NAD+ vs SS-31 (Elamipretide)
NAD+ (Cellular coenzyme (dinucleotide)) and SS-31 (Elamipretide) (Mitochondria-targeted tetrapeptide) are documented as co-studied in the PeptiDex library. This page puts the two entries side by side on class, molecular weight, half-life, origin, mechanism and studied research areas — every value taken from the entry it belongs to.
Why these two are co-studied
Cross-referenced for research context — not a usage or combination recommendation.
At a glance
| Attribute | NAD+ | SS-31 (Elamipretide) |
|---|---|---|
| Compound class | Cellular coenzyme (dinucleotide) | Mitochondria-targeted tetrapeptide |
| Research category | Longevity & Cellular | Longevity & Cellular |
| Length (amino acids) | Not documented | 4 amino acids |
| Molecular weight | 663.43 g/mol (free acid) | 639.8 g/mol (approx.) |
| Half-life | Not documented | Not documented |
| Origin | Nicotinamide adenine dinucleotide (NAD+) is a naturally occurring coenzyme present in all living cells, first described in the early 20th century in the context of fermentation and cellular respiration. It is not a peptide but a dinucleotide composed of a nicotinamide moiety and an adenine moiety joined through ribose and phosphate groups. | SS-31 (elamipretide, also known as MTP-131 or Bendavia) is a synthetic, cell-permeable, mitochondria-targeted tetrapeptide developed from the Szeto-Schiller (SS) family of aromatic-cationic peptides. It is one of the most studied members of that peptide series. |
“Not documented” means the PeptiDex entry records no value for that field. Nothing on this page is estimated, and no figure is carried over from one compound to the other.
How NAD+ works
NAD+ functions as a central redox cofactor, cycling between its oxidized (NAD+) and reduced (NADH) forms to shuttle electrons in glycolysis, the citric acid cycle, and oxidative phosphorylation. Beyond redox chemistry, NAD+ is a required substrate for enzymes that consume it, including sirtuins (NAD+-dependent deacylases), poly(ADP-ribose) polymerases (PARPs) involved in DNA repair, and CD38. Cellular NAD+ levels have been reported to decline with age in various tissues, which is a focus of aging research. It is synthesized de novo from tryptophan and through salvage pathways from precursors such as nicotinamide, nicotinic acid, and nicotinamide riboside.
How SS-31 (Elamipretide) works
SS-31/elamipretide selectively concentrates in the inner mitochondrial membrane, where it is reported to bind the phospholipid cardiolipin. By associating with cardiolipin, it is proposed to stabilize the structure of the inner membrane and cristae, support electron transport chain organization and efficiency, and reduce excessive reactive oxygen species production. These actions are intended to improve mitochondrial bioenergetics under conditions of mitochondrial dysfunction.
Mechanistic descriptions reflect published research-literature understanding and are quoted from each compound's own entry. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.
Where each one appears in the literature
The research contexts each entry documents. Listing a research area is not a claim of efficacy or a therapeutic indication, and the two lists are not scored against each other.
NAD+
SS-31 (Elamipretide)
What sets each apart
NAD+
Unlike the peptides in this category, NAD+ is a small-molecule coenzyme central to redox metabolism rather than a signaling peptide, and it is studied primarily via precursor supplementation.
SS-31 (Elamipretide)
SS-31 is a synthetic mitochondria-targeting tetrapeptide that physically localizes to the inner membrane and binds cardiolipin, and unlike most peptides here it has advanced into human clinical trials as elamipretide.
Frequently asked questions
What is NAD+ and what is it studied for?
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme central to cellular energy metabolism, redox reactions, and as a substrate for sirtuins and PARP enzymes involved in DNA repair. It is studied in models of aging, mitochondrial function, metabolic decline, and neuroprotection, where tissue NAD+ levels fall with age. It is a naturally occurring coenzyme, not a peptide.
Is NAD+ a peptide?
No. NAD+ is a dinucleotide coenzyme composed of two nucleotides (one bearing adenine, the other nicotinamide) joined through phosphate groups, not a chain of amino acids. It is grouped in longevity research catalogs alongside peptides because of its role in aging and mitochondrial studies, but it is a distinct chemical class.
How does NAD+ differ from precursors like NMN and NR?
NMN (nicotinamide mononucleotide) and NR (nicotinamide riboside) are biosynthetic precursors that cells convert into NAD+, whereas NAD+ is the finished coenzyme. Precursors are commonly studied as oral routes to raise intracellular NAD+, while NAD+ itself is studied via IV or subcutaneous routes in research settings. Direct cellular uptake of intact NAD+ is a subject of ongoing research.
What is SS-31 (elamipretide)?
SS-31 (elamipretide, also known by the codes Bendavia and SS-31) is a mitochondria-targeted tetrapeptide, D-Arg-Dmt-Lys-Phe-NH2, that concentrates in the inner mitochondrial membrane by binding cardiolipin. It is studied in models of mitochondrial dysfunction, heart failure, ischemia-reperfusion, and age-related bioenergetic decline.
How does SS-31 target mitochondria?
Its alternating cationic and aromatic residues give it strong affinity for cardiolipin, a phospholipid found almost exclusively on the inner mitochondrial membrane. By binding cardiolipin it is thought to stabilize cristae structure and improve electron-transport efficiency, reducing reactive oxygen species.
What is the sequence and molecular weight of SS-31?
SS-31 is the tetrapeptide D-Arg-2',6'-dimethyltyrosine-Lys-Phe-NH2 (D-Arg-Dmt-Lys-Phe-NH2), with molecular formula C32H49N9O5 and a molecular weight of about 639.8 g/mol. The unusual dimethyltyrosine and C-terminal amide are defining features.
Answers are the ones published on each compound's own PeptiDex entry. They are educational summaries of research-literature context and are not medical advice.