MOTS-C – 40mg

£39.95

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MOTS-C 40mg is a 16-amino-acid mitochondrial-derived research peptide studied in how cells sense energy stress, regulate glucose and fuel metabolism, and communicate signals from mitochondria to the nucleus, with major research involving AMPK, skeletal-muscle metabolism and exercise-response biology.

Strength: 40mg

Full name: Mitochondrial Open Reading Frame of the 12S rRNA-c

Peptide class: Mitochondrial-derived peptide

Peptide length: 16 amino acids

Sequence: Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg

Sequence notation: MRWQEMGYIFYPRKLR

Biological origin: Described from a short open reading frame within the mitochondrial 12S rRNA region

Research focus: AMPK-linked energy sensing, glucose and metabolic regulation, mitonuclear signalling, skeletal-muscle biology and metabolic-stress responses

Minimum purity standard: ≥99%

Form: Lyophilised solid

Batch traceability: Maintained

Documentation: COA & SDS available

For laboratory research use only. Not for human or veterinary use.
Why Pronoia
  • Independent Testing
  • COA & SDS Documentation
  • Temperature-Controlled Storage
  • Tracked UK Delivery
Quantity Discount (%) Price
1 — £39.95
2 5.01 % £37.95
3 - 4 9.99 % £35.96
5+ 14.99 % £33.96

Description

About MOTS-C

MOTS-C is a 16-amino-acid mitochondrial-derived peptide originally described from a short open reading frame within the mitochondrial 12S ribosomal RNA region.

Its sequence is Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg, commonly represented as MRWQEMGYIFYPRKLR.

Mitochondria are best known for their role in cellular energy production, but they also function as signalling centres that communicate information about metabolic conditions to the rest of the cell. MOTS-C is particularly interesting because it provides an experimental model for signalling associated with a peptide sequence originating from the mitochondrial genome.

Published research has linked MOTS-C with cellular energy sensing, glucose metabolism and AMPK — a major signalling system activated when cells experience changes in energy availability.

Research has also shown that MOTS-C can move into the cell nucleus during metabolic stress and influence nuclear gene expression, creating an experimental link between mitochondrial signalling and nuclear stress-response pathways.

Further research has expanded the MOTS-C landscape into skeletal-muscle metabolism, exercise responses, physical-capacity models and mitochondrial bioenergetics.

Together, these characteristics make MOTS-C relevant to experimental studies of metabolic homeostasis, energy-stress adaptation, mitochondria-to-nucleus communication and skeletal-muscle biology.

Pronoia supplies MOTS-C in a higher-total-content 40mg lyophilised research format with batch traceability and supporting documentation available for the supplied material.

Product Specification

Product: MOTS-C

Strength: 40mg

Full name: Mitochondrial Open Reading Frame of the 12S rRNA-c

Peptide class: Mitochondrial-derived peptide

Peptide length: 16 amino acids

Sequence: H-Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg-OH

Sequence notation: MRWQEMGYIFYPRKLR

Biological origin: Described from a short open reading frame within the mitochondrial 12S rRNA region

Research pathways: AMPK signalling, metabolic-stress responses and mitonuclear communication

Research focus: Energy sensing, glucose and metabolic regulation, skeletal-muscle biology and mitochondrial signalling

Form: Lyophilised solid

Pronoia minimum purity standard: ≥99%

Batch traceability: Maintained

SKU: PB-MOTS-40

Testing & Batch Documentation

Pronoia maintains a structured quality, testing and traceability process for MOTS-C, with supporting documentation retained for the supplied research material.

  • Batch-tested research material
  • Pronoia minimum accepted purity standard of ≥99%
  • Full batch traceability
  • Batch-separated and labelled inventory
  • Physical inventory routinely reconciled with digital stock records
  • Temperature-controlled cold storage
  • Certificate of Analysis (COA) and Safety Data Sheet (SDS) documentation available

The applicable Certificate of Analysis should be treated as the authoritative reference for the identity, purity and analytical results reported for an individual batch.

Research Context

MOTS-C was identified during research examining whether mitochondrial DNA contains short open reading frames associated with biologically active signalling peptides.

Its discovery contributed to a wider research field examining mitochondria not only as cellular energy-producing organelles, but also as active participants in metabolic signalling and communication.

AMPK and cellular energy sensing

One of the strongest areas of MOTS-C research concerns AMP-activated protein kinase, or AMPK.

AMPK acts as a cellular energy sensor. When energy availability changes, AMPK can alter metabolic pathways involved in glucose utilisation, fatty-acid metabolism and broader cellular energy balance.

Foundational MOTS-C research reported effects on folate-cycle and de novo purine metabolism, including accumulation of the AMP analogue AICAR and subsequent AMPK activation.

Experimental findings included:

  • Activation of AMPK-associated metabolic signalling
  • Changes in folate and purine metabolic pathways
  • Changes in glucose utilisation and glycolytic metabolism
  • Regulation of cellular metabolic homeostasis

These findings provided an important mechanistic connection between MOTS-C and cellular energy-sensing pathways.

Glucose regulation and metabolic models

MOTS-C has been investigated extensively in preclinical metabolic research.

In mouse models exposed to high-fat-diet conditions, researchers reported changes including:

  • Improved glucose handling
  • Improved insulin sensitivity
  • Reduced development of diet-associated metabolic dysfunction
  • Changes in body-weight and metabolic responses under the experimental conditions used

Skeletal muscle emerged as an important target tissue within this work.

These findings have made MOTS-C relevant to research examining interactions between mitochondrial signalling, skeletal-muscle glucose utilisation, insulin-responsive metabolism and whole-body metabolic homeostasis.

The findings derive primarily from preclinical systems and should not be interpreted as established metabolic or weight-management effects in humans.

Mitochondria-to-nucleus signalling

A particularly distinctive area of MOTS-C research concerns communication between mitochondria and the nuclear genome.

Under metabolic stresses including glucose restriction and oxidative stress, researchers reported that MOTS-C could translocate into the nucleus.

This nuclear movement was associated with AMPK activity.

Within the nucleus, MOTS-C influenced expression of genes involved in cellular stress responses.

Experimental findings included:

  • Stress-associated nuclear translocation of MOTS-C
  • AMPK-dependent regulation of the nuclear response
  • Changes in stress-responsive nuclear gene expression
  • Interaction with antioxidant-response-element-associated transcriptional systems
  • Interaction with NRF2-associated stress-response signalling

This makes MOTS-C particularly relevant to research into mitonuclear communication — the processes through which mitochondrial state can influence signalling and gene regulation elsewhere in the cell.

Exercise and skeletal-muscle research

Research has also examined the relationship between endogenous MOTS-C and physical activity.

In healthy young men undertaking cycling exercise, researchers reported increased endogenous MOTS-C in skeletal muscle following exercise together with a transient rise in circulating MOTS-C.

This provided human physiological evidence that the endogenous MOTS-C system responds dynamically to exercise.

Within the wider research programme, experimental administration of MOTS-C in mouse models has been associated with:

  • Improved physical performance across different age groups
  • Changes in skeletal-muscle metabolism
  • Changes in nuclear genes involved in metabolism and protein homeostasis
  • Improved adaptation to metabolic stress

The evidence types should be distinguished carefully: the human research demonstrated changes in the body’s endogenous MOTS-C response to exercise, while many intervention and performance-related findings derive from mouse and cell models.

Metabolic-stress and cellular adaptation

MOTS-C has also been studied in cells exposed to conditions including restricted glucose availability and oxidative stress.

These experiments investigate how cellular systems adapt when energy supply or metabolic conditions change.

Research has linked MOTS-C with:

  • AMPK-dependent stress responses
  • NRF2-associated antioxidant-response signalling
  • Stress-responsive gene regulation
  • Changes in cellular metabolism during nutrient restriction
  • Adaptive responses to metabolic and oxidative stress

This broadens MOTS-C research beyond glucose metabolism alone into the wider biology of cellular adaptation.

Newer skeletal-muscle mechanisms

More recent experimental research has continued to refine the molecular mechanisms associated with MOTS-C.

Researchers have identified casein kinase 2 (CK2) as a direct MOTS-C-binding protein and reported that CK2 activity contributes to MOTS-C-associated changes in skeletal-muscle glucose uptake and muscle homeostasis.

Additional recent research has examined mitochondrial bioenergetic performance in skeletal muscle and reported MOTS-C-associated changes dependent on AMPK and the metabolic transcriptional regulator PGC-1α.

These findings extend the research landscape from broad metabolic observations into more specific questions concerning mitochondrial efficiency, energy sensing and skeletal-muscle signalling.

Why MOTS-C is useful experimentally

The scientific interest in MOTS-C comes from the connection it provides between several normally distinct areas of biology:

  • Mitochondrial signalling
  • AMPK-linked cellular energy sensing
  • Glucose and fuel metabolism
  • Skeletal-muscle metabolic regulation
  • Mitochondria-to-nucleus communication
  • Metabolic and oxidative-stress responses
  • Exercise-associated mitochondrial biology
  • Mitochondrial bioenergetics

Rather than representing simply another metabolic peptide, MOTS-C provides an experimental framework for studying how mitochondrial status can influence cellular metabolism, nuclear signalling and adaptation to energetic stress.

The evidence base includes cell-culture, animal and human physiological research, but these evidence types differ substantially. Findings from experimental administration in preclinical models should not automatically be interpreted as equivalent human outcomes.

The published findings do not establish clinical efficacy, safety or suitability for human or veterinary use.

Storage & Handling

MOTS-C is supplied in lyophilised form and should be stored according to the conditions specified by Pronoia and the applicable batch documentation.

Pronoia stock is maintained in temperature-controlled cold storage and organised by identifiable batch prior to dispatch.

The material should be protected from unnecessary exposure to heat, moisture and light and handled using appropriate laboratory procedures.

Where batch-specific storage or handling information is supplied, that information should take precedence.

UK Delivery

MOTS-C is dispatched from Pronoia’s UK stock using tracked delivery.

Current availability and dispatch information are shown directly on the product page, with tracking supplied following dispatch.

Orders are prepared through Pronoia’s established research-product fulfilment process, with applicable delivery conditions remaining subject to Pronoia’s current delivery terms.

Research Use

MOTS-C supplied by Pronoia Bio is intended for laboratory research and experimental use only.

It is not supplied for human or veterinary use and should not be treated as a medicine or consumer healthcare product.

Pronoia does not provide dosage, treatment or administration guidance for this research material.

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