MOTS-c (Human)

• Research strengths include a defined native 16-residue sequence, a well-cited mitochondrial open-reading-frame origin and multiple testable pathways across metabolic-stress, insulin-sensitivity, exercise-adaptation and aging models
• Animal studies report effects on glucose homeostasis, diet-induced obesity, age-related muscle insulin resistance and physical performance, while human exercise studies describe endogenous MOTS-c measurements
• The appropriate evidence classification is predominantly preclinical; the registered native-MOTS-c Phase 2a study will require posted results before it can inform human efficacy or safety conclusions.

CAS

1627580-64-6

Formula

C₁₀₁H₁₅₂N₂₈O₂₂S₂

Molecular weight

2174.6 g/mol

Appearance

Lot-specific lyophilized research peptide; confirm appearance on the released-lot COA

Purity

Lot-specific chromatographic purity plus quantitative peptide content; confirm sequence, intact mass, counterion, water and methionine-oxidation profile separately · target, verify batch COA

Storage

Store and ship according to the lot COA and validated stability data for the exact sequence, salt, formulation, solvent, concentration and container. Generic 2-8 degrees Celsius, minus 20 degrees Celsius and prompt-use statements are not interchangeable. Avoid unvalidated freeze-thaw cycles and document excursions.

MOQ

1 kit (10 vials) per SKU

Lead time

10–18 days

MOTS-c is a 16-amino-acid mitochondrial-derived peptide encoded by a short open reading frame within the mitochondrial MT-RNR1 / 12S rRNA region and first reported by Lee et al. in Cell Metabolism in 2015. Research has linked it to folate-purine metabolism, AICAR- and AMPK-associated responses, metabolic homeostasis and stress-dependent nuclear signaling. The evidence base is predominantly cellular and animal. NCT07505745 provides current human research context as a recruiting, randomized Phase 2a study in adults with prediabetes and overweight or obesity; results are not yet posted. CB4211 is a distinct synthetic MOTS-c-derived analogue with its own early-phase development record and must be assessed separately from native MOTS-c.

• Relevant research domains include metabolic homeostasis, insulin sensitivity, exercise adaptation, aging biology, mitochondrial stress signaling and native-peptide versus analogue comparison
• Human exercise-associated measurements are observational
• NCT07505745 is recruiting 120 adults with prediabetes and overweight or obesity and has an estimated primary completion in 2027
• CB4211 remains a distinct derivative, so its early human data must be interpreted under its own identity and protocol.

The foundational cell and mouse study linked MOTS-c exposure to inhibition of folate-cycle and de novo purine metabolism, accumulation of AICAR and AMPK-associated metabolic responses. A later study reported that metabolic stress can drive MOTS-c nuclear translocation and interaction with stress-responsive transcriptional programs. Exact timing, motif dependence and downstream readouts belong to those experimental systems; they do not establish an administered-human mechanism, clinical benefit or universal exposure-response relationship.

• Human safety and pharmacokinetic characterization of native MOTS-c remains an open research question
• Animal tolerability and CB4211 Phase 1 observations belong to different evidence contexts and should be labelled accordingly
• WADA's 2026 Prohibited List includes MOTS-c under S4.4.1 AMPK activators, prohibited at all times
• TUE questions follow current official rules
• This supplied material is for laboratory research only.

Interactions reported in the literature

• Human co-administration evidence has not established compatibility with metformin, glucose-lowering medicines, NAD precursors, resveratrol, berberine, GH-axis peptides or other AMPK activators
• Shared-pathway relationships are useful for hypothesis design, while combination compatibility, assay interference and monitoring requirements remain protocol-specific
• Anti-doping status is a separate compliance consideration.

Laboratory: Manufacturer's QC laboratoryTests: HPLC purity · MS identity · endotoxin · fill amount

• 10 mg
• 15 mg
• 20 mg
• 40 mg

Previews are blurred on purpose so the documents cannot be reused; third-party reports show their first page only. Sales sends the clear full version for the product and strength you ask about.

Independent test fails? Full refund.

On every batch COA: HPLC purity · MS identity · endotoxin · fill amount · Verify LyoPep

Ask for the current packet, not a generic certificate

• A clear solution, white powder or HPLC area percentage cannot establish sequence identity, peptide content, sterility or biological equivalence to research material
• Require complete sequence and terminal state, salt/counterion, high-resolution intact mass and sequence-confirming MS/MS, chromatographic purity with raw data and impurity profile, quantitative peptide content, water and counterion, residual solvents and lot-specific stability
• Oxidation and other sequence-relevant degradants should be controlled
• Sterility, endotoxin and particulates require separate validated tests when claimed.

Store and ship according to the lot COA and validated stability data for the exact sequence, salt, formulation, solvent, concentration and container. Generic 2-8 degrees Celsius, minus 20 degrees Celsius and prompt-use statements are not interchangeable. Avoid unvalidated freeze-thaw cycles and document excursions.

State the destination and timing so receipt can be planned, then move the material into its stated storage condition on arrival.

• The 2015 Cell Metabolism paper is the foundational discovery and metabolic-homeostasis study. Later work addresses exercise and age-dependent function, plasma metabolomics, stress and aging mechanisms, CK2 binding and diabetic-heart models, predominantly preclinically. NCT07505745 is an official recruiting Phase 2a registry record with no results posted, not proof of efficacy. The CohBar release reports CB4211, a distinct MOTS-c-derived analogue, and is company-reported early-phase evidence only. The current official WADA list controls anti-doping status.

1. 01

   The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance

   Cell Metabolism · 2015 · peer-reviewed original research

   Open source
2. 02

   MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis

   Nature Communications · 2021 · peer-reviewed original research

   Open source
3. 03

   The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity

   Physiological Reports · 2019 · peer-reviewed original research

   Open source
4. 04

   Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging

   Journal of Translational Medicine · 2023 · systematic review

   Open source
5. 05

   MOTS-c modulates skeletal muscle function by directly binding and activating CK2

   iScience · 2024 · peer-reviewed original research

   Open source
6. 06

   Mitochondria-derived peptide MOTS-c restores mitochondrial respiration in type 2 diabetic heart

   Frontiers in Physiology · 2025 · peer-reviewed original research

   Open source
7. 07

   MOTS-c for Improving Insulin Sensitivity in Adults With Prediabetes and Overweight/Obesity (MOTS-MET)

   ClinicalTrials.gov · 2026 · clinical trial registry entry

   Open source
8. 08

   CohBar Announces Positive Topline Results from the Phase 1a/1b Study of CB4211 Under Development for NASH and Obesity

   GlobeNewswire (CohBar, Inc. investor/media release) · 2021 · company press release

   Open source

• How to read a peptide COA without confusing purity, identity and content
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