Mitochondrial & Cellular Energy Research Stack
€139,99
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Mitochondrial & Cellular Energy Research Stack
€139,99
The Mitochondrial & Cellular Energy Stack brings together three premier bioenergetic compounds: NAD+ (1000mg), SS-31 (10mg), and MOTS-c (10mg). Designed to target distinct layers of cellular vitality, this triple-action stack is researched for its multi-targeted influence on ATP production, cardiolipin stabilization, mitochondrial gene expression, and systemic metabolic adaptability.
Research Relevance: Investigated as a comprehensive model in longevity science and cellular bioenergetics, this stack addresses mitochondrial decline across three pivotal axis points: coenzyme availability (NAD+), structural membrane integrity (SS-31), and nuclear-mitochondrial signaling (MOTS-c).
Stack Specifications
| Product Name | Mitochondrial & Cellular Energy Stack |
| Bundle Contents | 1x NAD+ (1000mg) + 1x SS-31 (10mg) + 1x MOTS-c (10mg) |
| Type | Cellular & Mitochondrial Optimization Compounds |
| Purity | ≥ 99% (HPLC – COA available) |
| Molecular Weights | 663.43 g/mol (NAD+) | 639.80 g/mol (SS-31) | 2174.60 g/mol (MOTS-c) |
| Analyses | HPLC, MS |
| Format | Lyophilized powder (3 Vials) |
| Storage Conditions | 2-8°C (short term) or -20°C (long term) |
Confidential Lab Data - Specification Sheet
1. NAD+ (1000mg)
C21H27N7O14P2
Coenzyme Dinucleotide2. SS-31 (10mg)
C32H49N9O5
Mitochondrial Tetrapeptide3. MOTS-c (10mg)
C101H152N28O22S2
Mitochondrial-Derived PeptideSS-31 (Elamipretide) Amino Acid Sequence (4 Amino Acids)
Mitochondria-targeting tetrapeptide engineered with synthetic and D-amino acids.
1D-Arg
2Dmt
3Lys
4Phe
MOTS-c Amino Acid Sequence (16 Amino Acids)
Mitochondrial genome-encoded peptide consisting of 16 amino acids.
1Met
2Arg
3Trp
4Gln
5Glu
6Met
7Gly
8Tyr
9Ile
10Phe
11Tyr
12Pro
13Arg
14Lys
15Leu
16Arg
Mitochondrial Bioenergetics: Tri-Pathway Synergy
Mitochondrial decay is recognized as a hallmark of cellular aging and bioenergetic fatigue. The combination of NAD+, SS-31, and MOTS-c targets mitochondrial health from three distinct biological levels: substrate availability, structural protection, and metabolic gene signaling.
1. Cellular Fuel Substrate: NAD+ (1000mg)
Nicotinamide Adenine Dinucleotide (NAD+) is an essential coenzyme found in every living cell, responsible for mediating redox reactions and powering cellular energy transfer.
- ATP Generation: Serves as the primary electron carrier in glycolysis and the Krebs cycle, fueling oxidative phosphorylation within mitochondrial electron transport chains.
- Sirtuin Activation: Acts as a mandatory cofactor for sirtuins (SIRT1-SIRT7), regulating DNA repair, oxidative stress resilience, and deacetylating key metabolic enzymes.
2. Structural Membrane Stabilization: SS-31 (10mg)
SS-31 (Elamipretide) is a targeted tetrapeptide designed to selectively concentrate on the inner mitochondrial membrane (IMM).
- Cardiolipin Binding: Selectively binds to cardiolipin, a unique phospholipid in the inner membrane, preventing oxidative damage and optimizing cristae architecture.
- ROS Reduction: Reduces reactive oxygen species (ROS) at their source within electron transport complexes I and III, preserving mitochondrial structural integrity.
3. Metabolic Gene Signaling: MOTS-c (10mg)
MOTS-c is a 16-amino-acid peptide encoded within the mitochondrial 12S rRNA gene, functioning as an exercise-mimetic signaling hormone.
- AMPK Pathway Activation: Translocates to the cell nucleus during metabolic stress to activate AMPK and regulate systemic insulin sensitivity and glucose uptake.
- Metabolic Adaptability: Promotes fatty acid oxidation and metabolic homeostasis under conditions of physical or environmental stress.
Primary Research Focus Areas
1. Cellular Longevity & Anti-Senescence
- By sustaining NAD+ pools, protecting membrane lipid structures with SS-31, and modulating nuclear transcription via MOTS-c, this stack provides a robust model for investigating age-related bioenergetic decline.
2. Endurance & Metabolic Flexibility
- Research examines the combined effect of accelerated electron transport efficiency and upregulated glucose clearance in skeletal muscle models.
