substrate and signaling molecule that links neuronal activity, glial biology, and network function. In this review, we synthesize clinical, preclinical, and multi-omic evidence to reframe lactate as a dynamic regulator of AD pathophysiology. Emerging data demonstrate that lactate is differentially regulated across disease stages and cellular compartments, with early increases associated with amyloid pathology, reactive glia, and neuronal hyperexcitability. We highlight evidence that disease reactive microglia undergo glycolytic reprogramming and represent a major and spatially enriched source of lactate in the AD brain, challenging the traditional astrocyte-centric view of lactate metabolism. We further discuss how lactate participates in feed-forward mechanisms linking metabolism to inflammation, neuronal excitability, and protein aggregation, but also through epigenetic modifications such as lactylation. Importantly, we propose a context-dependent framework in which lactate exerts both beneficial and maladaptive effects on disease progression. While transient or well-regulated lactate supports synaptic function and cognitive processes, sustained or dysregulated elevations may contribute to neuroinflammation, network dysfunction, sleep loss, and disease progression. Finally, we evaluate the potential of lactate as both a biomarker and therapeutic target. Together, this perspective integrates metabolism, neuroinflammation, and systems-level dysfunction, positioning lactate as a key therapeutic target in AD.

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