N-Acetyl Cysteine (NAC)
Acetylated form of L-cysteine that serves as the rate-limiting precursor for glutathione synthesis. Provides the cysteine residue needed by glutamate-cysteine ligase (GCL) to form gamma-glutamylcysteine, which is then conjugated with glycine to produce glutathione (GSH). Also functions as a direct free radical scavenger and mucolytic agent. Modulates glutamatergic neurotransmission through the cystine-glutamate antiporter, providing psychiatric applications.
Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.
- alt
- ast
- ggt
- bilirubin
- homocysteine
- active-bleeding-disorder
- PMID:18990082N-Acetylcysteine: a review of clinical usefulness (an old drug with new tricks) — J Adv Pharm Technol Res, 2011
- PMID:25925411Oral N-acetyl cysteine reduces oxidative stress biomarkers — Free Radic Res, 2015
- PMID:16490323N-acetylcysteine as adjunctive treatment in bipolar depression — Biol Psychiatry, 2008
NAC is the glutathione precursor. Not glutathione itself — oral glutathione has abysmal bioavailability. NAC provides the cysteine that your body needs to build glutathione endogenously. This is the correct approach to glutathione repletion. The hepatoprotective data is so strong that NAC is the standard-of-care antidote for acetaminophen overdose in emergency departments. For enhancement contexts, it belongs in any liver support stack where hepatotoxic oral compounds are being used. The psychiatric data for OCD, addiction, and bipolar depression via glutamate modulation is a bonus mechanism that most supplement users are unaware of.
This is not medical advice
Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.
See N-Acetyl Cysteine (NAC) in a protocol matched to you