Converts alpha-amino-beta-carboxymuconate-epsilon-semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway. 2-amino-3-carboxymuconate 6-semialdehyde + H(+) = 2-aminomuconate 6-semialdehyde + CO2 Secondary metabolite metabolism; quinolate metabolism. Monomer. Highest expression in kidney with lower levels in liver and brain. By streptozocin-induced diabetes. Repressed by low protein diet. Belongs to the metallo-dependent hydrolases superfamily. ACMSD family.