Longevity and Anti-Aging Research
Compounds studied for cellular lifespan, mitochondrial function, and age-related biological decline
Longevity research sits at the intersection of telomere biology, mitochondrial metabolism, epigenetic regulation, and neuroendocrine signaling. Compounds in this category have been studied for their potential to slow or modulate the hallmarks of aging as described in foundational geroscience literature, including telomere attrition, mitochondrial dysfunction, cellular senescence, and epigenetic drift. Preclinical models ranging from cell culture systems to aging rodent cohorts have been used to examine these compounds in isolation and in combination. Researchers assembling multi-compound longevity panels typically select based on which biological mechanism is the primary study target.
Compounds in This Use Case
Each compound contributes a distinct mechanism relevant to this research objective.
NAD+
$279Role
Coenzyme studied for sirtuin activation, PARP-dependent DNA repair, and mitochondrial biogenesis in aging cell models.
Mechanism
Activates SIRT1 through SIRT7 deacylases and serves as the substrate for PARP enzymes central to DNA strand break repair, while supporting PGC-1alpha-driven mitochondrial biogenesis.
Epithalon
$199Role
Tetrapeptide studied for telomerase activation and extension of replicative cell lifespan in somatic cell models.
Mechanism
Activates telomerase (hTERT) in somatic cells that normally exhibit low telomerase expression, with documented telomere elongation and extended cell division capacity in vitro.
MOTS-c
$149Role
Mitochondrial-derived peptide studied for AMPK activation and metabolic longevity signaling from mitochondria to nucleus.
Mechanism
Translocates from mitochondria to the nucleus under metabolic stress, activating AMPK via an AICAR-related pathway to regulate glucose uptake, fatty acid oxidation, and metabolic gene expression.
GHK-Cu
$179Role
Copper-binding tripeptide studied for collagen synthesis, extracellular matrix remodeling, and broad anti-aging gene expression modulation.
Mechanism
Delivers Cu2+ ions to superoxide dismutase and other copper-dependent enzymes, upregulates collagen Type I and III synthesis in fibroblasts, and modulates expression of more than 4,000 human genes in cell-based assays including antioxidant and repair pathways.
Pinealon
$159Role
Pineal gland tripeptide studied for epigenetic gene regulation in neurons and neuroprotection in aging cell models.
Mechanism
Penetrates nuclear membranes and interacts directly with chromatin in neuronal models, modulating gene expression associated with neuronal survival, oxidative defense, and melatonin synthesis pathways.
Research Context
Longevity research has expanded significantly since the identification of conserved aging pathways including mTOR, AMPK, sirtuin, and telomere biology axes. Compounds that interact with these pathways are evaluated both in isolated cell systems and in organismal aging models, with some data from primate studies and human observational work. The multi-hallmark framework published by Lopez-Otin and colleagues provides the dominant theoretical structure for organizing longevity compound research.
Related Compound Comparisons
Explore side-by-side mechanism comparisons for the compounds in this use case.
Frequently Asked Questions
Source These Compounds
All compounds in this use case are available from Spartan Peptides at least 98% HPLC-verified purity. Domestic US supply with same-day dispatch before 2 PM. For in-vitro research use only.
All compounds are strictly for in-vitro research use only and not intended for human consumption.