Select Strength — 100mg
For in vitro laboratory research use only. Not for human consumption, diagnostic, or therapeutic use.
Research Data
Mechanisms of Action
Data presented from peer-reviewed in vitro studies. All findings are laboratory observations only.
Zhu et al. used non-invasive 31P MRS to measure brain NAD+ in living subjects, confirming age-dependent NAD+ decline and demonstrating that NAD+ repletion restored mitochondrial function. This foundational data established the rationale for NAD+ supplementation in longevity research.
NAD+ is the master coenzyme driving mitochondrial ATP production, DNA repair via PARP activation, sirtuin-mediated longevity signalling, and cellular redox balance. Plasma NAD+ levels decline approximately 50% between ages 40 and 60 — directly impairing all downstream pathways.
Analytical Data
| Specification | Value |
|---|---|
| CAS Number | 53-84-9 |
| Molecular Formula | C₂₁H₂₇N₇O₁₄P₂ |
| Molecular Weight | 663.43 g/mol |
| Purity (HPLC) | 99.3% |
| Appearance | White lyophilised powder |
| Solubility | Soluble in water (10 mg/mL) |
| Storage | −20°C long-term / 2–8°C short-term |
| Shelf Life | 36 months from production date |
| Research Grade | Yes — For In Vitro Use Only |
What Research Has Shown
Age-Related NAD+ Decline — PNAS, 2015
NAD+ Plasma Level Decline Between Ages 40 and 60
Comparative Activity Profile
In Vitro Safety Data
NAD+ is an endogenous coenzyme present in all living cells and is a required cofactor for over 500 enzymatic reactions. IV NAD+ has been used in clinical settings for decades. Primary research considerations relate to oxidative stability and storage handling rather than intrinsic toxicity.
Observed Adverse Indicators
Flushing (IV administration)
lowTransient GI discomfort
lowMild headache
lowSerious adverse events reported
low⚠️ Theoretical Concern
NAD+ is intrinsically safe as an endogenous molecule. The primary research consideration is its extreme sensitivity to oxidation and light degradation after reconstitution.
Researcher Reference
Sirtuins (SIRT1-7) are NAD+-dependent deacylases that regulate longevity pathways including FOXO transcription factors, PGC-1α (mitochondrial biogenesis), and histone modification. Every sirtuin reaction consumes one NAD+ molecule — meaning sirtuin activity is directly rate-limited by NAD+ availability.
NMN and NR are NAD+ precursors that cells convert to NAD+ via the salvage pathway. Direct NAD+ bypasses this conversion step. In terms of cell permeability, NMN enters cells via SLCO4A1 and CD73, while NR uses nucleoside transporters. Direct NAD+ is primarily used for extracellular signalling (CD38, PARP) and requires breakdown/resynthesis for intracellular use.
Lyophilised: −20°C up to 36 months. Reconstituted: 4°C, use within 14 days. Extremely sensitive to oxidation and light — store reconstituted solution in amber vials.
Peer-Reviewed Literature
All citations refer to published peer-reviewed in vitro research. Data presented for scientific reference only. No claims made regarding human therapeutic use.
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