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BiologicalX

Comparison

MOTS-c vs TUDCA

Side-by-side of MOTS-c and TUDCA. 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

TUDCA

  • Bile-acid molecule (taurine-conjugated UDCA) with chemical chaperone activity at the endoplasmic reticulum
  • Established pharmaceutical use for cholestasis and primary biliary cholangitis at 500-750 mg/day
  • Reduces ER stress and stabilizes misfolded proteins; the mechanistic basis for emerging ALS / retinal applications
  • Modest improvements in NAFLD markers and insulin sensitivity at 500-1,750 mg/day in small trials
  • Mitochondrial protection signal in animal models drives the longevity-supplement positioning
  • Generally well-tolerated; mild GI effects are the main dose-dependent issue

Side-by-side

Attribute MOTS-c TUDCA
Category peptide supplement
Also known as Mitochondrial Open Reading Frame of the Twelve S rRNA-c, MOTSc tauroursodeoxycholic acid, taurine-conjugated UDCA
Half-life (hr) 0.5 4
Typical dose (mg) 5 500
Dosing frequency 2-3x weekly daily, divided into 2 doses with food
Routes subcutaneous oral
Onset (hr) 1 1
Peak (hr) 4 2
Molecular weight 1880.18 499.7
Molecular formula C82H132N22O25S2 C26H45NO6S
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. Bile-acid signaling via FXR/TGR5 receptors; chemical chaperone reducing ER stress and unfolded protein response; mitochondrial protection through reduced outer-membrane permeabilization.
Legal status Not FDA approved; research-use-only grey market; not currently on WADA Prohibited List OTC dietary supplement (US); pharmaceutical in Italy and several Asian countries
WADA status unknown allowed
DEA / Rx Not scheduled (research chemical) OTC supplement
Pregnancy Insufficient data; not recommended Insufficient data for supplement use; UDCA used in cholestasis of pregnancy
CAS 1627580-64-6 14605-22-2
PubChem CID 139599184 9848818
Wikidata Q24832108 Q418751

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)

TUDCA

Common side effects

  • mild GI upset
  • diarrhea (dose-dependent)
  • constipation (rare)
  • nausea

Contraindications

  • complete biliary obstruction
  • pregnancy / lactation (insufficient supplement-dose data)
  • active GI disease without medical supervision

Interactions

  • cyclosporine, oral contraceptives, fat-soluble vitamins: modest absorption changes via altered bile-acid pool(minor)
  • phenylbutyrate: synergistic for ALS use (Relyvrio combination); consult clinician(moderate)

Which Should You Take?

TUDCA comes out ahead for most readers on the criteria we weight: 3 catalogued goals, OTC dietary supplement, 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 liver function, pick TUDCA.
  • If your priority is mitochondrial function, pick TUDCA.

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

Default choice: TUDCA. Lower friction to source, 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 TUDCA?

MOTS-c and TUDCA 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 TUDCA?

MOTS-c half-life is 0.5 hours; TUDCA half-life is 4 hours.

Can you stack MOTS-c with TUDCA?

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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