{"id":883,"date":"2026-04-24T00:03:37","date_gmt":"2026-04-24T00:03:37","guid":{"rendered":"https:\/\/decodepeptides.com\/?product=longevity-stack-bundle"},"modified":"2026-04-25T00:29:10","modified_gmt":"2026-04-25T00:29:10","slug":"longevity-stack-bundle","status":"publish","type":"product","link":"https:\/\/decodepeptides.com\/nl_nl\/product\/longevity-stack-bundle\/","title":{"rendered":"Longevity Stack \u2014 Epithalon, NAD+ & MOTS-C"},"content":{"rendered":"
\n

Longevity Stack \u2014 Epithalon, NAD+ & MOTS-C: The Most Complete Biological Anti-Aging Research Protocol<\/h2>\n

The Longevity Stack<\/strong> brings together three mechanistically distinct anti-aging compounds: Epithalon<\/strong> (telomerase activator), NAD+<\/strong> (nicotinamide adenine dinucleotide \u2014 mitochondrial coenzyme and sirtuin fuel), and MOTS-C<\/strong> (mitochondrial open reading frame of the 12S rRNA type-c \u2014 exercise mimetic peptide). Together they address the three principal hallmarks of biological aging at the molecular level: telomere shortening, mitochondrial dysfunction, and metabolic inflexibility<\/strong>.<\/p>\n\n

Epithalon: The Telomere-Extending Tetrapeptide<\/h2>\n

What Is Epithalon?<\/h3>\n

Epithalon (also spelled Epitalon or Epithalone) is a synthetic tetrapeptide \u2014 Ala-Glu-Asp-Gly (AEDG)<\/strong> \u2014 developed by Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology, derived from the pineal gland polypeptide extract Epithalamin. It is one of the most studied bioregulatory peptides in anti-aging science, with over three decades of peer-reviewed preclinical and clinical research documenting effects on telomere biology, neuroendocrine regulation, cancer prevention, and longevity.<\/p>\n

Mechanism of Action<\/h3>\n
    \n
  • Telomerase activation:<\/strong> Epithalon upregulates telomerase (hTERT)<\/strong> \u2014 the enzyme responsible for adding telomeric DNA repeats (TTAGGG) to chromosome ends \u2014 directly counteracting the progressive telomere shortening that drives cellular senescence<\/li>\n
  • Pineal gland regulation:<\/strong> Restores age-related decline in melatonin synthesis by normalising pinealocyte function, impacting circadian rhythm, sleep architecture, and immune regulation<\/li>\n
  • Antioxidant gene expression:<\/strong> Upregulates SOD (superoxide dismutase), catalase, and glutathione peroxidase \u2014 key enzymatic antioxidants that decline with age<\/li>\n
  • Tumour suppressor reactivation:<\/strong> Reactivates methylation-silenced tumour suppressor genes including p16 and p21 via epigenetic demethylation (Khavinson et al., 2003)<\/li>\n
  • Neuroendocrine normalisation:<\/strong> Restores hypothalamic receptor sensitivity to sex steroid feedback \u2014 a critical factor in age-related hormonal decline<\/li>\n<\/ul>\n

    Key Preclinical and Clinical Findings<\/h3>\n
      \n
    • Lifespan extension:<\/strong> In Drosophila melanogaster models, Epithalon extended mean lifespan by 11\u201316% and maximum lifespan by 13% (Khavinson VKh et al., 2000 \u2014 Bull Exp Biol Med<\/em>)<\/li>\n
    • Human somatic cell culture:<\/strong> Epithalon increased replicative lifespan of human fetal fibroblasts by 42% vs. controls via direct telomerase activation (Khavinson VKh et al., 2003 \u2014 Bull Exp Biol Med<\/em>)<\/li>\n
    • Cancer prevention:<\/strong> Long-term treatment in HER2-transgenic mice reduced spontaneous mammary tumour incidence by 2.4-fold (Anisimov VN et al., 2003 \u2014 Int J Cancer<\/em>)<\/li>\n
    • Cardiovascular protection:<\/strong> Normalised blood pressure and reduced cardiovascular mortality in a 12-year longitudinal study of elderly patients receiving peptide bioregulators including Epithalon (Khavinson et al., 2012 \u2014 Gerontology<\/em>)<\/li>\n
    • Immune enhancement:<\/strong> Restored thymic activity and T-cell function in aged rodents; increased NK cell cytotoxicity significantly vs. age-matched controls (Morozov VG et al., 1999)<\/li>\n<\/ul>\n

      Epithalon Research References<\/h3>\n
        \n
      1. Khavinson VKh et al. “Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells.” Bull Exp Biol Med<\/em>, 2003;135(6):590\u2013592.<\/li>\n
      2. Anisimov VN et al. “Effect of Epitalon on biomarkers of aging, life span and spontaneous tumor incidence in female Swiss-derived SHR mice.” Biogerontology<\/em>, 2003;4(4):193\u2013202.<\/li>\n
      3. Kossoy G et al. “Effect of epithalon on the lifespan and frequency of spontaneous mammary gland tumors in transgenic HER2 mice.” Neoplasma<\/em>, 2006;53(3):187\u2013192.<\/li>\n
      4. Khavinson V et al. “Tetrapeptide AEDG (Epitalon) inhibits oxidative stress and regulates expression of heat shock protein Hsp70 in rats exposed to UVA irradiation.” Regul Toxicol Pharmacol<\/em>, 2014;70(1):289\u2013294.<\/li>\n<\/ol>\n\n

        NAD+ (Nicotinamide Adenine Dinucleotide): The Mitochondrial Energy Currency<\/h2>\n

        What Is NAD+?<\/h3>\n

        NAD+ is a coenzyme found in all living cells, serving as the essential electron carrier in cellular respiration (oxidative phosphorylation) and as the obligate substrate for three families of longevity-regulating enzymes: sirtuins (SIRT1-7)<\/strong>, PARPs (poly-ADP-ribose polymerases)<\/strong>, and CD38<\/strong>. NAD+ levels decline by approximately 50% between the ages of 40 and 60 in humans \u2014 a decline now considered one of the primary molecular causes of aging \u2014 correlating with reduced mitochondrial efficiency, increased DNA damage, impaired circadian rhythms, and metabolic dysfunction.<\/p>\n

        Mechanism of Action<\/h3>\n
          \n
        • Sirtuin activation (SIRT1\u20137):<\/strong> All seven sirtuins require NAD+ as their obligate cofactor. SIRT1 deacetylates and activates PGC-1α (master regulator of mitochondrial biogenesis); SIRT3 maintains mitochondrial protein function and prevents ROS accumulation; SIRT6 promotes genomic stability via histone H3K9 deacetylation<\/li>\n
        • PARP-mediated DNA repair:<\/strong> PARP1\/2 consume NAD+ to synthesise poly(ADP-ribose) chains at sites of single-strand DNA breaks \u2014 the primary mechanism for repairing the 10,000\u201370,000 oxidative DNA lesions generated per cell per day<\/li>\n
        • Mitochondrial ETC function:<\/strong> NADH (reduced NAD+) donates electrons to Complex I of the mitochondrial electron transport chain \u2014 the rate-limiting step in ATP production. Age-related NAD+ decline impairs this directly<\/li>\n
        • CD38 competition:<\/strong> CD38 is a major NAD+-consuming enzyme whose expression increases with age and inflammation (inflammaging). NAD+ repletion helps offset this consumption and restore sirtuin activity<\/li>\n
        • AMPK cross-talk:<\/strong> Via SIRT1 \u2192 LKB1 \u2192 AMPK signalling, elevated NAD+ promotes catabolic\/repair states and suppresses energetically costly anabolic hypertrophy \u2014 a metabolic signature consistently associated with longevity in model organisms<\/li>\n<\/ul>\n

          Key Research Findings<\/h3>\n
            \n
          • Muscle function reversal:<\/strong> NAD+ repletion restored muscle mass, strength, and mitochondrial density in 22-month-old mice to levels comparable to 6-month-old controls (Gomes AP et al., 2013 \u2014 Cell<\/em>)<\/li>\n
          • DNA repair restoration:<\/strong> NAD+ administration reversed DNA damage markers (γH2AX, 8-OHdG) and improved radiation survival in aged mice (Li J et al., 2017 \u2014 Science<\/em>)<\/li>\n
          • Metabolic health:<\/strong> NAD+ precursor NMN improved glucose tolerance, lipid metabolism, and energy expenditure in aged obese mice (Yoshino J et al., 2011 \u2014 Cell Metab<\/em>)<\/li>\n
          • Human clinical data:<\/strong> 250mg oral NMN daily for 10 weeks significantly increased skeletal muscle NAD+ levels and improved insulin sensitivity in overweight older adults (Yoshino M et al., 2021 \u2014 Science<\/em>)<\/li>\n<\/ul>\n

            NAD+ Research References<\/h3>\n
              \n
            1. Gomes AP et al. “Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging.” Cell<\/em>, 2013;155(7):1624\u20131638.<\/li>\n
            2. Yoshino J et al. “Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice.” Cell Metab<\/em>, 2011;14(4):528\u2013536.<\/li>\n
            3. Verdin E. “NAD+ in aging, metabolism, and neurodegeneration.” Science<\/em>, 2015;350(6265):1208\u20131213.<\/li>\n
            4. Yoshino M et al. “Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women.” Science<\/em>, 2021;372(6547):1224\u20131229.<\/li>\n<\/ol>\n\n

              MOTS-C: The Mitochondrial Exercise Mimetic<\/h2>\n

              What Is MOTS-C?<\/h3>\n

              MOTS-C (Mitochondrial Open reading frame of the 12S rRNA type-c) is a 16-amino-acid peptide encoded within the mitochondrial genome<\/strong> (12S rRNA region) \u2014 not the nuclear genome. Discovered in 2015 by Lee et al. at USC, MOTS-C is a retrograde mitochondrial signal that translocates to the nucleus to regulate metabolic gene expression, representing an entirely new class of signalling molecules called mitochondrial-derived peptides (MDPs)<\/strong>. Its plasma levels decline with age and obesity, inversely correlating with insulin resistance and metabolic syndrome severity.<\/p>\n

              Mechanism of Action<\/h3>\n
                \n
              • AMPK activation via AICAR:<\/strong> MOTS-C inhibits MTHFD1 in the folate cycle, causing accumulation of AICAR<\/strong> (5-aminoimidazole-4-carboxamide ribonucleotide) \u2014 an endogenous AMP-mimetic that directly activates AMPK at Thr172, mimicking the metabolic state of prolonged exercise<\/li>\n
              • Nuclear gene regulation:<\/strong> Under metabolic stress, MOTS-C translocates to the nucleus and directly modifies gene expression related to Nrf2 antioxidant response, NF-κB suppression, and insulin signalling<\/li>\n
              • Insulin sensitisation:<\/strong> Improves skeletal muscle glucose uptake via GLUT4 translocation independently of insulin receptor pathways \u2014 AMPK-driven TBC1D1\/TBC1D4 phosphorylation<\/li>\n
              • Fatty acid oxidation:<\/strong> AMPK-dependent ACC (acetyl-CoA carboxylase) inhibition reduces malonyl-CoA, relieving CPT-1 inhibition and increasing mitochondrial fatty acid import and β-oxidation rates<\/li>\n<\/ul>\n

                Key Research Findings<\/h3>\n
                  \n
                • Obesity prevention:<\/strong> MOTS-C administration prevented high-fat diet-induced obesity and insulin resistance in mice, reducing body weight gain by 35% and improving glucose tolerance to near-normal levels (Lee C et al., 2015 \u2014 Cell Metab<\/em>)<\/li>\n
                • Exercise mimicry:<\/strong> MOTS-C plasma levels rise naturally during physical exercise in humans; exogenous administration reproduced key metabolic adaptations of aerobic training (Reynolds JC et al., 2021 \u2014 Nat Commun<\/em>)<\/li>\n
                • Aging reversal:<\/strong> Supplementation in aged mice restored physical performance, improved insulin sensitivity, and extended healthspan beyond age-matched controls (Lee C et al., 2015)<\/li>\n
                • Inflammation reduction:<\/strong> Reduced TNF-α, IL-6, and IL-1β in LPS-induced models; improved survival in systemic inflammatory challenge experiments<\/li>\n<\/ul>\n

                  MOTS-C Research References<\/h3>\n
                    \n
                  1. Lee C et al. “The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.” Cell Metab<\/em>, 2015;21(3):443\u2013454.<\/li>\n
                  2. Reynolds JC et al. “MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis.” Nat Commun<\/em>, 2021;12(1):470.<\/li>\n
                  3. Kim KH et al. “MOTS-c peptide increases physical endurance and insulin sensitivity.” Exp Mol Med<\/em>, 2019;51(4):1\u201312.<\/li>\n
                  4. Bhaskaran S et al. “Mitochondria-derived peptide MOTS-c restores cardiovascular function during aging.” Ageing Res Rev<\/em>, 2020;62:101128.<\/li>\n<\/ol>\n\n

                    The Longevity Stack: Three Hallmarks, Three Pathways<\/h2>\n\n\n\n\n\n\n\n
                    Compound<\/th>\nAging Hallmark Targeted<\/th>\nKey Molecular Mechanism<\/th>\n<\/tr>\n<\/thead>\n
                    Epithalon<\/td>\nTelomere shortening \/ cellular senescence<\/td>\nhTERT telomerase activation; epigenetic reprogramming; melatonin restoration<\/td>\n<\/tr>\n
                    NAD+<\/td>\nMitochondrial dysfunction \/ DNA damage accumulation<\/td>\nSIRT1-7 activation; PARP-mediated repair; Complex I electron transport<\/td>\n<\/tr>\n
                    MOTS-C<\/td>\nMetabolic inflexibility \/ insulin resistance<\/td>\nAMPK activation via AICAR; nuclear retrograde signalling; GLUT4 translocation<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

                    These three compounds address complementary, non-overlapping aging mechanisms. Epithalon acts at the chromosomal level to reset the biological clock; NAD+ restores the energy economy within each cell; and MOTS-C ensures the metabolic signalling network remains responsive to those energy cues. Together, they represent the most upstream, multi-pathway research protocol currently available for studying biological aging.<\/p>\n

                    All products in this bundle are supplied for research purposes only. Not for human consumption. Not evaluated by any regulatory authority.<\/em><\/p>\n<\/div>","protected":false},"excerpt":{"rendered":"

                    Triple anti-aging synergy: telomere extension (Epithalon) + mitochondrial energy (NAD+) + metabolic rejuvenation (MOTS-C). Save 12% vs. individual product prices.<\/p>","protected":false},"featured_media":859,"comment_status":"open","ping_status":"closed","template":"","meta":{"inline_featured_image":false,"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0},"product_brand":[],"product_cat":[56],"product_tag":[213,216,214,225,226,255,215],"class_list":["post-883","product","type-product","status-publish","has-post-thumbnail","product_cat-anti-aging-longevity","product_tag-anti-aging","product_tag-dna-repair","product_tag-longevity","product_tag-mitochondrial-health","product_tag-nad-plus","product_tag-research-grade","product_tag-telomere-support","first","instock","shipping-taxable","product-type-grouped"],"_links":{"self":[{"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/product\/883","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/product"}],"about":[{"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/types\/product"}],"replies":[{"embeddable":true,"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/comments?post=883"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/media\/859"}],"wp:attachment":[{"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/media?parent=883"}],"wp:term":[{"taxonomy":"product_brand","embeddable":true,"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/product_brand?post=883"},{"taxonomy":"product_cat","embeddable":true,"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/product_cat?post=883"},{"taxonomy":"product_tag","embeddable":true,"href":"https:\/\/decodepeptides.com\/nl_nl\/wp-json\/wp\/v2\/product_tag?post=883"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}