Alzheimer's disease (AD) remains one of the most challenging neurodegenerative disorders, affecting millions of people worldwide and placing a significant burden on healthcare systems . Characterized by the accumulation of amyloid-beta (Aβ) plaques and tau protein tangles in the brain, AD leads to progressive cognitive decline, memory loss, and behavioral changes . The underlying mechanisms of the disease remain incompletely understood, and despite substantial research efforts, treatments remain largely palliative, with few options to halt or reverse disease progression. One primary therapeutic target has been beta-secretase (BACE1), an enzyme critical to the production of Aβ peptides. However, many recent BACE1 inhibitors have failed clinical trials due to lack of efficacy , highlighting the need for new approaches that can both target AD pathology and maintain a favorable toxicity profile. Indoleamine 2,3-dioxygenase 1 (IDO1) is a pivotal enzyme that plays a significant role in both AD and in cancer research. In cancer research IDO1 is primarily known for its role in immune regulation and tumor immune evasion. IDO1 catalyzes the conversion of the essential amino acid tryptophan into kynurenine, a process that is often exploited by tumors to suppress immune responses and promote tolerance to tumor antigens . This enzymatic activity contributes to the establishment of a tumor-friendly microenvironment and facilitates the development of myeloidderived suppressor cells, which further inhibit anti-tumor immunity. Small-molecule inhibitors of IDO1 are currently under clinical evaluation, demonstrating potential to enhance the efficacy of existing cancer treatments, such as immunotherapy and chemotherapy . These inhibitors aim to reverse the immune suppression mediated by IDO1, thereby restoring the immune system's ability to recognize and attack tumor cells. IDO1plays a significant role in the pathogenesis of Alzheimer's disease (AD) as well since its dysregulation has been linked to neuroinflammation and neurodegeneration associated with AD . Neuroinflammation is a critical process in AD, where inflammatory responses contribute to neuronal damage and cognitive decline . Elevated IDO1 activity has been observed in the brains of AD patients, suggesting that it may exacerbate neuroinflammatory processes and neuronal toxicity. Recent studies have highlighted the therapeutic potential of targeting IDO1 to modulate these inflammatory responses. The inhibition of IDO1 has been shown to reduce neuroinflammation and improve cognitive outcomes in preclinical models of AD. For instance, coptisine, a novel IDO1 inhibitor, demonstrated efficacy in reducing microglial activation and amyloid plaque formation in AD mouse models, thereby ameliorating cognitive impairments .