PEPTIDES

NAD+ 
Nicotinamide adenine dinucleotide is a coenzyme molecule produced via biological fermentation using microbial or enzymatic systems that mimic natural biosynthetic pathways. As with all NAD+ forms, it functions as a critical redox cofactor involved in mitochondrial energy production, DNA repair, and enzymatic regulation.
Effects
NAD+ 500mg 
Energy Metabolism Studies: NAD+ participates in redox reactions within glycolysis, the citric acid cycle, and oxidative phosphorylation, facilitating ATP generation.
Sirtuin and PARP Activity: Functions as a substrate for NAD+-dependent enzymes (sirtuins and PARPs), regulating DNA repair and epigenetic signaling.
Mitochondrial Research: Aids in studies examining mitochondrial biogenesis, energy balance, and oxidative stress response.
Aging and Metabolic Investigations: Research indicates that replenishing NAD+ levels can influence age-related energy decline and stress resistance.
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MOTS‑c?
Mitochondrial Open Reading Frame of the 12S rRNA type‑c (MOTS‑c) is a 16‑amino‑acid peptide encoded within the mitochondrial 12S rRNA gene. Classified as a mitochondrial-derived peptide (MDP), MOTS‑c is released in response to metabolic or exercise stress and translocates to the nucleus, where it modulates gene expression related to stress adaptation, energy balance, and mitochondrial function.
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Effects of MOTS‑c
Energy and Metabolic Regulation: MOTS‑c activates the AICAR–AMPK pathway, increasing endogenous AICAR and enhancing energy expenditure, glucose utilization, and fatty acid oxidation in rodent models.
Insulin Sensitivity: In high-fat-fed mice, MOTS‑c improved insulin responsiveness and glucose tolerance compared to controls.
Muscle Endurance: Animal studies demonstrate enhanced mitochondrial performance, endurance capacity, and physical activity when MOTS‑c is combined with exercise.
Cardiovascular Support: By activating AMPK, MOTS‑c reduces vascular calcification and restores mitochondrial function in heart tissue.
Longevity‑Related Benefits: Endogenous MOTS‑c decreases with age; long-term administration in aged mice enhances metabolic resilience, improves fitness, and promotes healthspan.
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GHK‑Cu 
A naturally occurring copper-binding tripeptide composed of glycyl‑L‑histidyl‑L‑lysine complexed with copper (II) ions. It was first isolated from human plasma and has since been studied for its regulatory role in tissue repair, angiogenesis, and antioxidant pathways in laboratory models. Its small size and high affinity for copper make it an important research molecule for exploring wound healing and extracellular matrix remodeling processes.
Effects of GHK‑Cu?
Wound Healing and Tissue Regeneration: In animal studies, GHK‑Cu promotes fibroblast migration, collagen synthesis, and angiogenesis, leading to accelerated tissue repair.
Anti‑Inflammatory and Antioxidant Effects: Research shows GHK‑Cu can upregulate antioxidant enzymes such as superoxide dismutase and reduce pro-inflammatory cytokines, protecting tissues from oxidative stress.
Gene Expression Modulation: GHK‑Cu influences the expression of over 400 human genes related to tissue repair, immune response, and proteostasis, as reported in genomic studies.
Matrix Metalloproteinase Regulation: It has been observed to balance MMP activity, thereby protecting extracellular matrix components during the healing process.
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BPC‑157
 Body Protection Compound‑157 is a research-grade, synthetic 15‑amino‑acid peptide originally identified in human gastric juice and later synthesized for laboratory studies. Unlike many endocrine-related peptides, it’s primarily examined for its potential in tissue repair, inflammation modulation, and protective mechanisms across multiple organ systems.
Effects of BPC‑157?
Tissue Regeneration & Wound Healing: Preclinical studies in rodents report accelerated healing of tendons, ligaments, skin wounds, and muscle injuries, correlating with increased fibroblast growth, collagen synthesis, and angiogenesis.
Gastrointestinal Protection:Demonstrated anti‑ulcer and cytoprotective effects in gastric injury models, with regulated villus‑crypt structure and intestinal tissue preservation.
Angiogenesis & Vascular Repair: Stimulates vascular endothelial growth factor (VEGF) signaling and nitric oxide pathways, promoting blood vessel formation in ischemic and injury models.
Neuro‑ & Organ‑Protection:Experimental findings suggest BPC‑157 mitigates brain and nerve injury, maintains liver and kidney integrity under toxic stress, and reduces inflammatory markers.
Anti‑Inflammatory & Oxidative Stress Reduction:Modulates nitric oxide and inflammatory cytokines, displaying both antioxidant and analgesic effects in animal research.