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SYS · ONLINEPASS · 63.0%
Open Assay
Independent Testing / Est. 2026
BATCH04·26·B
PASS63.0%
N27
PeptidesLongevityNAD

NAD

/ Endogenous nicotinamide adenine dinucleotide; NAD+ research compound (injectable / IV)
TIER 2 · TranslationalN = 0 · TESTING PENDINGMW 663.40 g·mol⁻¹

ALIAS · NAD+ · Nicotinamide Adenine Dinucleotide · NAD(H)

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Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

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§ A · Identity
Primary sequence— sequence not captured —
MW · 663.40CLASS · Endogenous nicotinamide adenine dinucleotide; NAD+ research compound (injectable / IV)CATEGORY · Longevity

Tier 2. NAD+ itself is the endogenous cofactor; clinical interest centres on small RCTs of NAD+ pathway interventions (intravenous NAD, niacin/NAD+, and the precursor NMN and NR — covered separately). Notable small trials include Pirinen 2020 (niacin in mitochondrial myopathy) and Brakedal 2022 (niacin/NAD+ in Parkinson disease). NAD as a parenteral product is not FDA-approved and is sold in the US through dietary-supplement and IV-clinic channels.

§ B · Mechanism of action

NAD+ is an obligate redox cofactor in cellular metabolism, accepting and donating electrons in the form of NADH and NADP(H) and serving as a substrate for the sirtuin family of NAD+-dependent deacetylases, the PARP family of poly-ADP-ribose polymerases, and the CD38 / CD73 ectoenzymes. The geroscience hypothesis around NAD+ supplementation rests on the observation that tissue NAD+ levels decline with age and in several disease states, and that pharmacologic restoration may improve mitochondrial function, sirtuin-mediated transcription, and DNA-damage-response capacity. Whether parenteral NAD+ raises tissue NAD+ pools more efficiently than the orally bioavailable precursors NMN and NR is not well-established in human pharmacokinetic studies.

§ C · Human clinical evidence

Tier 2. Pirinen 2020 (niacin / NAD+ supplementation in adult-onset mitochondrial myopathy, Cell Metabolism) and Brakedal 2022 (niacin in early Parkinson disease, Cell Metabolism) are the modern small-trial anchors for NAD+ pathway intervention. Outcome data are hypothesis-generating rather than approval-grade; sample sizes are small and primary endpoints are biomarker-driven rather than hard clinical endpoints. Direct intravenous NAD+ infusion programmes in IV-clinic settings have generated anecdote and uncontrolled case series rather than indexed RCTs.

§ D · Primary literature
PubMed32640244Pirinen E et al.Niacin Cures Systemic NAD+ Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy · Cell Metabolism · human-phase-2Oral niacin restored systemic NAD+ levels and improved muscle strength and mitochondrial biogenesis markers in adult-onset mitochondrial myopathy over four months.Limitations: Small open-label cohort (n=10); single-centre; biomarker and strength endpoints rather than hard functional outcomes.2020
PubMed35235774Brakedal B et al.The NADPARK study: A randomized phase I trial of nicotinamide riboside supplementation in Parkinson's disease · Cell Metabolism · human-phase-1Oral nicotinamide riboside increased cerebral NAD+ levels and altered cerebral metabolism on MR spectroscopy and FDG-PET in early Parkinson disease over 30 days.Limitations: Phase 1; n=30; biomarker endpoints; not powered for clinical disease-progression outcomes.2022
§ F · Safety signal

In published small RCTs of niacin and NAD+ precursors, well tolerated with the expected niacin flushing pattern when relevant. Long-term safety of sustained NAD+ pathway elevation has not been characterised in large populations. Theoretical concerns from chronic SIRT and CD38 substrate availability — including effects on tumour metabolism in occult malignancy — remain hypothetical.

§ H · Regulatory status

Regulatory status

FDA status:
Not FDA-approved
§ I · Notable gaps and controversies

Direct parenteral NAD+ as sold in US IV-clinic and supplement channels has minimal peer-reviewed pharmacokinetic data. The geroscience case rests largely on the NMN and NR oral-precursor literature, which uses different molecules with different absorption pathways. The label 'NAD therapy' covers a range of regimens that the published trial evidence does not collectively support.