Description
NAD+ (Nicotinamide Adenine Dinucleotide) is a central coenzyme in nearly every cell of the body. NAD+ is substrate for sirtuins (SIRT1-SIRT7), PARPs (Poly-ADP-Ribose Polymerases), and CD38 - enzymes central to DNA repair, mitochondrial function, and aging regulation.
Per study reports NAD+ levels decline with age by about 50% between youth and 50th year of life. Restoring NAD+ levels is one of the best-investigated anti-aging pathways. The NAD+ precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR) are orally available with bioavailability problems - direct NAD+ injection bypasses these.
Preclinical studies document broad effects: improved mitochondrial function, elevated sirtuin activity with follow-on effects on gene expression, extension of median lifespan in animal models, neuroprotective action in Alzheimer research setups.
Typical application is subcutaneous or intravenous (in clinic settings as IV drip) in 8-12 week courses or continuous application with reduced doses.
Known effects: at too-rapid administration “NAD+ flush” (heat feeling, pressure in chest and abdomen), mild tachycardia. In standard doses very well tolerated.
You can order NAD+ Inject as an oily injection solution in 10-pack at 100mg/ml.
This information is for research and educational purposes only. No medical recommendations.
Risks & Safety
NAD+ Inject is considered well tolerated per study reports at standard doses. As an endogenous coenzyme, no pronounced toxicity profile is described, and the central point is the speed of administration.
Observed in studies and user reports:
- NAD+ flush: with overly rapid administration, a “NAD+ flush” with a heat sensation and pressure in the chest and abdomen is reported, which markedly subsides with slower dosing.
- Circulation: in connection with the flush, mild tachycardia is occasionally described.
- Injection site: mild redness, pressure or transient irritation at the injection site is the most common local observation.
- No long-term data: most of the available evidence comes from animal models and short application periods, and robust long-term human studies barely exist.
This classification does not replace medical advice. Risk and responsibility for any actual use lie entirely with the buyer.
Studies
- Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice - Cell Metabolism 2016, Mills et al: 12-month NMN administration study in mice with broad effects on age-associated physiological endpoints.
- NAD+ and sirtuins in aging and disease - Trends in Cell Biology 2014, Imai & Guarente: Mechanistic review on NAD+, sirtuins, PARPs and age-related NAD+ decline.
- Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women - Science 2021, Yoshino et al: Randomized placebo-controlled human study of NMN in postmenopausal prediabetic women.
- Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging - Cell 2013, Gomes et al (Sinclair lab): NAD+ decline and disrupted nucleus-mitochondria communication in the aging model.
- Nicotinamide riboside is uniquely and orally bioavailable in mice and humans - Nature Communications 2016, Trammell et al (Brenner lab): First human study on oral NAD+ precursor pharmacokinetics with NR.
