Editing Openai/692df380-fd64-8008-b788-94e93ef3ff89 (section)

==== 7. Practical implications for a longevity strategy ====

Given your interest is actionable healthspan interventions:
# Do not treat “KMO inhibitor” as a near-term biohacking target. At present it belongs firmly in the drug-development / clinical-trial bucket, not the “n=1 self-experimentation” bucket.
# Target the same biology via safer levers for now: - Inflammaging control: optimize standard anti-inflammatory levers (visceral adiposity, glycemic control, periodontal disease, sleep apnea, air pollution exposure, etc.). All reduce IDO/TDO activation upstream of KMO and should lower toxic KP flux indirectly. - Exercise: recent work suggests endurance/combined training normalizes KP metabolites (e.g., beneficial 3-HAA signaling) and is being explicitly framed as a KP-modulating longevity tool. Wiley Online Library<ref>{{cite web|title=Wiley Online Library|url=https://onlinelibrary.wiley.com/doi/10.1111/apha.70041|publisher=Wiley Online Library|access-date=2025-12-28}}</ref> - General NAD⁺ support: while speculative, balancing de novo vs salvage NAD⁺ pathways (dietary niacin, NR/NMN where appropriate) may interact with KP dynamics, but this area is unsettled and should not be over-interpreted. SpringerLink<ref>{{cite web|title=SpringerLink|url=https://link.springer.com/article/10.1007/s11357-025-01735-1|publisher=link.springer.com|access-date=2025-12-28}}</ref>
# Watch-list for future data: - Phase II trials of KNS366 or other KMO inhibitors in: - Acute inflammatory conditions (e.g., severe pancreatitis, critical illness) - Neurodegenerative diseases (HD, PD, AD) - Possibly frailty or sarcopenia cohorts - Longitudinal KP profiling in human aging interventions (exercise, caloric restriction mimetics, rapalogs, SGLT2i, etc.) to see whether KMO-branch suppression correlates with better outcomes.

===== Bottom line =====

KMO inhibition is one of the more compelling mechanistic nodes in the kynurenine pathway for neuroprotection and inflammation control, and it clearly improves health and survival in several disease models. But as of now, there is no direct evidence that KMO inhibitors improve human healthspan or lifespan, and there are plausible cognitive and mood risks if KYNA is pushed too high.

If you want to engage with this space today, the rational approach is as an observer and potential future trial participant, not as an early adopter of an unproven class.