NAD+

C₂₁H₂₈N₇O₁₄P₂⁺/C₂₁H₂₉N₇O₁₄P₂

Key Benefits

Mitochondrial Energy Production

Essential for oxidative phosphorylation. It shuttles electrons in the electron transport chain (ETC), driving ATP synthesis. Low NAD⁺ = mitochondrial dysfunction = fatigue, insulin resistance, and premature aging.

DNA Repair and Genomic Stability

Fuels PARP enzymes that detect and repair DNA strand breaks. As DNA damage accumulates with age, higher NAD⁺ levels improve repair fidelity, reduce mutational load, and protect telomeres. This is critical for longevity and cancer prevention.

Sirtuin Activation and Epigenetic Regulation

Sirtuins (SIRT1–7) are NAD⁺-dependent enzymes that deacetylate histones and key transcription factors like FOXO and p53. This switches cells into a pro-longevity state: enhanced autophagy, stem cell preservation, inflammation suppression, and improved stress resistance.

Neuro-protection and Cognitive Enhancement

Supports brain health by maintaining axonal integrity, promoting neurogenesis, and activating SIRT1 in neurons. It also buffers against excitotoxicity, neuroinflammation, and age-related cognitive decline. In models of Alzheimer’s, Parkinson’s, and stroke, NAD⁺ restoration showed neuroprotective effects.

Biologic Description

Nicotinamide adenine dinucleotide (NAD⁺) is a vital coenzyme found in every cell of the human body. It plays a central role in redox reactions—acting as an electron shuttle during cellular respiration—as well as serving as a substrate for key enzymes involved in DNA repair, epigenetic regulation, circadian rhythm, and cell survival. NAD⁺ exists in two forms: NAD⁺ (oxidized) and NADH (reduced), forming a redox pair essential to mitochondrial ATP production.

Beyond energy metabolism, NAD⁺ is a critical signaling molecule. It serves as a required cofactor for sirtuins (SIRT1–7), PARPs (poly ADP-ribose polymerases), and CD38/CD157 ectoenzymes, all of which are deeply involved in aging, inflammation, and cell death pathways.

As we age, NAD⁺ levels decline significantly in tissues—by as much as 50% by middle age—leading to mitochondrial dysfunction, loss of genomic integrity, and impaired stem cell maintenance. This decline is thought to be one of the core biological underpinnings of aging itself.

Dosage Guidelines

NAD⁺ in powdered lyophilized form is used subcutaneously for metabolic support, mitochondrial repair, cognitive enhancement, and anti-aging research. Most research protocols use between 10mg to 100mg per injection, depending on goals and tolerance.

Lower doses (10–50 mg) may be used for cellular maintenance or combined with NMN/NR in metabolic protocols. Higher doses (50–100 mg) are reserved for repair-intensive goals such as neurological recovery or systemic inflammation mitigation.

Starting Dose

10-100 mg

5 Days on 2 Days Off

6-8 Weeks

Side Effects

While NAD⁺ is a naturally occurring molecule, supraphysiologic restoration or aggressive elevation may produce unintended effects, especially in methylation-sensitive individuals.

Observed research effects:

Transient fatigue or flu-like symptoms (common with IV NAD⁺ drips)
Nausea or cramping (when administered too quickly or via non-buffered routes)
Methyl donor depletion leading to mood or detox issues
PARP overactivation in certain cancer models (caution in oncology)

Additionally, overactivation of CD38, an NAD-consuming enzyme, has been linked to immunosenescence and may blunt the benefit of NAD⁺ elevation unless addressed concurrently (e.g., using apigenin or CD38 inhibitors in research).

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