MS10 - MOTS-C - 10 MG - Research Use Only

Name: MS10 - MOTS-C - 10 MG - Research Use Only
Brand: Peptific
SKU: MS10
Price: 16 USD
Availability: OutOfStock

MOTS-c is a 16-amino-acid mitochondrial-derived peptide (encoded in mitochondrial 12S rRNA) studied in animal models as an exercise mimetic — activating AMPK, improving insulin sensitivity, and declining with age.

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$16.00

MOTS-c-

$16.00

✓HPLC purity tested
✓COA per lot, on request
✓Lyophilized, sealed
✓US shipping, tracked

Only mitochondria-encoded peptide — mechanistically distinct from all nuclear-gene-derived research compounds
Activates AMPK in skeletal muscle — the same pathway as metformin and exercise, via an insulin-independent mechanism
Studied as exercise mimetic in rodent models — improves glucose tolerance and metabolic markers in sedentary animals
Plasma MOTS-c declines with age, rises with exercise — relevant to aging biology and mitochondrial signaling research
Investigated for visceral adiposity reduction and insulin sensitivity improvement in diet-induced obesity rodent models

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In your order

What ships when you order MOTS-c

Lyophilized vial
Sterile-filtered, freeze-dried peptide in glass vial, sealed under inert gas.
Lot ID on every vial
Printed lot ID ties this exact vial to its analytical record.
COA on request
Independent third-party HPLC certificate, matched to your lot, sent on request.
Carrier-tracked shipping
Shipped from a US facility with full carrier tracking and protective packaging.

The Peptific standard

Why researchers buy from Peptific instead of grey-market vendors

Peptide quality is invisible until it isn’t. Lot identity, purity, fill integrity, and chain of custody are the difference between usable research material and wasted budget.

Third-party HPLC tested
Every lot is tested for identity and purity by an independent analytical lab. Certificate of Analysis available on request, tied to the exact lot you receive.
Lyophilized and lot-tracked
Sterile-filtered, freeze-dried, sealed under inert gas. Each vial carries its own lot ID — full chain of custody from fill to delivery.
US-based fulfillment
Orders ship from a temperature-controlled US facility with carrier tracking. No drop-shipping, no opaque overseas relay.
Real support, not a ticket queue
A real person responds to research questions, lot questions, and order questions — usually same business day. No bot triage.

How it works

The MOTS-c mechanism

MOTS-c activates AMPK and the folate-methionine cycle, promoting insulin-independent glucose uptake in skeletal muscle. In rodent studies, MOTS-c administration improves insulin sensitivity, reduces adiposity, and activates metabolic pathways normally engaged by exercise. Plasma MOTS-c declines with age, rises with physical activity — positioning it as a mitochondrial-nuclear metabolic communication signal.

Compound profile

Class: Mitochondrial-derived peptide (MDP)
Encoding: Mitochondrial 12S rRNA gene — not nuclear genome encoded
Amino acids: 16
Molecular weight: ~2,174 Da
Primary mechanism: AMPK activation, folate-methionine cycle, insulin-independent glucose uptake
Discovery: Lee et al., Cell Metabolism, 2015
Research category: Mitochondrial biology, aging, exercise mimetic, metabolic disease
Storage: Lyophilized: −20°C. Reconstituted: 2–8°C, use within 30 days

Product definition

What is MOTS-c?

MOTS-c (Mitochondrial ORF of the 12S rRNA Type-C) is a 16-amino-acid peptide discovered by Changhan David Lee's group at USC, encoded by a small open reading frame within the 12S rRNA gene of the mitochondrial genome. Unlike all prior research peptides, it is not a nuclear gene product — it is a mitochondria-encoded signaling molecule that translocates from mitochondria to the nucleus and into systemic circulation, functioning as a retrograde signal from the mitochondria to the rest of the organism. The functional research profile documents AMPK activation as the primary downstream effect in skeletal muscle — the same kinase activated by metformin and physical exercise. MOTS-c-treated rodents show improved glucose tolerance, increased skeletal muscle glucose uptake (GLUT4 translocation), reduced diet-induced obesity, and enhanced physical performance in exercise capacity models. The discovery that plasma MOTS-c rises with exercise and declines with age across multiple mammalian species has made it a central compound in the emerging field of mitochondria-aging research.

Research audience

Who studies MOTS-c?

MOTS-c is used by researchers in mitochondrial biology, aging science, metabolic disease, AMPK pharmacology, exercise physiology, and insulin resistance research. It is the foundational compound for studying mitochondrial-derived peptide signaling and is particularly relevant for investigators studying how mitochondrial function communicates with systemic metabolism.

Research context

What does the preclinical literature say about MOTS-c?

MOTS-c was discovered in 2015 by Changhan David Lee's group at USC and published in Cell Metabolism. The discovery that the mitochondrial genome encodes a secreted peptide that functions as a systemic metabolic regulator was a conceptual advance for mitochondrial biology — prior to this, the mitochondrial genome was assumed to encode only structural components of the oxidative phosphorylation machinery. Subsequent research has established MOTS-c as the best-characterized member of the MDP class. In rodent obesity models, systemic MOTS-c administration reverses high-fat diet-induced obesity, improves glucose homeostasis, and increases physical exercise capacity — effects attributed to AMPK activation in skeletal muscle and adipose tissue. The folate-methionine cycle activation provides a mechanism for MOTS-c's effects on AMPK independent of direct adenylate kinetics. Human aging studies have documented age-related decline in plasma MOTS-c levels and inverse correlation between MOTS-c levels and obesity/metabolic syndrome markers, supporting the hypothesis that declining MDP signaling contributes to metabolic aging. Phase I clinical research with MOTS-c is ongoing, making it one of the few mitochondrial-derived peptides with early human data in the pipeline.

Common questions

What makes MOTS-c mechanistically different from other metabolic peptides?

Every other research peptide is encoded by the nuclear genome and produced in ribosomes. MOTS-c is encoded in the mitochondrial genome — a 16,569 bp circular genome that encodes only 37 genes total, previously thought to exclusively encode oxidative phosphorylation components. MOTS-c's discovery demonstrated that the mitochondrial genome produces a systemic signaling peptide, which is a mechanistic class distinction with fundamental implications for understanding mitochondria-to-nucleus retrograde communication and aging biology.

How does MOTS-c compare to humanin and other MDPs?

Humanin (HN) was the first characterized MDP, discovered in 2001. MOTS-c is a later discovery with a distinct amino acid sequence and mechanism. Humanin's primary research context is neuroprotection and Alzheimer's disease; MOTS-c's primary context is metabolic regulation and exercise biology. Both decline with age, but they differ in their downstream signaling pathways and tissue distribution. MOTS-c is the most studied MDP for metabolic/aging research; humanin is the reference for neuroprotective MDP research.

Are there any published human data on MOTS-c?

Observational human data exist: plasma MOTS-c levels decline with age in human cross-sectional studies and show inverse correlation with metabolic syndrome markers. Exercise-induced MOTS-c elevation has been documented in human plasma samples. Interventional clinical trials are in early stages as of the current research landscape. Published preclinical rodent data constitutes the bulk of the mechanistic research base.