NAD+

NAD+ (Nicotinamide Adenine Dinucleotide): Comprehensive Research Guide

Nicotinamide Adenine Dinucleotide (NAD+) is a vital coenzyme found in every living cell, playing a fundamental role in cellular energy metabolism, DNA repair, gene expression, and cellular signaling. This dinucleotide, consisting of two nucleotides joined through their phosphate groups, is essential for over 500 enzymatic reactions in the human body and is a key regulator of cellular health, aging, and longevity. NAD+ levels naturally decline with age, and this decline has been implicated in numerous age-related diseases, including metabolic disorders, neurodegenerative diseases, cardiovascular disease, and cancer. NAD+ supplementation has emerged as a promising strategy for boosting cellular NAD+ levels, improving metabolic health, and potentially slowing the aging process.

At Hanpro Peptides, we provide the highest purity NAD+ for research purposes only. Our products are manufactured in state-of-the-art facilities and undergo rigorous quality testing to ensure 99%+ purity. This comprehensive guide covers everything researchers need to know about NAD+, including its molecular structure, mechanisms of action, research applications, proper handling, and frequently asked questions.

Molecular Structure and Properties

NAD+ (Nicotinamide Adenine Dinucleotide) is a dinucleotide consisting of two nucleotides joined through their 5′-phosphate groups. One nucleotide contains an adenine base, and the other contains a nicotinamide base. The molecular formula of NAD+ is C₂₁H₂₇N₇O₁₄P₂, with a molecular weight of approximately 663.43 g/mol. NAD+ is the oxidized form of the coenzyme, while NADH (Nicotinamide Adenine Dinucleotide, reduced) is the reduced form. The interconversion between NAD+ and NADH is central to cellular energy metabolism, as NAD+ accepts electrons from metabolic reactions to become NADH, and NADH donates electrons to the electron transport chain to produce ATP (adenosine triphosphate), the cell’s primary energy currency.

The structure of NAD+ consists of: (1) A nicotinamide ring (the biologically active portion of the molecule), which can accept a hydride ion (H⁻) to become NADH; (2) A ribose sugar attached to the nicotinamide ring via a glycosidic bond; (3) A phosphate group attached to the 5′ carbon of the ribose; (4) A second phosphate group linked to the first phosphate via a phosphoanhydride bond; (5) A second ribose sugar attached to the second phosphate; (6) An adenine base attached to the second ribose via a glycosidic bond. The positively charged nitrogen in the nicotinamide ring (hence the “+” in NAD+) is essential for the molecule’s ability to accept electrons and participate in redox reactions. NAD+ is highly soluble in water and physiological buffers, and it is stable under acidic conditions but can degrade under alkaline conditions or at high temperatures.

NAD+ can also be phosphorylated to form NADP+ (Nicotinamide Adenine Dinucleotide Phosphate), which has an additional phosphate group attached to the 2′ carbon of the adenine-containing ribose. NADP+ and its reduced form NADPH are primarily involved in anabolic (biosynthetic) reactions and antioxidant defense, while NAD+ and NADH are primarily involved in catabolic (energy-producing) reactions and cellular signaling. NAD+ can also be covalently attached to proteins through a process called ADP-ribosylation, which is involved in DNA repair, gene expression, and cellular signaling. The enzyme poly(ADP-ribose) polymerase (PARP) uses NAD+ as a substrate to synthesize poly(ADP-ribose) (PAR) chains on target proteins, which is a key step in DNA repair and cellular stress responses.

Mechanisms of Action

NAD+ exerts its effects through multiple interconnected mechanisms, making it a fundamental regulator of cellular health and function. Understanding these mechanisms is crucial for designing effective research studies and interpreting results.

1. Cellular Energy Metabolism: The primary and most well-established role of NAD+ is as a coenzyme in cellular energy metabolism. NAD+ is essential for glycolysis, the citric acid cycle (Krebs cycle), and oxidative phosphorylation, the three main pathways that produce ATP (adenosine triphosphate), the cell’s primary energy currency. In glycolysis, NAD+ accepts electrons from glucose to become NADH, and the resulting pyruvate is further metabolized in the citric acid cycle, where NAD+ again accepts electrons to become NADH. The NADH produced in these pathways then donates electrons to the electron transport chain in the mitochondria, where the energy from the electrons is used to pump protons across the inner mitochondrial membrane, creating an electrochemical gradient that drives ATP synthesis. Without sufficient NAD+, these energy-producing pathways cannot function, and cells cannot produce enough ATP to meet their energy needs, leading to cellular dysfunction and eventually cell death.

2. DNA Repair and Genome Stability: NAD+ is a critical substrate for enzymes involved in DNA repair and genome stability, particularly the poly(ADP-ribose) polymerases (PARPs) and the sirtuins. PARPs are a family of enzymes that use NAD+ as a substrate to catalyze the transfer of ADP-ribose units to target proteins, a process called poly(ADP-ribosylation) or PARylation. PARylation is a key step in the DNA damage response, as it recruits DNA repair proteins to sites of DNA damage and helps coordinate the repair process. When DNA is damaged (e.g., by oxidative stress, radiation, or chemical mutagens), PARPs are activated and use NAD+ to synthesize PAR chains on histones and other DNA repair proteins, which helps to relax the chromatin structure and recruit repair enzymes to the damage site. Without sufficient NAD+, PARPs cannot function effectively, and DNA damage accumulates, leading to genome instability, cellular dysfunction, and potentially cancer or cell death. The sirtuins, another family of NAD+-dependent enzymes, also play a role in DNA repair and genome stability by deacetylating histones and other proteins involved in DNA repair and chromatin remodeling.

3. Sirtuin Activation and Epigenetic Regulation: NAD+ is an essential cofactor for the sirtuins, a family of NAD+-dependent deacetylases and ADP-ribosyltransferases that play key roles in epigenetic regulation, gene expression, cellular metabolism, stress resistance, and longevity. There are seven sirtuins in mammals (SIRT1-SIRT7), each with distinct subcellular localizations and functions. SIRT1, the most well-studied sirtuin, is primarily localized in the nucleus and cytoplasm, and it deacetylates a wide range of target proteins, including histones (H3K9, H4K16), transcription factors (p53, FOXO, NF-κB, PGC-1α), and metabolic enzymes. By deacetylating these target proteins, SIRT1 regulates gene expression, cellular metabolism, stress resistance, apoptosis, and aging. SIRT2 is primarily cytoplasmic and deacetylates tubulin and other cytoplasmic proteins, while SIRT3, SIRT4, and SIRT5 are mitochondrial and regulate mitochondrial metabolism, energy production, and antioxidant defense. SIRT6 and SIRT7 are nuclear and regulate DNA repair, genome stability, and ribosome biogenesis. The activity of all sirtuins is strictly dependent on NAD+, and as NAD+ levels decline with age, sirtuin activity also declines, leading to changes in gene expression, cellular metabolism, and stress resistance that contribute to aging and age-related diseases. By boosting NAD+ levels, NAD+ supplementation can increase sirtuin activity, potentially reversing some of the age-related changes in gene expression and cellular function.

4. Cellular Signaling and Stress Resistance: NAD+ plays a key role in cellular signaling and stress resistance through its effects on sirtuins, PARPs, and other NAD+-dependent enzymes. By regulating the activity of these enzymes, NAD+ modulates various cellular signaling pathways, including the insulin/IGF-1 signaling pathway, the AMPK (AMP-activated protein kinase) pathway, the mTOR (mammalian target of rapamycin) pathway, and the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway. These pathways regulate cellular metabolism, growth, proliferation, inflammation, stress resistance, and apoptosis. NAD+ also plays a role in calcium signaling, as it is a precursor for cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), two second messengers that regulate intracellular calcium release from the endoplasmic reticulum and lysosomes, respectively. By regulating these signaling pathways, NAD+ helps cells adapt to stress, maintain homeostasis, and survive under adverse conditions. As NAD+ levels decline with age, the ability of cells to respond to stress and maintain homeostasis also declines, contributing to aging and age-related diseases.

5. Mitochondrial Function and Biogenesis: NAD+ is essential for mitochondrial function and biogenesis, as it is a key cofactor for the citric acid cycle and oxidative phosphorylation, the two main pathways that produce ATP in the mitochondria. NAD+ also regulates mitochondrial biogenesis (the creation of new mitochondria) through its effects on SIRT1 and PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha), a master regulator of mitochondrial biogenesis. SIRT1 deacetylates and activates PGC-1α, which then coactivates various transcription factors (including NRF-1, NRF-2, and PPARs) to increase the expression of genes involved in mitochondrial biogenesis, oxidative phosphorylation, and energy metabolism. As NAD+ levels decline with age, SIRT1 activity decreases, leading to reduced PGC-1α activity and decreased mitochondrial biogenesis, which contributes to the decline in mitochondrial function and energy production observed with aging. By boosting NAD+ levels, NAD+ supplementation can increase SIRT1 activity, activate PGC-1α, and promote mitochondrial biogenesis, potentially improving mitochondrial function and energy production in aged or dysfunctional cells.

6. Inflammation and Immune Function: NAD+ plays a key role in regulating inflammation and immune function through its effects on sirtuins, PARPs, and other NAD+-dependent enzymes. SIRT1, in particular, has been shown to have potent anti-inflammatory effects by deacetylating and inhibiting the activity of NF-κB, a key transcription factor that regulates the expression of pro-inflammatory cytokines, chemokines, and adhesion molecules. By inhibiting NF-κB activity, SIRT1 reduces the production of pro-inflammatory mediators and suppresses chronic inflammation, which is a key driver of aging and many age-related diseases. NAD+ also plays a role in immune cell function, as it is essential for the energy metabolism and effector functions of immune cells, including T cells, B cells, macrophages, and neutrophils. As NAD+ levels decline with age, immune cell function also declines, leading to increased susceptibility to infections, reduced vaccine response, and chronic low-grade inflammation (inflammaging). By boosting NAD+ levels, NAD+ supplementation can improve immune cell function and reduce chronic inflammation, potentially improving immune health and reducing the risk of inflammatory diseases.

7. Circadian Rhythm Regulation: NAD+ plays a key role in regulating the circadian rhythm (the body’s internal 24-hour clock) through its effects on SIRT1 and the circadian clock machinery. The circadian rhythm is regulated by a complex network of transcription-translation feedback loops, including the core clock genes CLOCK, BMAL1, PER, and CRY. SIRT1 interacts with the CLOCK/BMAL1 complex and regulates the circadian expression of clock genes and clock-controlled genes by deacetylating histones and clock proteins at the promoters of these genes. The activity of SIRT1 is strictly dependent on NAD+, and NAD+ levels themselves exhibit circadian oscillations, with higher levels during the active phase (daytime in humans) and lower levels during the rest phase (nighttime in humans). This circadian oscillation in NAD+ levels helps to synchronize cellular metabolism and gene expression with the daily light-dark cycle. As NAD+ levels decline with age, the circadian oscillation in NAD+ levels becomes dampened, leading to disruptions in circadian rhythm, sleep patterns, and metabolic regulation. By boosting NAD+ levels, NAD+ supplementation can help restore the circadian oscillation in NAD+ levels, potentially improving circadian rhythm, sleep quality, and metabolic health.

Research Applications

NAD+ has been investigated in numerous preclinical and clinical studies for its potential therapeutic applications across various medical fields. The following sections highlight the most important areas of research.

1. Aging and Longevity

One of the most significant and widely studied applications of NAD+ is in the field of aging and longevity research. NAD+ levels naturally decline with age in humans and other mammals, and this decline has been implicated in numerous age-related processes, including cellular senescence, mitochondrial dysfunction, DNA damage accumulation, epigenetic changes, chronic inflammation, and metabolic dysregulation. The “NAD+ decline theory of aging” proposes that the age-related decline in NAD+ levels is a key driver of the aging process, and that boosting NAD+ levels can slow or reverse some of the age-related changes in cellular function and potentially extend lifespan.

Numerous preclinical studies in model organisms (including yeast, worms, flies, and mice) have shown that boosting NAD+ levels (through supplementation with NAD+ precursors such as nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), or nicotinamide (NAM), or through direct NAD+ supplementation) can extend lifespan and improve healthspan (the period of life spent in good health). In mice, NAD+ supplementation has been shown to extend lifespan by 10-30%, depending on the strain, dose, and timing of supplementation, and to improve various markers of health, including metabolic health, mitochondrial function, physical endurance, cognitive function, and stress resistance. NAD+ supplementation has also been shown to delay the onset of age-related diseases in mice, including metabolic disorders, neurodegenerative diseases, cardiovascular disease, and cancer.

The mechanisms by which NAD+ supplementation exerts its anti-aging and longevity effects are believed to involve: (1) Activation of sirtuins, particularly SIRT1, SIRT3, and SIRT6, which regulate gene expression, cellular metabolism, stress resistance, DNA repair, and genome stability; (2) Improvement of mitochondrial function and biogenesis, increasing cellular energy production and reducing oxidative stress; (3) Enhancement of DNA repair and genome stability, reducing the accumulation of DNA damage and mutations with age; (4) Reduction of chronic inflammation (inflammaging), through inhibition of NF-κB and other pro-inflammatory pathways; (5) Improvement of cellular metabolism and insulin sensitivity, reducing the risk of metabolic disorders; (6) Enhancement of cellular stress resistance, through activation of various stress response pathways, including the heat shock response, the unfolded protein response, and autophagy; (7) Regulation of circadian rhythm and sleep, which are important for overall health and longevity.

While the preclinical evidence for the anti-aging and longevity effects of NAD+ supplementation is strong, the clinical evidence in humans is still limited. Several small clinical trials have shown that supplementation with NAD+ precursors (NR or NMN) can increase blood NAD+ levels by 20-50% and improve various markers of metabolic health, including insulin sensitivity, blood lipid profiles, and inflammatory markers. However, larger and longer-term clinical trials are needed to determine whether NAD+ supplementation can slow the aging process, extend lifespan, or prevent age-related diseases in humans. Several large-scale clinical trials are currently underway to investigate the effects of NAD+ supplementation on aging, longevity, and age-related diseases, and the results of these trials will provide important information about the potential therapeutic benefits of NAD+ supplementation in humans.

2. Metabolic Health and Diabetes

NAD+ plays a critical role in cellular metabolism and energy homeostasis, and NAD+ deficiency has been implicated in the development of metabolic disorders, including obesity, insulin resistance, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD). NAD+ supplementation has emerged as a promising strategy for improving metabolic health and treating metabolic disorders, based on its ability to boost cellular NAD+ levels, activate sirtuins, improve mitochondrial function, and regulate cellular metabolism.

Numerous preclinical studies in animal models of obesity and type 2 diabetes have shown that NAD+ supplementation (or supplementation with NAD+ precursors such as NR or NMN) can improve insulin sensitivity, reduce blood glucose levels, reduce body weight and fat mass, improve lipid profiles, and reduce liver fat accumulation. In mice fed a high-fat diet, NAD+ supplementation has been shown to prevent the development of obesity, insulin resistance, and type 2 diabetes, and to reverse existing metabolic dysfunction. NAD+ supplementation has also been shown to improve glucose tolerance and insulin sensitivity in genetically obese and diabetic mice, and to reduce the severity of NAFLD and non-alcoholic steatohepatitis (NASH) in animal models.

The mechanisms by which NAD+ supplementation improves metabolic health include: (1) Activation of SIRT1, which deacetylates and activates PGC-1α (a master regulator of mitochondrial biogenesis and energy metabolism), FOXO transcription factors (which regulate stress resistance and metabolism), and other metabolic regulators; (2) Activation of SIRT3, SIRT4, and SIRT5 in the mitochondria, which regulate mitochondrial metabolism, energy production, and antioxidant defense; (3) Improvement of mitochondrial function and biogenesis, increasing cellular energy production and reducing oxidative stress; (4) Enhancement of insulin signaling and glucose uptake in skeletal muscle, adipose tissue, and the liver, through activation of the insulin/PI3K/Akt signaling pathway; (5) Reduction of gluconeogenesis (glucose production) in the liver, through inhibition of the expression of gluconeogenic genes such as PEPCK and G6Pase; (6) Reduction of inflammation and oxidative stress in metabolic tissues, through inhibition of NF-κB and other pro-inflammatory pathways; (7) Regulation of appetite and food intake, through effects on the hypothalamus and other brain regions involved in energy homeostasis.

Several small clinical trials have investigated the effects of NAD+ precursor supplementation (NR or NMN) on metabolic health in humans, with promising results. In overweight or obese adults, supplementation with NR (1000-2000 mg/day for 6-12 weeks) has been shown to increase blood NAD+ levels by 20-50%, improve insulin sensitivity in skeletal muscle, reduce blood pressure and arterial stiffness, and reduce inflammatory markers. In patients with type 2 diabetes, supplementation with NR (1000 mg twice daily for 12 weeks) has been shown to improve blood lipid profiles and reduce inflammatory markers, although the effects on glycemic control were less consistent. Supplementation with NMN (250 mg/day for 12 weeks) has also been shown to improve insulin sensitivity and reduce blood glucose levels in prediabetic women. While these results are promising, larger and longer-term clinical trials are needed to determine the optimal dose, duration, and formulation of NAD+ supplementation for the treatment of metabolic disorders, and to confirm the long-term safety and efficacy of NAD+ supplementation in humans.

3. Neurodegenerative Diseases and Cognitive Health

NAD+ plays a critical role in neuronal function and survival, as neurons are highly dependent on mitochondrial energy production and are particularly vulnerable to oxidative stress, DNA damage, and mitochondrial dysfunction. NAD+ deficiency has been implicated in the development and progression of various neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis (ALS). NAD+ supplementation has emerged as a promising strategy for treating neurodegenerative diseases and preserving cognitive health, based on its ability to boost neuronal NAD+ levels, activate sirtuins, improve mitochondrial function, reduce oxidative stress and inflammation, and enhance DNA repair and neuronal survival.

Numerous preclinical studies in animal models of neurodegenerative diseases have shown that NAD+ supplementation (or supplementation with NAD+ precursors such as NR or NMN) can reduce neuronal loss, improve cognitive function, and delay disease progression. In mouse models of Alzheimer’s disease, NAD+ supplementation has been shown to reduce amyloid-beta plaque formation, reduce tau hyperphosphorylation and neurofibrillary tangle formation, reduce neuroinflammation, improve synaptic function, and improve spatial learning and memory. NAD+ supplementation has also been shown to extend lifespan and improve cognitive function in mouse models of Alzheimer’s disease. In mouse models of Parkinson’s disease, NAD+ supplementation has been shown to protect dopaminergic neurons from degeneration, reduce alpha-synuclein aggregation, reduce neuroinflammation, and improve motor function. In mouse models of Huntington’s disease, NAD+ supplementation has been shown to reduce mutant huntingtin aggregation, reduce neuronal loss, improve motor function, and extend lifespan. In mouse models of ALS, NAD+ supplementation has been shown to protect motor neurons from degeneration, reduce neuroinflammation, improve motor function, and extend lifespan.

The mechanisms by which NAD+ supplementation exerts its neuroprotective effects include: (1) Improvement of mitochondrial function and biogenesis in neurons, increasing cellular energy production and reducing oxidative stress; (2) Activation of SIRT1, which deacetylates and activates PGC-1α (promoting mitochondrial biogenesis), FOXO transcription factors (promoting stress resistance and antioxidant defense), and other neuroprotective regulators; (3) Activation of SIRT3 in the mitochondria, which regulates mitochondrial metabolism, energy production, and antioxidant defense; (4) Reduction of oxidative stress and reactive oxygen species (ROS) production in neurons, through enhancement of antioxidant defense systems (including SOD, catalase, and glutathione); (5) Reduction of neuroinflammation, through inhibition of NF-κB and other pro-inflammatory pathways in microglia and astrocytes; (6) Enhancement of DNA repair and genome stability in neurons, through activation of PARPs and sirtuins involved in the DNA damage response; (7) Promotion of neuronal survival and inhibition of apoptosis, through regulation of the Bcl-2 family of proteins and other apoptotic regulators; (8) Improvement of synaptic function and plasticity, through regulation of synaptic protein expression and neurotransmitter release.

While the preclinical evidence for the neuroprotective effects of NAD+ supplementation is strong, the clinical evidence in humans is still limited. Several small clinical trials have shown that supplementation with NAD+ precursors (NR or NMN) can increase blood NAD+ levels and improve various markers of metabolic and cardiovascular health, but the effects on cognitive function and neurodegenerative diseases have not been extensively studied. A few small clinical trials in patients with Alzheimer’s disease or mild cognitive impairment have shown that supplementation with NR or NMN can improve cognitive function and reduce biomarkers of neurodegeneration, but larger and longer-term clinical trials are needed to confirm these results. Several large-scale clinical trials are currently underway to investigate the effects of NAD+ supplementation on cognitive health and neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease, and the results of these trials will provide important information about the potential therapeutic benefits of NAD+ supplementation in these conditions.

4. Cardiovascular Health

NAD+ plays a critical role in cardiovascular health, as the heart is one of the most energy-demanding organs in the body and is highly dependent on mitochondrial energy production. NAD+ deficiency has been implicated in the development and progression of various cardiovascular diseases, including heart failure, myocardial infarction (heart attack), atherosclerosis, hypertension, and cardiac hypertrophy. NAD+ supplementation has emerged as a promising strategy for treating cardiovascular diseases and preserving cardiac function, based on its ability to boost cardiac NAD+ levels, activate sirtuins, improve mitochondrial function, reduce oxidative stress and inflammation, and enhance cardiac stress resistance.

Numerous preclinical studies in animal models of cardiovascular disease have shown that NAD+ supplementation (or supplementation with NAD+ precursors such as NR or NMN) can improve cardiac function, reduce cardiac damage, and delay disease progression. In mouse models of heart failure, NAD+ supplementation has been shown to improve cardiac contractility, reduce cardiac hypertrophy (enlargement of the heart), reduce cardiac fibrosis (scarring), and improve exercise capacity and survival. In mouse models of myocardial infarction (heart attack), NAD+ supplementation has been shown to reduce infarct size, preserve cardiac function, reduce cardiac remodeling, and improve survival. In mouse models of atherosclerosis, NAD+ supplementation has been shown to reduce atherosclerotic plaque formation, reduce vascular inflammation, improve endothelial function, and reduce the risk of plaque rupture. In mouse models of hypertension, NAD+ supplementation has been shown to reduce blood pressure, improve vascular function, and reduce cardiac and renal damage. In mouse models of cardiac hypertrophy (induced by pressure overload or exercise), NAD+ supplementation has been shown to reduce pathological cardiac hypertrophy, preserve cardiac function, and reduce the risk of heart failure.

The mechanisms by which NAD+ supplementation exerts its cardiovascular protective effects include: (1) Improvement of mitochondrial function and biogenesis in cardiomyocytes (heart muscle cells), increasing cellular energy production and reducing oxidative stress; (2) Activation of SIRT1, which deacetylates and activates PGC-1α (promoting mitochondrial biogenesis), FOXO transcription factors (promoting stress resistance and antioxidant defense), and other cardioprotective regulators; (3) Activation of SIRT3 in the mitochondria, which regulates mitochondrial metabolism, energy production, and antioxidant defense in cardiomyocytes; (4) Reduction of oxidative stress and reactive oxygen species (ROS) production in the heart and blood vessels, through enhancement of antioxidant defense systems; (5) Reduction of inflammation in the heart and blood vessels, through inhibition of NF-κB and other pro-inflammatory pathways; (6) Improvement of endothelial function and vascular health, through increased production of nitric oxide (NO) and reduced endothelial dysfunction; (7) Reduction of cardiac hypertrophy and fibrosis, through inhibition of pro-hypertrophic and pro-fibrotic signaling pathways (including the calcineurin/NFAT pathway and the TGF-β/Smad pathway); (8) Enhancement of cardiac stress resistance and inhibition of apoptosis in cardiomyocytes, through regulation of stress response pathways and apoptotic regulators; (9) Regulation of cardiac energy metabolism, shifting the heart from fatty acid oxidation to glucose oxidation (which is more oxygen-efficient), particularly in the setting of heart failure or myocardial ischemia.

While the preclinical evidence for the cardiovascular protective effects of NAD+ supplementation is strong, the clinical evidence in humans is still limited. Several small clinical trials have shown that supplementation with NAD+ precursors (NR or NMN) can increase blood NAD+ levels and improve various markers of cardiovascular health, including blood pressure, arterial stiffness, endothelial function, and inflammatory markers. In patients with heart failure, supplementation with NR (1000 mg twice daily for 12 weeks) has been shown to improve exercise capacity, reduce symptoms of heart failure, and improve quality of life, although the effects on cardiac function were less consistent. In patients with hypertension, supplementation with NR has been shown to reduce systolic blood pressure by 5-10 mmHg and improve arterial stiffness. While these results are promising, larger and longer-term clinical trials are needed to determine the optimal dose, duration, and formulation of NAD+ supplementation for the treatment of cardiovascular diseases, and to confirm the long-term safety and efficacy of NAD+ supplementation in these conditions. Several large-scale clinical trials are currently underway to investigate the effects of NAD+ supplementation on cardiovascular health and disease, and the results of these trials will provide important information about the potential therapeutic benefits of NAD+ supplementation in cardiovascular disease.

5. Other Research Applications

In addition to the well-established applications in aging, metabolic health, neurodegenerative diseases, and cardiovascular disease, NAD+ has been investigated in several other research areas, with promising preliminary results.

Cancer: NAD+ plays a complex role in cancer, as it is essential for the energy metabolism and survival of cancer cells, but it is also required for DNA repair and genome stability, which can prevent the development of cancer. NAD+ levels are often elevated in cancer cells (to support their high metabolic demands), and NAD+ depletion has been investigated as a potential cancer therapy, as it can selectively kill cancer cells while sparing normal cells. Conversely, NAD+ supplementation has been investigated as a potential strategy for preventing cancer (by enhancing DNA repair and genome stability) and for reducing the side effects of chemotherapy and radiation therapy (by protecting normal cells from DNA damage). The role of NAD+ in cancer is complex and context-dependent, and more research is needed to determine the optimal use of NAD+ supplementation or NAD+ depletion in cancer prevention and treatment.

Liver Disease: NAD+ plays a critical role in liver metabolism and function, and NAD+ deficiency has been implicated in the development and progression of various liver diseases, including NAFLD, NASH, alcoholic liver disease, and liver fibrosis. NAD+ supplementation has been shown to improve liver function, reduce liver fat accumulation, reduce liver inflammation and fibrosis, and improve liver regeneration in animal models of liver disease. In patients with NAFLD or NASH, supplementation with NAD+ precursors has been shown to reduce liver fat content and liver enzymes, and to improve markers of liver health. Larger clinical trials are needed to confirm these results and to determine the optimal use of NAD+ supplementation in liver disease.

Kidney Disease: NAD+ plays a critical role in kidney function, as the kidneys are highly dependent on mitochondrial energy production for their transport and reabsorption functions. NAD+ deficiency has been implicated in the development and progression of acute kidney injury (AKI) and chronic kidney disease (CKD). NAD+ supplementation has been shown to protect against AKI (induced by ischemia-reperfusion injury or nephrotoxic drugs) and to slow the progression of CKD in animal models, by improving mitochondrial function, reducing oxidative stress and inflammation, and enhancing renal cell survival and regeneration. In patients with CKD, supplementation with NAD+ precursors has been shown to improve renal function and reduce markers of kidney damage, although larger clinical trials are needed to confirm these results.

Skeletal Muscle and Exercise Performance: NAD+ plays a critical role in skeletal muscle function and energy metabolism, and NAD+ deficiency has been implicated in the age-related decline in muscle mass and function (sarcopenia). NAD+ supplementation has been shown to improve mitochondrial function, increase muscle mass and strength, improve exercise endurance, and reduce muscle damage and fatigue in animal models and in some human studies. In older adults, supplementation with NAD+ precursors has been shown to improve muscle strength, physical performance, and exercise capacity, although the results have been somewhat inconsistent. Larger clinical trials are needed to determine the optimal use of NAD+ supplementation for improving muscle health and exercise performance, particularly in older adults.

Skin Health and Aging: NAD+ plays a critical role in skin cell function and skin health, and NAD+ deficiency has been implicated in skin aging, including the development of wrinkles, loss of elasticity, and impaired wound healing. NAD+ supplementation (both oral and topical) has been shown to improve skin health, reduce wrinkles, improve skin elasticity and hydration, and promote wound healing in animal models and in some human studies. Topical NAD+ supplementation has also been shown to protect the skin from UV-induced damage and to reduce the risk of skin cancer. Larger clinical trials are needed to confirm these results and to determine the optimal use of NAD+ supplementation for skin health and anti-aging.

Immune Function and Inflammation: NAD+ plays a critical role in immune cell function and inflammation, and NAD+ deficiency has been implicated in immune dysfunction and chronic inflammation. NAD+ supplementation has been shown to improve immune cell function, reduce chronic inflammation, and enhance the immune response to infections and vaccines in animal models and in some human studies. In older adults, supplementation with NAD+ precursors has been shown to improve immune function and reduce markers of chronic inflammation (inflammaging), although larger clinical trials are needed to confirm these results.

Product Specifications

Product Name	NAD+ (Nicotinamide Adenine Dinucleotide)
Full Name	β-Nicotinamide Adenine Dinucleotide (Oxidized Form)
Molecular Formula	C21H27N7O14P2
Molecular Weight	663.43 g/mol
Purity	≥99%
Appearance	White to off-white lyophilized powder
Solubility	Soluble in water (50 mg/mL) and physiological buffers
Storage	Store at -20°C upon receipt, protected from light and moisture. After reconstitution, store at 2-8°C for up to 7 days, or at -20°C for up to 3 months.
Available Sizes	100mg, 250mg, 500mg, 1g, 5g
Quality Control	HPLC, Mass Spectrometry, COA provided

Reconstitution and Handling Guidelines

Proper reconstitution and handling are essential for maintaining the stability and efficacy of NAD+. NAD+ is sensitive to light, moisture, and high temperatures, and it can degrade over time if not stored properly. Follow these guidelines carefully to ensure optimal results in your research.

Reconstitution Procedure:

1. Allow the vial to reach room temperature before opening (approximately 15-20 minutes), protected from light.
2. Wipe the rubber stopper with an alcohol swab and allow it to dry.
3. Using a sterile syringe, inject the appropriate volume of sterile water, phosphate-buffered saline (PBS), or other suitable buffer into the vial. For a 100mg vial, add 1mL of solvent to achieve a concentration of 100mg/mL. For a 500mg vial, add 5mL of solvent for a 100mg/mL concentration.
4. Gently swirl the vial until the powder is completely dissolved. Do not shake vigorously, as this can cause foaming and degradation. The solution should be clear and colorless.
5. Once fully dissolved, inspect the solution for any particles or discoloration. If you notice any particles or significant discoloration, do not use the solution.

Storage After Reconstitution:

• Store reconstituted NAD+ in a refrigerator at 2-8°C (36-46°F), protected from light.
• When stored properly at 2-8°C, reconstituted NAD+ remains stable for up to 7 days.
• For longer storage (up to 3 months), aliquot the solution into individual doses and store at -20°C, protected from light. Avoid repeated freeze-thaw cycles, as this can degrade the molecule.
• Do not store reconstituted NAD+ in direct sunlight or at room temperature for extended periods, as exposure to light and heat can cause degradation.

Handling Precautions:

• Always wear gloves and use sterile technique when handling NAD+.
• Use only sterile syringes and needles for reconstitution and administration.
• Do not mix NAD+ with other compounds in the same vial unless you have verified compatibility and stability. NAD+ is particularly sensitive to alkaline conditions and high temperatures, so avoid mixing with strongly alkaline solutions.
• If you are using NAD+ for in vitro studies, dilute it to the desired concentration using appropriate buffer solutions. Note that NAD+ is most stable at slightly acidic pH (pH 4-6), and it can degrade at neutral or alkaline pH over time.
• NAD+ can be administered via intravenous (IV), intramuscular (IM), or subcutaneous (SC) injection for in vivo studies. For IV administration, use a slow infusion to avoid adverse reactions. Rotate injection sites for IM or SC administration to minimize local reactions.
• NAD+ is light-sensitive, so protect the vial and solution from direct light during handling and storage. Use amber or foil-wrapped vials if possible.

Frequently Asked Questions (FAQ)

Q1: What is NAD+ and why is it important?

A: NAD+ (Nicotinamide Adenine Dinucleotide) is a vital coenzyme found in every living cell, playing a fundamental role in cellular energy metabolism, DNA repair, gene expression, and cellular signaling. It is often referred to as the “molecule of life” or the “energy currency of the cell” because it is essential for over 500 enzymatic reactions in the human body. NAD+ is involved in two main types of cellular processes: (1) Redox reactions, where NAD+ accepts electrons from metabolic reactions to become NADH (the reduced form), and NADH donates electrons to the electron transport chain in the mitochondria to produce ATP (adenosine triphosphate), the cell’s primary energy currency. This process is essential for glycolysis, the citric acid cycle, and oxidative phosphorylation, the three main pathways that produce energy in cells. (2) Non-redox reactions, where NAD+ is used as a substrate by enzymes such as sirtuins (NAD+-dependent deacetylases), PARPs (poly(ADP-ribose) polymerases), and CD38 (a cyclic ADP-ribose synthase). These enzymes use NAD+ to regulate gene expression, DNA repair, cellular signaling, inflammation, and stress resistance. NAD+ levels naturally decline with age, and this decline has been implicated in numerous age-related diseases, including metabolic disorders, neurodegenerative diseases, cardiovascular disease, and cancer. NAD+ supplementation has emerged as a promising strategy for boosting cellular NAD+ levels, improving metabolic health, and potentially slowing the aging process.

Q2: What is the difference between NAD+, NADH, NADP+, and NADPH?

A: NAD+, NADH, NADP+, and NADPH are all related dinucleotide coenzymes, but they have distinct structures and functions in the cell: (1) NAD+ (Nicotinamide Adenine Dinucleotide, oxidized form) is the oxidized form of the coenzyme, with a positively charged nitrogen in the nicotinamide ring. It accepts electrons from metabolic reactions to become NADH. NAD+ is primarily involved in catabolic (energy-producing) reactions, such as glycolysis, the citric acid cycle, and oxidative phosphorylation, and in cellular signaling processes, such as sirtuin activation and PARP-mediated DNA repair. (2) NADH (Nicotinamide Adenine Dinucleotide, reduced form) is the reduced form of NAD+, with an extra hydride ion (H⁻) attached to the nicotinamide ring. It donates electrons to the electron transport chain in the mitochondria to produce ATP. NADH is primarily involved in catabolic (energy-producing) reactions, and it is the primary electron donor for oxidative phosphorylation. (3) NADP+ (Nicotinamide Adenine Dinucleotide Phosphate, oxidized form) is similar to NAD+, but it has an additional phosphate group attached to the 2′ carbon of the adenine-containing ribose. Like NAD+, NADP+ accepts electrons to become NADPH. NADP+ is primarily involved in anabolic (biosynthetic) reactions, such as fatty acid synthesis, cholesterol synthesis, and nucleotide synthesis, and in antioxidant defense. (4) NADPH (Nicotinamide Adenine Dinucleotide Phosphate, reduced form) is the reduced form of NADP+. It donates electrons for biosynthetic reactions and for the regeneration of reduced glutathione (the cell’s primary antioxidant). NADPH is primarily involved in anabolic (biosynthetic) reactions and antioxidant defense, and it is the primary electron donor for reductive biosynthesis and for the glutathione antioxidant system. In summary, NAD+/NADH are primarily involved in catabolic (energy-producing) reactions and cellular signaling, while NADP+/NADPH are primarily involved in anabolic (biosynthetic) reactions and antioxidant defense. The ratio of NAD+ to NADH in the cell is an important indicator of cellular metabolic state, with a high NAD+/NADH ratio indicating a high-energy state (oxidative metabolism), and a low NAD+/NADH ratio indicating a low-energy state (glycolytic metabolism). Similarly, the ratio of NADP+ to NADPH is an important indicator of cellular antioxidant capacity, with a high NADPH/NADP+ ratio indicating a high antioxidant capacity.

Q3: How does NAD+ supplementation work, and what are the benefits?

A: NAD+ supplementation works by increasing the levels of NAD+ in cells and tissues, which can improve cellular energy metabolism, activate sirtuins and other NAD+-dependent enzymes, enhance DNA repair, reduce inflammation and oxidative stress, and improve overall cellular function. NAD+ levels naturally decline with age, and this decline has been implicated in numerous age-related diseases. By boosting NAD+ levels, NAD+ supplementation can potentially reverse some of the age-related changes in cellular function and improve health. The potential benefits of NAD+ supplementation include: (1) Improved cellular energy metabolism and mitochondrial function, increasing ATP production and reducing fatigue; (2) Activation of sirtuins (SIRT1-SIRT7), which regulate gene expression, cellular metabolism, stress resistance, DNA repair, and longevity; (3) Enhanced DNA repair and genome stability, reducing the accumulation of DNA damage and mutations with age; (4) Reduction of chronic inflammation (inflammaging), through inhibition of NF-κB and other pro-inflammatory pathways; (5) Improvement of metabolic health, including improved insulin sensitivity, reduced blood glucose levels, improved lipid profiles, and reduced liver fat accumulation; (6) Neuroprotective effects, including improved cognitive function, reduced neuroinflammation, and protection against neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease; (7) Cardiovascular protective effects, including improved cardiac function, reduced blood pressure, improved endothelial function, and reduced risk of cardiovascular disease; (8) Improved muscle mass and strength, exercise performance, and recovery from exercise; (9) Improved skin health, including reduced wrinkles, improved elasticity and hydration, and protection against UV-induced damage; (10) Improved immune function and reduced susceptibility to infections; (11) Potential anti-aging and longevity effects, based on preclinical studies showing extended lifespan and improved healthspan in model organisms. It is important to note that while the preclinical evidence for the benefits of NAD+ supplementation is strong, the clinical evidence in humans is still limited, and more research is needed to confirm the long-term safety and efficacy of NAD+ supplementation in humans. Additionally, NAD+ supplementation is not a substitute for a healthy lifestyle, including a balanced diet, regular exercise, adequate sleep, and stress management, which are all important for maintaining healthy NAD+ levels and overall health.

Q4: What is the recommended dosage for NAD+ in research studies?

A: The optimal dosage of NAD+ varies depending on the specific research application, animal model, route of administration, and desired outcome. In preclinical animal studies, dosages have ranged from 10 mg/kg to 1000 mg/kg body weight per day, depending on the species and study design. For rodent studies, typical dosages range from 100 mg/kg to 500 mg/kg per day, administered via oral gavage, intraperitoneal injection, or subcutaneous injection. For larger animal models (such as non-human primates), dosages are typically lower, ranging from 10 mg/kg to 100 mg/kg per day. For in vitro studies, concentrations typically range from 1 μM to 10 mM, with most studies using concentrations between 10 μM and 1 mM. It is important to note that these are research dosages and should not be interpreted as recommendations for human use. In clinical studies, NAD+ is typically administered via intravenous (IV) infusion at dosages ranging from 100 mg to 1000 mg per infusion, with infusions administered 1-3 times per week. Oral NAD+ supplementation is less common due to poor bioavailability (NAD+ is broken down in the digestive tract before it can be absorbed), and most oral supplementation studies use NAD+ precursors such as nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN) instead, which have better oral bioavailability and can increase cellular NAD+ levels more effectively. For oral supplementation with NAD+ precursors, typical dosages range from 100 mg to 2000 mg per day, with most studies using dosages between 250 mg and 1000 mg per day. Researchers should consult published literature and conduct dose-response studies to determine the optimal dosage for their specific research application. It is also important to note that the route of administration can significantly affect the bioavailability and efficacy of NAD+, with IV administration providing the highest bioavailability, followed by subcutaneous and intramuscular injection, and oral administration providing the lowest bioavailability due to degradation in the digestive tract. Always follow institutional guidelines and ethical protocols when conducting research with NAD+.

Q5: What are the most common side effects of NAD+ supplementation?

A: NAD+ is generally well-tolerated in both preclinical and clinical studies, with a low incidence of side effects. The most common side effects of NAD+ supplementation are mild and transient, and they include: (1) Flushing and warmth of the skin, particularly of the face, neck, and chest, which is similar to the “niacin flush” caused by high doses of nicotinic acid (vitamin B3). This flushing is caused by vasodilation (widening of blood vessels) and is usually mild and transient, lasting 15-30 minutes. The incidence and severity of flushing can be reduced by slowing the rate of IV infusion, taking an aspirin or non-steroidal anti-inflammatory drug (NSAID) before supplementation, or by gradually increasing the dose over time. (2) Nausea and gastrointestinal discomfort, particularly at higher doses or with rapid IV infusion. These symptoms are usually mild and transient, and they can be reduced by slowing the rate of infusion, taking the supplement with food, or by gradually increasing the dose over time. (3) Headache and dizziness, particularly at higher doses or with rapid IV infusion. These symptoms are usually mild and transient, and they can be reduced by slowing the rate of infusion, staying hydrated, or by gradually increasing the dose over time. (4) Fatigue and tiredness, particularly in the first few days of supplementation, as the body adjusts to the increased NAD+ levels. This is usually mild and transient, and it typically resolves within a few days to a week. (5) Injection site reactions, including redness, swelling, itching, or pain at the injection site, particularly with subcutaneous or intramuscular injection. These reactions are usually mild and transient, and they can be reduced by rotating injection sites and using proper injection technique. Serious side effects are rare, but they can include: (1) Allergic reactions, including rash, itching, hives, swelling of the face/lips/tongue, and difficulty breathing. If any of these symptoms occur, discontinue use immediately and seek medical attention. (2) Hypotension (low blood pressure), particularly with rapid IV infusion or at very high doses. This can cause dizziness, lightheadedness, fainting, or even shock in severe cases. The risk of hypotension can be reduced by slowing the rate of infusion and monitoring blood pressure during supplementation. (3) Hepatotoxicity (liver damage), which has been reported in rare cases with very high doses of NAD+ or with long-term use. This is usually reversible upon discontinuation of supplementation, but it is important to monitor liver function with long-term or high-dose use. (4) Interactions with medications, particularly with blood pressure medications, blood thinners, and diabetes medications. NAD+ can lower blood pressure and blood glucose levels, so the dose of these medications may need to be adjusted when used in combination with NAD+ supplementation. It is important to note that these side effects are based on limited clinical data, and more research is needed to fully understand the long-term safety and side effect profile of NAD+ supplementation. Researchers should always follow proper safety protocols and consult institutional safety guidelines when working with NAD+.

Q6: Is NAD+ legal for research purposes?

A: Yes, NAD+ is legal for research purposes in most countries, including the United States, when purchased from reputable suppliers and used strictly for laboratory research. NAD+ is a naturally occurring coenzyme found in all living cells, and it is not a controlled substance or a prescription medication. NAD+ is available as a dietary supplement in many countries, including the United States, where it is regulated as a dietary supplement by the Food and Drug Administration (FDA) under the Dietary Supplement Health and Education Act (DSHEA) of 1994. However, it is important to note that while NAD+ is available as a dietary supplement, the quality and purity of over-the-counter NAD+ supplements can vary significantly, and many supplements may not contain the amount of NAD+ listed on the label or may contain contaminants. For research purposes, it is important to purchase high-purity NAD+ from reputable suppliers that provide a Certificate of Analysis (COA) with each batch, verifying the purity, identity, and quality of the product. Researchers must ensure that their use of NAD+ complies with all applicable local, state, and federal regulations, as well as institutional guidelines and ethical protocols. For in vivo research involving animals, researchers must follow institutional animal care and use committee (IACUC) guidelines, and for human subjects research, researchers must follow institutional review board (IRB) guidelines and obtain informed consent from participants. At Hanpro Peptides, we sell high-purity NAD+ exclusively for research purposes, and all purchasers must agree to use the product only for legitimate scientific research. It is important to note that while NAD+ is available as a dietary supplement, it has not been evaluated by the FDA for the treatment, cure, or prevention of any disease, and it should not be used as a substitute for medical advice or treatment. Additionally, the use of NAD+ for intravenous (IV) therapy or other clinical applications should only be done under the supervision of a qualified healthcare provider.

Q7: What is the shelf life of NAD+, and how should it be stored?

A: When stored properly, lyophilized (freeze-dried) NAD+ has a shelf life of up to 2 years from the date of manufacture when stored at -20°C in a freezer, protected from light and moisture. It is important to keep NAD+ in its original sealed vial, protected from light, moisture, and temperature fluctuations. NAD+ is sensitive to light, moisture, and high temperatures, and exposure to these factors can cause degradation and reduce the potency of the product. For short-term storage (up to 3 months), NAD+ can be stored at 2-8°C (refrigerator), protected from light and moisture. For long-term storage (up to 2 years), NAD+ should be stored at -20°C (freezer), protected from light and moisture. It is important to avoid repeated freeze-thaw cycles, as this can cause degradation. After reconstitution, NAD+ should be stored in a refrigerator at 2-8°C, protected from light, and used within 7 days. For longer storage of reconstituted NAD+ (up to 3 months), it is recommended to aliquot the solution into individual doses and store at -20°C, protected from light. However, repeated freeze-thaw cycles should be avoided, as they can degrade the molecule. Always check the product’s expiration date and Certificate of Analysis (COA) for specific storage recommendations. At Hanpro Peptides, all our products are shipped with cold packs to maintain stability during transit, and each vial comes with a detailed COA specifying the manufacture date, expiration date, and purity level. It is important to note that NAD+ should not be stored at room temperature for extended periods, as exposure to heat, light, and moisture can lead to degradation of the molecule and reduced efficacy. The reconstituted solution should be inspected regularly for any signs of degradation, including discoloration, cloudiness, or particle formation. If any of these signs are observed, the solution should be discarded and not used for research purposes. Additionally, NAD+ is most stable at slightly acidic pH (pH 4-6), and it can degrade at neutral or alkaline pH over time, so it is important to use appropriate buffers when working with reconstituted NAD+.

Related Products for Research

For researchers investigating cellular metabolism, aging, longevity, and related conditions, we recommend exploring these related peptides and compounds:

• Epithalon – A synthetic peptide derived from the pineal gland, known for its anti-aging and telomere-lengthening properties. Often studied in combination with NAD+ for comprehensive anti-aging and longevity research.
• GHK-Cu (Copper Peptide) – A naturally occurring tripeptide with copper, known for its anti-aging, wound healing, and tissue regeneration properties. Often studied in combination with NAD+ for skin health and anti-aging research.
• Semaglutide – A GLP-1 receptor agonist, known for its effects on blood glucose control and weight loss. Often studied in combination with NAD+ for metabolic health and anti-aging research.
• Tirzepatide – A dual GLP-1/GIP receptor agonist, known for its potent effects on blood glucose control and weight loss. Often studied in combination with NAD+ for metabolic health and anti-aging research.
• Ipamorelin – A growth hormone secretagogue that stimulates the release of growth hormone, supporting muscle growth, fat loss, and recovery. Often studied in combination with NAD+ for body composition and anti-aging research.
• CJC-1295 Without DAC – A growth hormone-releasing hormone (GHRH) analog that increases growth hormone and IGF-1 levels, supporting muscle growth, fat loss, and recovery. Frequently studied in combination with Ipamorelin and NAD+.
• BPC 157 – A 15-amino-acid peptide derived from gastric juice, known for its remarkable healing properties. Often studied in combination with NAD+ for tissue repair and anti-aging research.
• TB-500 (Thymosin Beta-4) – A 43-amino-acid peptide known for its connective tissue healing and flexibility-promoting properties. Often studied in combination with NAD+ for tissue repair and anti-aging research.

Quality Assurance at Hanpro Peptides

At Hanpro Peptides, we are committed to providing researchers with the highest quality peptides and compounds available. Our NAD+ is manufactured in state-of-the-art facilities using advanced synthesis and purification technology, ensuring consistent quality and purity batch after batch. We use only the highest quality raw materials and严格的质量控制流程 to ensure that our NAD+ meets or exceeds the highest industry standards for purity, identity, and quality.

Our Quality Control Process Includes:

• High-Performance Liquid Chromatography (HPLC): Every batch is analyzed by HPLC to verify purity ≥99%. This ensures that our products are free from impurities and contaminants that could affect research results.
• Mass Spectrometry (MS): Mass spectrometry is used to confirm the molecular weight and identity of each compound, ensuring that the product matches the expected molecular structure.
• UV-Visible Spectroscopy: For NAD+ and other compounds with characteristic UV absorption spectra, we conduct additional UV-Vis spectroscopy analysis to verify identity and purity.
• Certificate of Analysis (COA): Every product comes with a detailed COA that includes the batch number, manufacture date, expiration date, purity level, and test results. Researchers can use this information to verify product quality and document their research materials.
• Microbiological Testing: Our products undergo rigorous microbiological testing to ensure they are free from bacteria, fungi, and other microorganisms.
• Endotoxin Testing: For compounds intended for in vivo studies, we conduct endotoxin testing to ensure that levels are within acceptable limits for research use.
• Heavy Metal Testing: For compounds intended for in vivo studies, we conduct heavy metal testing to ensure that levels of lead, mercury, cadmium, arsenic, and other heavy metals are within acceptable limits.

We also offer custom synthesis services for researchers who require specific compounds, modifications, or formulations. Our team of experienced chemists can synthesize a wide range of peptides, nucleotides, coenzymes, and other bioactive compounds, tailored to your specific research needs. We can also provide custom formulations, including liposomal formulations, nanoparticle formulations, and controlled-release formulations, to improve the bioavailability and efficacy of your research compounds.

Disclaimer

Important Notice: All products sold by Hanpro Peptides are intended for laboratory research purposes only. They are not intended for human consumption, diagnostic use, or therapeutic application. While NAD+ is available as a dietary supplement in some countries, our research-grade NAD+ is not intended for clinical use or human consumption, and it should only be used in preclinical research or approved clinical trials in accordance with applicable regulations and institutional guidelines.

Researchers are responsible for ensuring that their use of our products complies with all applicable local, state, and federal regulations, as well as institutional guidelines and ethical protocols. Our products should only be used by qualified researchers in properly equipped laboratory settings. Animal research should be conducted in accordance with institutional animal care and use committee (IACUC) guidelines, and human subjects research should be conducted in accordance with institutional review board (IRB) guidelines and under an active investigational new drug (IND) application where required.

The information provided in this product description is for educational and informational purposes only and is based on published scientific literature and preliminary clinical trial results. It does not constitute medical advice, and we make no claims regarding the therapeutic effects or safety of our products for human use. Any references to potential therapeutic applications are based on preclinical and clinical research and are not intended to suggest that these products are safe or effective for human consumption.

By purchasing and using our products, you acknowledge and agree that you are a qualified researcher, that you will use our products only for legitimate scientific research, and that you assume all responsibility for ensuring compliance with applicable regulations and ethical guidelines.

If you have any questions about our products, quality control processes, or custom synthesis services, please contact our customer support team. We are committed to providing researchers with the highest quality products and exceptional customer service to support your important research endeavors.