SS-31, MOTS-c and NAD+ Research Set — Research Use Only

Background

Mitochondrial decline is one of the most well-documented hallmarks of aging. As mitochondria lose efficiency, energy output drops, oxidative stress rises, and cells shift toward less efficient metabolic pathways. The three compounds are each studied at a different point in mitochondrial biology: membrane-level protection, AMPK pathway activation, and NAD+-dependent sirtuin signaling.

Compound Profiles

SS-31 (Elamipretide) — Inner Membrane Stabilization

SS-31 binds cardiolipin — a phospholipid critical for inner mitochondrial membrane integrity — preserving the electron transport chain architecture, reducing ROS production, and restoring ATP synthesis in aging mitochondria. Multiple animal models have demonstrated reversal of age-related mitochondrial dysfunction with SS-31.

MOTS-c — Mitochondrial-Derived Peptide & AMPK Activation

MOTS-c is encoded within the mitochondrial genome and acts as a cellular stress sensor, translocating to the nucleus to activate AMPK and regulate glucose and lipid metabolism. In mice, MOTS-c has been reported to alter AMPK signalling and metabolic gene expression.

NAD+ — The Energy Currency Cofactor

NAD+ fuels Complex I in the electron transport chain and is the substrate for SIRT3 — the primary mitochondrial deacetylase regulating fatty acid oxidation, the TCA cycle, and ROS detoxification. NAD+ levels decline significantly with age..

Research Applications

• Age-related mitochondrial decline studies
• Oxidative stress and ROS production research
• AMPK pathway and metabolic flexibility studies
• Cardiac and skeletal muscle mitochondrial function
• Exercise mimetic and metabolic adaptation studies