ACMSD (aminocarboxymuconate semialdehyde decarboxylase) is a key metabolic enzyme that catalyzes the conversion of alpha-amino-beta-carboxymuconate-epsilon-semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS), thereby controlling tryptophan catabolism along the kynurenine pathway 1. By converting ACMS to a benign catabolite, ACMSD prevents the non-enzymatic cyclization of ACMS into quinolinate (QA), a potent endogenous neurotoxin implicated in neurodegenerative diseases 1. Mechanistically, ACMSD functions as a key rate-limiting enzyme that regulates cellular NAD+ levels through the de novo NAD+ synthesis pathway, with activation enhancing mitochondrial function and sirtuin activity 2. ACMSD is primarily expressed in liver and kidney 2. Therapeutically, ACMSD inhibition increases hepatic NAD+ synthesis and reverses metabolic dysfunction-associated steatotic liver disease/steatohepatitis (MASLD/MASH), mitigating fibrosis, inflammation, and DNA damage 3. Genetically, ACMSD mutations have been associated with Parkinson's disease risk 4 and familial cortical myoclonic tremor with epilepsy and parkinsonism 5, suggesting that impaired ACMSD function leads to quinolinate accumulation and neurological dysfunction. Additionally, ACMSD knockdown alleviates acute kidney injury through suppression of the TCA cycle and promotion of NAD+ synthesis 6. These findings establish ACMSD as a promising therapeutic target across multiple disease contexts.