Performance & Vitality · Reviewed by Ian K. Tseng, MD

What Is NAD+? The Coenzyme That Is Not a Peptide

NAD+ appears on nearly every peptide menu, including ours, and it is not a peptide at all. It is a coenzyme — a different class of molecule entirely — and the reason it keeps company with peptides is practical rather than biochemical. Since the distinction affects how you should evaluate claims about it, it is worth starting there.

Published August 4, 2026 · Medical review by Ian K. Tseng, MD, Medical Director

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The short answer

NAD+ — nicotinamide adenine dinucleotide — is a coenzyme present in every living cell, not a peptide. It is central to the redox reactions that produce cellular energy and serves as a required substrate for enzyme families including the sirtuins and PARPs. Cellular NAD+ levels decline with age. It is administered intravenously, by subcutaneous injection, and through oral precursor compounds, and these routes differ meaningfully in bioavailability.

Coenzyme, not peptide

Peptides are chains of amino acids. NAD+ is a dinucleotide — a molecule built from two nucleotides joined through phosphate groups, one containing adenine and the other nicotinamide, which is derived from vitamin B3. Structurally it has nothing in common with a peptide.

It appears alongside peptides on wellness menus because it occupies a similar clinical position: an injectable compound aimed at cellular energy and healthy aging, prescribed and administered in similar settings. The grouping is operational, not biochemical. We flag it because "is this a peptide" is a reasonable question and the honest answer is no.

What NAD+ actually does

NAD+ has two broad roles. The first is as an electron carrier in redox reactions. In cellular respiration, NAD+ accepts electrons to become NADH, carries them to the mitochondrial electron transport chain, and releases them to drive ATP production. Essentially every cell depends on this cycle continuously; without adequate NAD+, energy production itself is constrained.

The second role is as a consumed substrate. Certain enzyme families do not merely use NAD+ catalytically but cleave it, consuming it in the process. The sirtuins — implicated in metabolic regulation and studied extensively in aging research — are NAD+-dependent. So are the PARP enzymes involved in DNA repair. Because these enzymes consume NAD+ rather than recycling it, sustained demand on them draws down the available pool.

The age-related decline

Tissue NAD+ levels decline with age across multiple studied tissues. The mechanisms proposed involve both reduced synthesis and increased consumption — notably by PARP enzymes responding to accumulated DNA damage, and by other NAD+-consuming enzymes whose activity increases with age.

This decline is the basis of research interest in restoring NAD+ levels. It is important to be careful about the inferential step, though: that a molecule declines with age and is required for processes that also decline does not by itself establish that supplementing it reverses those processes. Research examining that question in humans is ongoing and remains an active area rather than a settled one.

Delivery routes and why they differ

NAD+ is administered several ways, and the differences are not trivial. Intravenous administration delivers it directly to the bloodstream, bypassing digestive breakdown; infusions are typically slow, because rapid administration is associated with uncomfortable effects including chest tightness and nausea. We offer this route as part of our IV therapy menu.

Subcutaneous injection is used for smaller, more frequent dosing without an infusion appointment. Nasal and oral routes exist as well, and oral supplementation more commonly uses precursor molecules — nicotinamide riboside and nicotinamide mononucleotide — rather than NAD+ itself, on the rationale that the intact molecule is poorly absorbed orally. Whether precursors meaningfully raise tissue NAD+ in humans, and by how much, is precisely the question the current research is working on.

Route selection is a clinical decision, and for many patients an IV route within an existing wellness program is more appropriate than a prescribed injectable protocol.

Frequently asked questions

Is NAD+ a peptide?

No. NAD+ is a coenzyme — a dinucleotide built from two nucleotides joined through phosphate groups, one containing adenine and the other nicotinamide, derived from vitamin B3. Peptides are chains of amino acids. NAD+ appears alongside peptides on wellness menus because it occupies a similar clinical position as an injectable compound aimed at cellular energy, not because of any structural relationship.

What does NAD+ do in the body?

Two main things. It acts as an electron carrier in cellular respiration, accepting electrons to become NADH and delivering them to the mitochondrial electron transport chain to drive ATP production. It also serves as a consumed substrate for enzyme families including the sirtuins, which are studied in metabolic regulation and aging, and the PARP enzymes involved in DNA repair. These enzymes cleave NAD+ rather than recycling it, drawing down the available pool.

Why do NAD+ levels decline with age?

Proposed mechanisms involve both reduced synthesis and increased consumption — notably by PARP enzymes responding to accumulated DNA damage, and by other NAD+-consuming enzymes whose activity rises with age. That a molecule declines with age and is required for processes that also decline does not by itself establish that supplementing it reverses those processes; research on that question in humans is ongoing.

What is the difference between IV NAD+ and oral NAD+ supplements?

Intravenous administration delivers NAD+ directly to the bloodstream, bypassing digestive breakdown, and infusions are given slowly because rapid administration is associated with chest tightness and nausea. Oral supplementation more commonly uses precursor molecules — nicotinamide riboside and nicotinamide mononucleotide — rather than NAD+ itself, since the intact molecule is poorly absorbed orally. How much precursors raise tissue NAD+ in humans is an active research question.

Clinical references

Medically reviewed by Ian K. Tseng, MD, Medical Director of Soothe IV's peptide therapy program. The clinical statements in this article are supported by the following sources:

Covarrubias AJ, Perrone R, Grozio A, Verdin E. NAD+ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology. 2021. pmc.ncbi.nlm.nih.gov
Rajman L, Chwalek K, Sinclair DA. Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metabolism. 2018. pmc.ncbi.nlm.nih.gov
U.S. Food & Drug Administration. Human Drug Compounding. www.fda.gov

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This article is educational and is not medical advice. Statements have not been evaluated by the FDA. Peptide therapy is a physician-supervised medical service; specific protocols are determined individually after a Good Faith Examination and bloodwork, and not all applicants qualify. Some compounded medications used in physician-prescribed protocols are not FDA-approved. Data from clinical trials on FDA-approved medications should not be used to make assessments related to compounded medications. Soothe IV's peptide program is available nationwide via telehealth; prescriptions are issued by physicians licensed in your state.