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Comparison

MOTS-c vs N-Acetyl Cysteine

Side-by-side of MOTS-c and N-Acetyl Cysteine. Every row below is pulled from the compound schema and will update as our data grows. For deeper reads, follow through to each compound page.

Effects at a glance

MOTS-c

  • 16-amino-acid peptide encoded in mitochondrial DNA (12S rRNA region); discovered 2015
  • Activates AMPK in skeletal muscle and liver; improves insulin sensitivity in rodent models
  • Circulating endogenous levels decline with age, motivating the longevity-restoration hypothesis
  • CohBar's MOTS-c analog CB4211 discontinued after phase 1b NASH readout did not meet endpoints
  • Anecdotal protocols use 5 to 10 mg subcutaneously 2 to 3 times weekly
  • Not on the WADA Prohibited List as of 2026; future scrutiny likely given exercise-mimetic mechanism

N-Acetyl Cysteine

  • Replenishes intracellular glutathione by supplying cysteine, the rate-limiting amino acid for synthesis
  • First-line antidote for acetaminophen toxicity, restoring hepatic glutathione before fulminant injury occurs
  • Reduces sputum viscosity in chronic bronchitis and COPD at 600 to 1200 mg/day over months
  • Modest symptom reductions in OCD and trichotillomania at 1200 to 2400 mg/day across small RCTs
  • Mixed evidence for psychiatric adjunct use in bipolar depression and schizophrenia negative symptoms
  • Inhaled forms can trigger bronchospasm in active asthma; oral use is the standard biohacker route

Side-by-side

Attribute MOTS-c N-Acetyl Cysteine
Category peptide supplement
Also known as Mitochondrial Open Reading Frame of the Twelve S rRNA-c, MOTSc NAC
Half-life (hr) 0.5 5.6
Typical dose (mg) 5 1200
Dosing frequency 2-3x weekly 1 to 3 times daily, split dosing preferred
Routes subcutaneous oral, iv
Onset (hr) 1 1
Peak (hr) 4 2
Molecular weight 1880.18 163.19
Molecular formula C82H132N22O25S2 C5H9NO3S
Mechanism Mitochondrial-derived peptide that activates AMPK in skeletal muscle and liver, improves insulin sensitivity, and translocates to the nucleus under metabolic stress to modulate nuclear gene expression in retrograde mitochondrial signaling. Deacetylated to cysteine, the rate-limiting precursor for glutathione synthesis; also directly scavenges reactive oxygen species and modulates glutamate signaling.
Legal status Not FDA approved; research-use-only grey market; not currently on WADA Prohibited List OTC in most jurisdictions; restricted periods in US history (FDA reclassified 2022)
WADA status unknown allowed
DEA / Rx Not scheduled (research chemical) OTC supplement (US, post-2022); Rx indications also exist (acetaminophen overdose, mucolytic)
Pregnancy Insufficient data; not recommended Used clinically in pregnancy for specific indications; consult clinician
CAS 1627580-64-6 616-91-1
PubChem CID 139599184 12035
Wikidata Q24832108 Q413299

Safety profile

MOTS-c

Common side effects

  • injection-site irritation
  • transient fatigue
  • headache (anecdotal)

Contraindications

  • pregnancy
  • lactation
  • active malignancy (theoretical)
  • severe hypoglycemia risk on concurrent insulin or sulfonylurea

Interactions

  • insulin: additive insulin sensitization may increase hypoglycemia risk(moderate)
  • metformin: both activate AMPK; theoretical additive metabolic effect, no controlled data(minor)
  • sulfonylureas: increased hypoglycemia risk via additive insulin sensitization(moderate)

N-Acetyl Cysteine

Common side effects

  • sulfur-like taste or odor
  • nausea
  • flatulence
  • diarrhea

Contraindications

  • active asthma attack (inhaled form can trigger bronchospasm)
  • known NAC hypersensitivity

Interactions

  • nitroglycerin: potentiates vasodilation, risk of hypotension and headache(moderate)
  • activated charcoal: reduces NAC absorption when used for acetaminophen overdose(moderate)
  • anticoagulants: theoretical additive antiplatelet effect at high doses(minor)

Which Should You Take?

N-Acetyl Cysteine comes out ahead for most readers on the criteria we weight: 3 catalogued goals, OTC, oral dosing, with a Tier-A outcome catalogued. MOTS-c is the right call when one of the conditionals below applies.

  • If your priority is metabolic health and glucose control, pick MOTS-c.
  • If your priority is mitochondrial function, pick MOTS-c.
  • If your priority is post-training recovery, pick N-Acetyl Cysteine.
  • If your priority is liver function, pick N-Acetyl Cysteine.

Edge case: If you want to avoid research-only / gray-market sourcing, N-Acetyl Cysteine is the more accessible choice.

Default choice: N-Acetyl Cysteine. Wider use case, a Tier-A evidence outcome catalogued, and broader goal coverage. Reach for MOTS-c only if your priority sits squarely in the goals it owns above.

This verdict is generated from each compound's schema (goals, legal status, evidence outcomes, dosing route). It updates automatically as our compound data evolves; the deeper read sits on each individual compound page.

Common questions

What is the difference between MOTS-c and N-Acetyl Cysteine?

MOTS-c and N-Acetyl Cysteine differ in category (peptide vs supplement), mechanism, and typical dosing. See the side-by-side table for full details.

Which has a longer half-life, MOTS-c or N-Acetyl Cysteine?

MOTS-c half-life is 0.5 hours; N-Acetyl Cysteine half-life is 5.6 hours.

Can you stack MOTS-c with N-Acetyl Cysteine?

Stack compatibility depends on mechanism overlap, legal status, and individual response. Check each compound page for specific interactions and contraindications before combining.

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