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BiologicalX

Comparison

MOTS-c vs TB-500

Side-by-side of MOTS-c and TB-500. 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

TB-500

  • 17-amino-acid fragment of endogenous Thymosin Beta-4, an actin-sequestering peptide
  • Preclinical models show accelerated tendon, ligament, and dermal wound healing
  • Equine veterinary use for soft-tissue injury is the most documented real-world application
  • Anecdotal human protocols use 2 to 5 mg twice weekly subcutaneously for 4 to 6 weeks
  • WADA banned under S2 (peptide hormones, growth factors) since 2018
  • No completed phase II or III human RCTs as of 2026; long-term safety unestablished

Side-by-side

Attribute MOTS-c TB-500
Category peptide peptide
Also known as Mitochondrial Open Reading Frame of the Twelve S rRNA-c, MOTSc Thymosin Beta-4 fragment, TB4-Frag, Thymosin Beta 4
Half-life (hr) 0.5 2
Typical dose (mg) 5 2.5
Dosing frequency 2-3x weekly 2x weekly (anecdotal protocols)
Routes subcutaneous subcutaneous, intramuscular
Onset (hr) 1 -
Peak (hr) 4 -
Molecular weight 1880.18 4963.4
Molecular formula C82H132N22O25S2 C212H350N56O78S
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. Sequesters G-actin monomers, modulates cell migration and angiogenesis, and upregulates VEGF and myosin transcription. Promotes endothelial differentiation and stem-cell migration to injury sites in preclinical models.
Legal status Not FDA approved; research-use-only grey market; not currently on WADA Prohibited List Not FDA approved; research-use-only grey market; banned by WADA
WADA status unknown banned
DEA / Rx Not scheduled (research chemical) Not FDA approved; not scheduled; research-chemical status
Pregnancy Insufficient data; not recommended Insufficient data
CAS 1627580-64-6 885340-08-9
PubChem CID 139599184 62707662
Wikidata Q24832108 Q7799921

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)

TB-500

Common side effects

  • injection-site irritation
  • fatigue (anecdotal)
  • lethargy in early dosing (anecdotal)

Contraindications

  • pregnancy
  • active malignancy (theoretical angiogenic concern)
  • no established human safety profile

Interactions

  • BPC-157: Frequently co-administered in anecdotal healing protocols; no controlled interaction data(minor)

Which Should You Take?

MOTS-c and TB-500 score evenly on the criteria we weight (goal breadth, legal accessibility, evidence depth). The conditionals below should drive the decision more than any aggregate score.

  • If your priority is healthspan extension, pick MOTS-c.
  • If your priority is metabolic health and glucose control, pick MOTS-c.
  • If your priority is post-training recovery, pick TB-500.
  • If your priority is tendon repair, pick TB-500.

Edge case: Half-lives differ materially (MOTS-c ~0.5 hr vs TB-500 ~2 hr). TB-500 reaches steady state faster; MOTS-c is easier to dial in if tolerability is uncertain.

Default choice: either is defensible. MOTS-c edges out on goal breadth + legal accessibility; TB-500 is the right call if your priority sits in the goals listed 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 TB-500?

MOTS-c and TB-500 differ in category (peptide vs peptide), mechanism, and typical dosing. See the side-by-side table for full details.

Which has a longer half-life, MOTS-c or TB-500?

MOTS-c half-life is 0.5 hours; TB-500 half-life is 2 hours.

Can you stack MOTS-c with TB-500?

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

Go deeper