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N-Methylglycine
An endogenous glycine derivative that inhibits the type-1 glycine transporter (GlyT-1), enhancing NMDA-receptor co-agonism. It is studied as a prescription-style PSYCHIATRIC ADJUNCT — with genuine add-on RCTs in schizophrenia (and smaller signals in OCD and depression) — not as a casual nootropic. Evidence is real but narrow and emerging.
What the evidence says
Most Sarcosine studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from high-quality meta-analyses and randomised trials published 2004–2026 with a typical study size of 25 participants.
Based on 25 studies · 3 meta-analyses · 19 RCTs · 2,424 total participants
Confidence
High confidenceBy outcome
A 2020 meta-analysis of 7 double-blind RCTs (326 patients) shows a real adjunctive benefit on schizophrenia symptoms, but the evidence base is small, single-source, and cognition/mood signals stay preliminary.
20 rigorous studies
18 randomized trials · 2 meta-analyses · 0 systematic reviews
Our evidence rating for Sarcosine is accountable to this entire body of rigorous research indexed in PubMed — not a hand-picked subset.
PubMed · as of Jul 2026
No trials currently enrolling · 11 completed on ClinicalTrials.gov
1 of the completed trials have posted results
Registered trials show research momentum for Sarcosine, not proof of effect — a registration is a plan, and posted results are sponsor-reported, not peer-reviewed. They are never counted toward the evidence rating above.
Browse these trials on ClinicalTrials.govClinicalTrials.gov · as of Sep 2026
Sarcosine (N-methylglycine) is a naturally occurring intermediate of glycine metabolism. Its mechanism is specific and well-defined: it inhibits the type-1 glycine transporter (GlyT-1), raising synaptic glycine and thereby potentiating the glycine co-agonist site of the NMDA glutamate receptor.
Because NMDA hypofunction is implicated in schizophrenia, sarcosine has been studied as an ADD-ON to antipsychotics — and this is its strongest evidence: a 2020 meta-analysis of 7 double-blind RCTs (326 patients) found a significant improvement in overall clinical symptoms (SMD 0.51), though the cognitive benefit was positive but non-significant, and notably it did NOT augment clozapine.
Smaller studies suggest possible benefit in OCD (an open-label trial) and major depression (a small citalopram-controlled RCT). Important framing: sarcosine is researched as an adjunct to psychiatric treatment under clinical supervision, NOT as a recreational focus/mood supplement.
People with serious psychiatric conditions should not self-treat. The evidence base, while real, is modest in size and mostly from a single research group.
Blocks the type-1 glycine transporter, raising synaptic glycine availability.
Higher synaptic glycine enhances NMDA-receptor function at its glycine site — relevant to NMDA-hypofunction models of schizophrenia.
How Sarcosine works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Only use as part of a clinician-supervised treatment plan — not a substitute for prescribed medication.
Likely not beneficial as add-on; consult a prescriber before use.
Not studied — avoid.
Sarcosine did NOT augment clozapine in the meta-analysis and may not be appropriate as add-on to clozapine — discuss with a prescriber.
Studied AS an add-on to first/second-generation antipsychotics; combine only under clinical supervision.
Tip: Usually transient; reduce dose if persistent
Tip: Take with food
Sarcosine has an evidence score of 5/10 — moderate evidence based on 24 indexed studies, including 1 meta-analysis. An endogenous glycine derivative that inhibits the type-1 glycine transporter (GlyT-1), enhancing NMDA-receptor co-agonism. It is studied as a prescription-style PSYCHIATRIC ADJUNCT — with genuine add-on RCTs in schizophrenia (and smaller signals in OCD and depression) — not as a casual nootropic. Evidence is real but narrow and emerging. Representative study: PMID 32122256.
The commonly studied dose of Sarcosine is 500-2000 mg/day in trials (schizophrenia commonly 2 g/day add-on; OCD trials 500-2000 mg/day). Individual needs vary — start at the lower end of the range and adjust based on how you respond.
The best time to take Sarcosine is in the morning. Take it with food. Daily dosing used in trials; taking with food is reasonable for tolerability.
Sarcosine is generally safe at recommended doses, with a few precautions worth noting. Reported side effects are uncommon and include headache, mild GI upset. Use caution if any of these apply to you: Patients on clozapine (meta-analysis found no benefit when added to clozapine; some signal of worsening reported elsewhere); Pregnancy/breastfeeding (not studied); Self-treatment of serious psychiatric illness without clinical supervision.
Alpha-GPC
Likely helpsCrosses the blood-brain barrier to fuel acetylcholine synthesis — supports focus, memory, and power output in athletes.
Citicoline
Probably helpsDual precursor to acetylcholine and phosphatidylcholine — enhances memory, focus, and brain cell membrane repair.
Huperzine A
Likely helpsAcetylcholinesterase inhibitor from club moss, studied mainly for Alzheimer's and dementia; cognitive evidence is mixed and limited by trial quality.
Phosphatidylserine
Mostly mechanism / observationalKey brain membrane phospholipid that facilitates neurotransmitter release, memory formation, and post-exercise cortisol reduction.
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Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 25 studies · how we score · editorial policy
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
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