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Free U.S. shipping on orders over $150Nicotinamide adenine dinucleotide (oxidized form), commonly abbreviated as NAD⁺, is a naturally occurring coenzyme found in all living cells. It has gained interest in research due to its roles in mediating various cellular anti-aging processes.
It plays a central role in redox reactions, acting as an electron carrier in metabolic processes such as glycolysis, the Krebs cycle, and oxidative phosphorylation [1, 2, 3].
Structurally, NAD⁺ consists of two nucleotides joined through their phosphate groups: one nucleotide contains an adenine base, and the other contains nicotinamide [4].
Image source [4]
In cellular systems, NAD⁺ functions as a substrate for a range of enzymes, including:
In its oxidized form (NAD⁺), the molecule accepts electrons and is converted into its reduced counterpart, NADH, which subsequently donates those electrons to the mitochondrial electron transport chain for ATP production [8].
However, NAD⁺ itself remains a molecule of focus for research exploring its direct biochemical interactions within various intracellular compartments, including the cytoplasm, nucleus, and mitochondria.
Intracellular NAD⁺ levels decline with cellular aging, demonstrated in several mammalian tissues [9]. Various anti-aging hormeses, such as caloric restriction and cold exposure, work partly by increasing cellular NAD+.
This observation has created interest in longevity research and has launched multiple investigations into NAD⁺ precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) in both animals and humans [10], [11].
Age-associated declines in NAD⁺ levels have been linked to impaired mitochondrial function, increased oxidative stress, and reduced sirtuin activity [9].
Lower NAD⁺ concentrations correlate with diminished autophagy, shortened telomeres, and lowered PARP DNA repair activity [12, 13]. Age-related NAD⁺ depletion also impairs endothelial function and contribute to chronic low-grade inflammation [14].
Although NAD+ is a PARP substrate, it’s unclear whether increasing physiologic NAD+ concentration can meaningfully improve DNA repair.
A clinical trial with 21 healthy smokers orally supplemented nicotinic acid (0, 50, or 100 mg/day) over 14 weeks to track various biological and DNA associated parameters. After 14 weeks, results found [15]:
Although nicotinamide supplementation did not activate markers of DNA repair, larger sample size studies and comparison to healthy individuals are needed.
NAD+ supplementation can tangibly improve whole-body metabolic health.
An RCT of 30 overweight or obese adults over 45 received 1,000 mg/day of β-nicotinamide mononucleotide (MIB-626) (2 x 500 mg tablets twice daily) vs. placebo for 28 days to see whether NAD⁺ levels could be safely boosted and improve markers of cardiometabolic health [16].
Results showed that MIB-626 supplementation:
NAD+ supplementation is a powerful way to curb addictive behaviors.
A pilot study investigated the effects of intravenous NAD+ and enkephalinase combination infusions on cravings and psychological outcomes in 50 individuals with Substance Use Disorder (SUD) [17].
The cohort included a diverse group of poly-drug-dependent individuals. Behavioral changes were evaluated using Likert scales, measuring craving, anxiety, and depression levels before and after infusion therapy.
IV NAD+ infusions resulted in:
All reductions followed a dose-dependent linear trend, with greater improvements observed over time. The study shows the potential application of NAD/NADH as a stand-alone treatment in attenuating symptoms of addiction.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). NAD+ is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
Orders are processed within 1–3 business days after payment confirmation. Orders placed after 3:00 PM Pacific time or on weekends and holidays will begin processing the next business day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
What is P21 peptide? P21 is a synthetic peptide designed as a mimetic of ciliary neurotrophic factor (CNTF), a neurotrophin involved in neuronal survival, synaptic maintenance, and central repair pathways. While native CNTF is a large protein with limited permeability and complex receptor interactions, P21 distills CNTF’s key functional domains into a short, bioactive sequence engineered for stability and targeted signaling [1]. One of the biggest advantages of P21 is its ability to cross the blood–brain barrier (BBB). Its small molecular size allows it to access central nervous system tissues more efficiently than full-length neurotrophic proteins [2]. This distinguishes P21 from broader neurotrophic blends such as cerebrolysin, which rely on multi-peptide mixtures and indirect peripheral effects [3]. Cerebrolysin contains fragments derived from porcine brain proteins and act through diffuse signaling. P21, in contrast, is a receptor-specific mimetic designed to emulate a single neurotrophin’s core actions. P21 Peptide Benefits Neurogenesis and Synaptic Plasticity P21’s ability to activate CNTF-related neurotrophic pathways can help support neuronal growth, differentiation, and long-term structural adaptability. A core feature of P21’s activity is promoting neurogenesis, especially within brain regions where adult neural stem cells remain active [4]. P21 also interacts with pathways involved in synaptic plasticity, the process by which neurons strengthen, weaken, or remodel their connections in response to new information [2]. Because P21 is small enough to cross the blood–brain barrier, these effects occur in a more targeted and timely fashion. Alzheimer's Disease P21 has attracted scientific interest for its potential relevance to pathways implicated in Alzheimer’s disease. P21’s interaction with STAT3 and other CNTF-responsive intracellular cascades may help reinforce processes that protect neurons from [5]: Oxidative strain Impaired energy metabolism Synaptic deterioration all hallmarks frequently in Alzheimer’s models. Another area of interest is P21’s potential influence on amyloid- and tau-associated stress responses. An in vivo study in a 3xTg-AD transgenic mouse model of Alzheimer’s disease evaluated effects of 12 months of chronic oral P21. Female 3xTg-AD mice and wild-type controls were given P21 in their diet for 12 months, starting at 9-10 months of age when AD symptoms developed [6]. P21 diets resulted in: Significantly decreased accumulation of abnormal hyperphosphorylated tau Significant reduction in soluble Aβ levels and plaque load Elevated brain-derived neurotrophic factor (BDNF) and decreased GSK3β activity Restored cognitive performance and neurogenesis These findings support P21 as a promising neurotrophic peptide mimetic with therapeutic potential to shift Alzheimer’s disease pathology from neurodegeneration toward regeneration. Developmental disorders P21 has also generated interest in research exploring neurodevelopmental pathways, because CNTF signaling plays a role in neuronal differentiation, axonal guidance, and early circuit formation [7]. During development, CNTF influences how neural progenitors mature into functional neurons and how connections between brain regions are refined. A combined in vitro/in vivo study evaluated the therapeutic potential of P21 in a mouse model of CDKL5 deficiency disorder (CDD) [8]. CDD is an X-linked disorder that results in seizures, developmental and intellectual delays, and usually requires lifelong care. P21 administration resulted in: Successful rescue of multiple CDKL5-related cellular deficits in neurons: Restored proliferation Normalized cell survival Improved neuronal maturation Corrected abnormalities in GSK3β signaling There were limited effects in vivo, as P21 resulted in minimal behavioral improvement. This could be due to differences in bioavailability, timing, or developmental windows between in vitro and in vivo systems. P21 is not just limited to rare neurodevelopmental disorders. Prenatal to early postnatal treatment with the CNTF-derived peptide mimetic P021 was tested in Ts65Dn mice, a Down syndrome model that also develops Alzheimer’s-like memory deficits [9]. Early P021 intervention rescued developmental delays in pups and restored hippocampus-dependent memory in adulthood. The treatment: Prevented presynaptic protein loss Reduced GSK3β activity Increased neuroplasticity markers including BDNF and phosphorylated CREB in both young (3 weeks) and adult mice These results demonstrate that enhancing neurotrophic support during critical periods of early brain development can prevent lifelong cognitive impairment and Alzheimer’s-like pathology associated with trisomy 21.
Snapshot: PEG-MGF (PEGylated Mechano-Growth Factor) is a regulated IGF-1 Ec-derived peptide used in preclinical research to study IGF-1R, PI3K/Akt, and MAPK/ERK signaling in tissue-repair and regeneration models. Experimental studies have explored its roles in skeletal muscle recovery, periodontal ligament remodeling, bone and cartilage repair, and injury-response pathways. What Is PEG-MGF? PEG-MGF (Polyethylene Glycol–Modified Mechano-Growth Factor) is a chemically-modified peptide related to the IGF-1 Ec splice-variant sequence (also called MGF). In research settings, it is used as a pathway probe to study IGF-axis signaling, skeletal muscle regeneration programs, and injury-response biology in both in vitro and in vivo models [1, 2, 3]. Pegylation is applied to increase peptide persistence and stability, allowing for longer exposure windows compared with non-pegylated fragments in time-course and distribution studies [4]. Experimental studies most often evaluate PEG-MGF in contexts including skeletal muscle injury and repair, cardiac ischemia and hypoxia, bone healing and osteoblast activity, cartilage and chondrocyte migration, and periodontal ligament cell differentiation. Mechanistically, its actions are linked to IGF-1 receptor activation and downstream PI3K/Akt and MAPK/ERK signaling pathways, which are associated with cell growth, migration, and survival responses [3]. PEG-MGF Peptide Benefits & Side Effects PEG-MGF has been investigated in preclinical and mechanistic research models, with findings suggesting potential roles in muscle repair and regeneration [5], modulation of inflammatory mediator expression and immune-cell clearance kinetics [6], osteoblast proliferation [7], chondrocyte migration and mechanotransduction pathways [2], and apoptosis and remodeling in cardiac injury models [8]. In experimental settings, key considerations include the fact that IGF-axis activation is linked to cell-proliferation signaling, which warrants caution in models involving abnormal or uncontrolled cell growth [2]. Effects may also vary depending on delivery method and PEGylation format, and current evidence remains largely limited to controlled preclinical studies. These findings are model-specific and should be interpreted within a lab-research context. Hypertrophy and Muscle Damage Repair PEG-MGF and related MGF-derived peptides are frequently studied in models of muscle injury and repair. These experiments typically measure changes in inflammation, oxidative stress, and expression of genes involved in tissue recovery and remodelling [2]. Cell-based studies using myoblasts and muscle-cell cultures also study cell growth, migration, and IGF-1R-linked PI3K/Akt and MAPK/ERK signaling, which are pathways associated with hypertrophy and regeneration rather than performance enhancement [2]. Across multiple studies, MGF peptides support satellite-cell activation, proliferation, and fusion, which are key steps in muscle maintenance and repair [5, 3]. In primary human muscle cell cultures, the MGF-24aa-E peptide increased the proliferative lifespan of satellite cells and delayed cellular aging in younger tissue, while promoting hypertrophy across all age groups [5]. These effects are interpreted as enhanced regenerative capacity, particularly relevant to age-related muscle loss and sarcopenia [5]. Other experimental models show that early increases in MGF splice-variant expression tend to coincide with the initial, proliferation-focused phase of muscle repair, followed later by differentiation and myofiber maturation [3]. MGF-related peptides have also been studied in cardiac injury settings. In animal models of myocardial infarction, delivery of MGF E-domain peptides has been associated with better preservation of cardiac function, smaller regions of compromised tissue, reduced cell-death signaling, and slower progression of adverse remodeling [8, 9]. In some studies, localized delivery using peptide-eluting biomaterial structures further improved hemodynamic recovery following injury [9]. Overall findings suggest benefits for repair, survival, and regeneration-linked signaling programs both in skeletal and cardiac muscle, with applications focused on tissue-healing rather than performance outcomes. Periodontal Regeneration MGF-related peptides have also been studied in periodontal ligament (PDL) regeneration models, particularly under mechanical loading conditions such as occlusal force. In vitro and in vivo studies show that MGF produced in response to mechanical stimulation can enhance PDL remodelling and promote periodontal ligament stem-cell proliferation and fibrogenic differentiation [10, 11]. These effects are linked to Fyn-FAK-mediated mechanochemical signaling, activation of ERK1/2 and p38 pathways, and the Fyn-RhoA-YAP phosphorylation axis, which together support matrix remodeling and fibroblast-like differentiation [10]. Collectively, these findings suggest a potential role for MGF-centered signaling as an adjunct approach in periodontal regeneration research. Anabolic and Regenerative Effects PEG-MGF peptides have been studied in multiple injury- and regeneration-focused models. In cardiac ischemia, MGF expression rises rapidly and peptide delivery has been associated with reduced apoptosis, preservation of myocardium, improved hemodynamics, and possible stimulation of precursor cell recruitment [4]. In neural and hypoxia-ischemia models, MGF shows neuroprotective activity independent of IGF-1R signaling, supporting cell survival pathways [4]. MGF has also been reported to influence chondrocyte and mesenchymal-cell differentiation, matrix remodelling, and cytoskeletal dynamics under stress or damage conditions [4]. References 1 Liu, X., Zeng, Z., Zhao, L., Chen, P. and Xiao, W. (2019) Impaired skeletal muscle regeneration induced by macrophage depletion could be partly ameliorated by MGF injection. Front. Physiol., Frontiers Media SA 10, 601 2 Liu, Y., Duan, M., Zhang, D. and Xie, J. (2023) The role of mechano growth factor in chondrocytes and cartilage defects: a concise review. Acta Biochim. Biophys. Sin. (Shanghai), China Science Publishing & Media Ltd. 55, 701–712 3 Matheny, R. W., Jr, Nindl, B. C. and Adamo, M. L. (2010) Minireview: Mechano-growth factor: a putative product of IGF-I gene expression involved in tissue repair and regeneration. Endocrinology, The Endocrine Society 151, 865–875 4 Zabłocka, B., Goldspink, P. H., Goldspink, G. and Górecki, D. C. (2012) Mechano-Growth Factor: an important cog or a loose screw in the repair machinery? Front. Endocrinol. (Lausanne), Frontiers Media SA 3, 131 5 Kandalla, P. K., Goldspink, G., Butler-Browne, G. and Mouly, V. (2011) Mechano Growth Factor E peptide (MGF-E), derived from an isoform of IGF-1, activates human muscle progenitor cells and induces an increase in their fusion potential at different ages. Mech. Ageing Dev. 132, 154–162 6 Lin, Y.-C., Chen, B.-M., Tran, T. T. M., Chang, T.-C., Al-Qaisi, T. S. and Roffler, S. R. (2023) Accelerated clearance by antibodies against methoxy PEG depends on pegylation architecture. J. Control. Release, Elsevier BV 354, 354–367 7 Deng, M., Zhang, B., Wang, K., Liu, F., Xiao, H., Zhao, J., et al. (2011) Mechano growth factor E peptide promotes osteoblasts proliferation and bone-defect healing in rabbits. Int. Orthop., Springer Science and Business Media LLC 35, 1099–1106 8 Carpenter, V., Matthews, K., Devlin, G., Stuart, S., Jensen, J., Conaglen, J., et al. (2008) Mechano-growth factor reduces loss of cardiac function in acute myocardial infarction. Heart Lung Circ., Elsevier BV 17, 33–39 9 Peña, J. R., Pinney, J. R., Ayala, P., Desai, T. A. and Goldspink, P. H. (2015) Localized delivery of mechano-growth factor E-domain peptide via polymeric microstructures improves cardiac function following myocardial infarction. Biomaterials, Elsevier BV 46, 26–34 10 Feng, F., Tu, T., Wang, H., Song, R., Li, J., Zhu, Y., et al. (2024) Mechano-growth factor regulates periodontal ligament stem cell proliferation and differentiation through Fyn-RhoA-YAP signaling. Biochem. Biophys. Res. Commun., Elsevier BV 733, 150450 11 Zhao, Y., Zhang, S., Cheng, B., Feng, F., Zhu, Y., Liu, Y., et al. (2024) Mechanochemical coupling of MGF mediates periodontal regeneration. Bioeng. Transl. Med., Wiley 9, e10603
What is Pinealon Peptide? Pinealon is a synthetic, bioactive, tripeptide (Glu-Asp-Arg) derived from the pineal gland [3]. It is classified as a peptide bioregulator due to its unique ability to bypass typical cell-surface or cytoplasmic receptors [3]. Instead, evidence suggests that it’s exceptionally small structure enables the molecule to cross both cellular and nuclear membranes [3]. Lab studies find that Pinealon can enter the cell nucleus, where it is thought to interact with DNA or DNA-associated proteins [3]. This ability to reach the genome provides a potential explanation for its wide-ranging effects, which align better with gene-expression changes rather than modulating traditional signalling pathways [3]. Inside the nucleus, Pinealon seems to modulate genes involved in antioxidant defenses, cell repair, and protection from cellular stress [1]. Animal model research reveals reductions in reactive oxygen species and apoptosis, and increased activity of endogenous antioxidant enzymes [4]. It appears to reduce the activity of caspase-3, an enzyme involved in programmed cell death, across several tissue types, suggesting a potential role in supporting cell survival under stressful conditions [4]. Pinelon may impact pathways related to healthy cell cycling and interact with the pineal gland to influence its function and regulate circadian rhythm [5]. Pinealon peptide benefits Its unique mechanism, which bypasses conventional cell-surface receptors, has led to growing interest in its potential roles in neuroprotection, metabolism, stress resilience, and cognitive support. Learning and Memory Through directly interacting with DNA to influence gene expression involved in neural function, Pinealon may support learning and memory. Studies suggest it can reduce oxidative stress in brain tissue, preserve neuronal viability, and modulate pathways related to information retention. In a study of prenatal rats exposed to high levels of homocysteine, maternal administration of Pinealon improved offspring cognitive function, enhancing performance in spatial orientation and navigation tasks while reducing reactive oxygen species and neuronal necrosis in the cerebellum [6]. Another found Pinealon was able to produce improvements in the Morris labyrinth task, showing faster acquisition of navigation tasks compared to untreated controls and those treated with a comparator peptide [7]. Improvements were also accompanied by reductions in caspase-3 activity in brain regions, suggesting that this peptide supports neuronal survival and resilience under hypoxic stress [4]. In a review, authors highlight findings to suggest that Pinealon enhances learning indices, decreases age- and stress-related neuronal apoptosis, and improves overall memory performance in animal models. It is thought these benefits are related to Pinealon’s ability to penetrate the nucleus and modulate gene expression, upregulating protective pathways and antioxidant systems while stabilizing cell-cycle and cell-death processes [8]. Neuroprotection Studies have found that Pinealon may help protect neurons through multiple and complementary mechanisms, primarily demonstrated in preclinical models. One major pathway involves reducing oxidative stress, a key contributor to neuronal injury and neurodegeneration. In cell studies, Pinealon was found to decrease ROS accumulation, reduce necrotic cell death, and modulate ERK1/2 activation, a signalling pathway involved in cell survival and stress response [1]. These findings suggest Pinealon may help maintain neuronal integrity under conditions of metabolic or oxidative stress, through direct genomic interactions that influence cell-cycle regulation [1]. Experimental hypoxia models further demonstrate neuroprotective effects. In hypobaric hypoxia and aged rat studies, Pinealon was able to increase neuronal resistance to oxygen deprivation, potentially by stimulating superoxide dismutase and glutathione peroxidase, and by limiting NMDA receptor-mediated excitotoxicity [7]. Pinealon was also found to normalize pro-inflammatory cytokines such as IL-6 and TNF‑α, indicating a dual role reducing programmed cell death and neuroinflammation [4]. At a molecular level, Pinealon is thought to modulate gene expression pathways associated with neurodegeneration [8]. Evidence suggests it can interact with histones and RNA, influencing pathways such as MAPK/ERK, as well as pro-apoptotic proteins and antioxidant genes [8]. This makes it a candidate for further study in neurodegenerative conditions. Antioxidant and Anti-aging Pinealon shows promise as an antioxidant and cellular longevity support. It supports brain cell viability by reducing reactive oxygen species (ROS) and limiting cell death, while also influencing cell survival pathways like ERK1/2 [1]. It also shows benefits for strengthening cell membranes and preventing lipid peroxidation, helping support the brain’s resistance to oxidative stress [8]. Pinealon has been shown to modulate the activity of antioxidant enzymes, including SOD and GPx, and support antioxidant genes like SOD2 and GPX1 [8]. In aging and low-oxygen models, it protects neurons by reducing excitotoxicity, lowering caspase‑3 activity, and normalizing inflammatory signals, which supports cell survival and new neuron growth [4]. In human neurons from older donors, it also reduces DNA damage and helps maintain dendritic structures [9]. Overall, Pinealon combines antioxidant, anti-aging, and anti-inflammatory effects, though human studies are still limited.