MOTS-c

SKU: REF-MOTSC

Metabolic · Energy · Longevity

MOTS-c is a mitochondria-derived peptide used to support metabolic health, fat loss, and exercise performance by mimicking some of the cellular effects of exercise. It signals cells to take up more glucose, burn more fat, and activate stress-resistance pathways associated with metabolic resilience. It's a popular longevity and performance peptide for people looking to support their energy metabolism and healthy aging.

$200 / 40 mg vial

Dosing

Native MOTS-c, human dosing – No citable dose

No citable figure. No published, citable human dosing exists for native MOTS-c peptide. This is a case where the correct answer is that no citable dose exists; do not treat any number in circulation for native MOTS-c as validated.

Community reported

Community titration (peptidedosages.com)
Timeframe Dosage Frequency Note
Weeks 1-2 200 mcg once daily Starting dose1
Weeks 3-4 400 mcg once daily
Weeks 5-6 600 mcg once daily
Weeks 7-8 800 mcg once daily
Weeks 9-10+ 1,000 mcg (1.0 mg) once daily Stated maximum2
  1. Subcutaneous. Cycle length 8-12 weeks, extension to 16 weeks optional.
  2. A first-person community report describes escalating to 60 units (3 mg) daily on advice this was 'a pretty standard dose,' with severe, incapacitating fatigue at both 40 and 60 units; that poster settled on 0.5 mg as their actual working dose. Frequency convention (daily vs. 5-on/2-off) and reports of '15 mg per week' are also unsettled among regular community users.

Batches on hand

Availability

30 vials on hand.

MKM-MS40-26072630 vials
Full research

Evidence tier

Animal and in-vitro only

The substantial metabolic and longevity evidence base for native MOTS-c (obesity prevention, insulin sensitization, exercise capacity, lifespan) comes entirely from rodent and cell studies. The only human interventional data in the MOTS-c family belongs to CB4211, a structurally distinct synthetic analog developed by CohBar Inc. whose development was subsequently discontinued; this data does not describe the native peptide sold commercially as MOTS-c. One registered native-peptide human trial (NCT07505745, Phase 2a, prediabetes and overweight/obesity) is recruiting with no results reported at the time of this research.

Original dosing schedule

The Dosing table above this section now shows a community- or vendor-sourced schedule (peptidedosages.com). The regulatory-label or clinical-trial dosing this entry was originally built on is kept here, unchanged, rather than removed.

Clinical trial

CB4211 (distinct synthetic analog), Phase 1a/1b trial dosing
Timeframe Dosage Frequency Note
Ongoing 0.2-3 mg/kg/day Phase 1a/1b ascending dose Different molecule12
  1. CB4211 is a distinct synthetic analog, not native MOTS-c; this dosing does not transfer to the native peptide.
  2. Phase 1a used single/multiple ascending doses; Phase 1b was 25 mg subcutaneously once daily for 28 days.

Identity

Full name MOTS-c (Mitochondrial Open reading frame of the Twelve S ribosomal RNA type-c)
Class Mitochondrial-derived peptide (AMPK-pathway metabolic signaling peptide)
Molecular weight 2174.6 g/mol
Sequence MRWQEMGYIFYPRKLR

Mechanism of action

Plain language

MOTS-c appears to act as a chemical messenger from the mitochondria to the rest of the cell, signaling metabolic stress in a way that mimics some of the effects of exercise: increased glucose uptake, increased fat burning, and activation of cellular stress-resistance programs.

Technical

Under metabolic stress, MOTS-c is proposed to translocate to the nucleus and activate AMP-activated protein kinase (AMPK), the cell's central energy-sensing kinase. A specific proposed mechanism is that MOTS-c inhibits the folate cycle and its coupled de novo purine biosynthesis pathway, causing accumulation of AICAR, itself a known AMPK activator, thereby indirectly driving AMPK activation. This folate-cycle/AICAR mechanism is a proposed model rather than a fully established one. Downstream, MOTS-c has been reported to promote GLUT4 translocation to the plasma membrane in an AMPK-dependent manner (one study reporting a dependency on mitofusin), increasing insulin-stimulated glucose uptake in skeletal muscle and reducing lipogenesis in adipose tissue.

Sources: PMC9905433, MOTS-c: A, PMC8275580, Mitofusion is

Why: No human data, native form

No published, citable human dosing, efficacy, or pharmacokinetic data exists for native MOTS-c, the 16-amino-acid peptide sold commercially. The entire metabolic evidence base (obesity prevention, insulin sensitization, exercise capacity, lifespan) comes from rodent and cell studies. One native-peptide human trial, a Phase 2a study in prediabetes and overweight/obesity, is registered and recruiting, with no results reported at the time of this research.

Sources: Cell Metabolism (2015),, 2015, ClinicalTrials.gov NCT07505745, MOTS-c

Why: Human data belongs to a different molecule

Every piece of human interventional data cited anywhere for "MOTS-c," a Phase 1a dose-escalation study in 65 healthy adults and a Phase 1b trial in 20 obese subjects with NAFLD, was collected using CB4211, a structurally distinct synthetic analog developed by CohBar Inc. whose development program was subsequently discontinued. That data describes CB4211, not the native peptide marketed and sold as MOTS-c, and should not be read as human efficacy, safety, or dosing evidence for the native peptide.

Sources: BioSpace, CohBar Completes, BioSpace, CohBar Announces

Why: Mouse-only mechanism evidence

The proposed AMPK-activation mechanism, and the associated findings of prevented diet-induced obesity, improved insulin sensitivity, increased exercise capacity, and extended lifespan, all come from mouse studies. A human observational finding exists (higher serum MOTS-c correlating with greater muscle mass, force, and jumping power) but this is correlational and non-interventional, not a treatment trial.

Sources: Cell Metabolism (2015),, 2015, Nature, Experimental &, 2025

What it’s used for

Off-label / community use

  • Widely sold and marketed in the peptide-retail community, as the native 16-amino-acid peptide, for "metabolic health," fat loss, exercise performance, and longevity. None of these community uses of native MOTS-c are supported by completed human efficacy trials; the only human interventional data that exists for the MOTS-c family belongs to CB4211, a structurally distinct synthetic analog, not the native peptide sold commercially.

Pharmacokinetics

Native MOTS-c human pharmacokinetics

Not established

No citable figure. No citable human pharmacokinetic data (Tmax, half-life, bioavailability) for native MOTS-c was identified in the peer-reviewed literature accessed during this research. A commonly repeated vendor claim of approximately 80% subcutaneous bioavailability could not be traced to a primary source and is flagged as unsourced.

Route

Animal / in-vitro

Animal studies: intraperitoneal or subcutaneous injection. CB4211 human trials (distinct analog): subcutaneous.

Sources: Cell Metabolism (2015),, 2015

Reconstitution

Reconstitution does not apply to this compound: No validated human clinical dose exists for native MOTS-c, so no defensible unit-on-a-U-100-syringe mapping can be given. This research document explicitly flags reconstitution data as a genuine gap for this compound: any dose-to-units mapping found on vendor pages maps a commercial vial (commonly 5 mg or 10 mg lyophilized, reconstituted with bacteriostatic water to 10 mg/mL) to an unpublished, community-derived dose, not a clinically validated one.

Storage and post-reconstitution stability

Unopened storage

Vendor sources describe storing lyophilized powder frozen (around -20 degrees C) for long-term storage or refrigerated (2-8 degrees C) if reconstituting within weeks; treat as commercial claims only, not peer-reviewed or pharmacopeial data.

Post-reconstitution stability – Not established

Vendor sources describe refrigerating the reconstituted solution, protecting from light, and avoiding freeze-thaw cycles.

No citable figure. No specific post-reconstitution day figure was found for MOTS-c; only qualitative vendor guidance (frozen long-term, refrigerated if using within weeks) exists. No peer-reviewed or pharmacopeial stability data for reconstituted MOTS-c was identified.

Safety

Notable risks

  • No formal human dose-escalation toxicology (organ pathology, clinical chemistry, hematology panels) has been published for native MOTS-c, and no LD50 or maximum-tolerated-dose determination was identified in the peer-reviewed literature.
  • For the distinct CB4211 analog, Phase 1a/1b reported no serious adverse events at doses up to 25 mg/day subcutaneously for 28 days, but persistent, mild injection-site reactions (painless bumps, believed related to depot persistence of drug at the injection site) were common enough to prompt a temporary trial hold and protocol amendment in 2018 before the study resumed and completed in 2019. This safety record belongs to CB4211, not native MOTS-c.

    Sources: BioSpace, CohBar Announces

  • Multiple secondary sources describe MOTS-c as listed under the World Anti-Doping Agency's Prohibited List, Section S4 (Hormone and Metabolic Modulators), as an AMPK activator, alongside AICAR and BAM15. This research could not directly access and quote the primary WADA list text, so this status is reported as described by secondary sources rather than independently verified against the primary WADA document, and should be re-verified before being treated as settled fact.

This is a research and educational reference, not medical advice. Nothing on this site is a recommendation to use any compound.