Evidence-based educational profiles for the biohacking stack. No hype — just mechanism of action, research status, common protocols, and honest safety context. All compounds are Research Use Only.
Compounds studied for telomere biology, immune aging, and cellular longevity. Many originate from decades of Russian and Eastern European gerontology research — now the subject of growing global interest. Evidence ranges from robust preclinical data to emerging human trials.
A synthetic tetrapeptide derived from the pineal gland's epithalamin, studied for telomerase activation, telomere elongation, and circadian regulation. One of the most-researched longevity peptides in the Russian gerontology canon — 40+ years of preclinical and limited human data. Scheduled for FDA PCAC review July 24, 2026.
A 16-amino-acid peptide encoded within mitochondrial DNA — not nuclear DNA. Studied for AMPK activation, metabolic homeostasis, insulin sensitivity, and exercise-mimicking effects. Circulating levels decline with age. Unique: the first mitochondria-derived peptide to act as a systemic hormone-like signal.
A naturally occurring thymic peptide studied for T-cell maturation, adaptive immunity enhancement, and immune senescence reversal. Approved as Zadaxin in 35+ countries. Thymic output declines with age — Tα1 is among the most clinically studied immune peptides for restoring immune competence in aging research contexts.
A naturally occurring copper-binding tripeptide that modulates 4,000+ human genes — more than any other known compound studied in this context. Research covers collagen synthesis, anti-inflammatory signaling, stem cell activation, and gene expression normalization. Plasma levels decline by 70% between age 20 and 60.
The Research Protocol Planner lets you build a structured compound schedule. The Peptide Calculator handles unit math for subcutaneous peptides. Free to use.
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme essential to every energy-producing reaction in the cell. It's also required for sirtuin activation and PARP-mediated DNA repair. Levels decline ~50% by age 50. Precursors — NMN and NR — are the primary research strategies for raising intracellular NAD+.
The foundational coenzyme in cellular energy metabolism. Required for glycolysis, the TCA cycle, and oxidative phosphorylation. Also a substrate for sirtuin deacetylases (SIRT1-7) and PARP enzymes that repair DNA strand breaks. IV and subcutaneous routes studied for direct cellular loading. The parent molecule — precursors are converted into NAD+ intracellularly.
A direct NAD+ precursor one step upstream in the biosynthesis pathway. Converts to NAD+ via the enzyme NMNAT. Studied in rodent models for metabolic function, DNA repair capacity, and muscle mitochondrial function. First controlled human trial (Keio University, 2020) demonstrated safety and NAD+ elevation at 250 mg/day. Ongoing human trials include Harvard/Washington University aging cohorts.
An alternative NAD+ precursor that enters the biosynthesis pathway via NRK enzymes, bypassing the rate-limiting NAMPT step. Has the most human clinical data of the NAD+ precursors — Phase 1/2 trials at Washington University in older adults demonstrated 50% NAD+ elevation in 4 weeks at 2,000 mg/day. Unlike NMN, NR is degraded in the gut to nicotinamide before intestinal absorption.
Both raise NAD+ in humans. The route (oral vs sublingual vs IV) meaningfully affects bioavailability. Discuss the evidence with fellow researchers in the Biohacker Hub.
Peptides studied for neuroprotection, BDNF upregulation, synaptogenesis, and cognitive biology. Evidence-based only — this is not a list of "smart drugs." These are compounds with defined mechanisms of action studied in laboratory and clinical contexts. Effects in healthy non-patient populations remain an active research question.
A synthetic heptapeptide derived from the ACTH 4-10 fragment, engineered for CNS stability. Studied for BDNF and NGF upregulation, neuroprotection against oxidative stress, and melanocortin receptor modulation. Pharmaceutical approval in Russia for stroke recovery and cognitive decline. One of the most evidence-backed peptide nootropics studied.
A synthetic heptapeptide derived from tuftsin, studied for GABAergic modulation, BDNF expression, and anxiolytic effects without benzodiazepine-class side effects. Developed by the Russian Academy of Sciences. Pharmaceutical status in Russia. Studied for generalized anxiety disorder in controlled trials — one of the few peptides with clinical trial data in anxiety research.
An angiotensin IV analog developed at Washington State University. Studied for synaptogenesis — specifically, promotion of new dendritic spine formation via the HGF/MET signaling pathway. Reported in preclinical studies to be 10 million times more potent than BDNF at inducing synaptogenesis. Brain-penetrant. Caution: research is exclusively preclinical; human data is absent.
A synthetic 11-amino-acid fragment of Ciliary Neurotrophic Factor (CNTF) studied for neurogenesis stimulation in the hippocampus, BDNF upregulation, and cognitive performance in rodent aging models. Proposed to increase neural progenitor cell activity in the dentate gyrus. Research is exclusively preclinical — no human data. One of the most potent neurogenic research peptides studied to date.
A synthetic small molecule (not a peptide) studied for hippocampal neurogenesis stimulation. Phase II trial in MDD (Major Depressive Disorder) showed increased hippocampal volume at 40mg/day over 12 weeks. Mechanism is incompletely understood — proposed to increase neurogenesis via an unidentified pathway distinct from BDNF. The Phase IIb failed primary endpoints but showed signal on secondary cognitive measures.
The Peptide Interaction Checker covers Semax, Selank, and Dihexa interactions with other compounds. The Selank + Semax stack is the most commonly studied cognitive peptide combination. Read the stack profile →
Peptides studied for tissue remodeling, collagen biology, wound healing, and dermal rejuvenation. Several of these — particularly GHK-Cu — have exceptionally deep research records that extend beyond cosmetics into whole-body gene expression modulation. TB-500 appears here as well due to its systemic role in tissue repair.
Studied for collagen synthesis stimulation, elastin and proteoglycan production, MMP regulation for skin remodeling, and anti-inflammatory gene expression. Dr. Loren Pickart's foundational research (1970s–2000s) established GHK-Cu as a master regulator of skin biology. At physiological concentrations it activates over 4,000 human genes — many controlling skin structure, wound healing, and inflammation.
A synthetic fragment of one of the most abundant intracellular proteins in mammals — thymosin beta-4. Studied for its central role in actin filament dynamics, cell migration, angiogenesis (new blood vessel formation), and tissue repair. Relevant to skin healing because it promotes dermal fibroblast migration and keratinocyte proliferation — key to wound closure and scar remodeling.
Topical application and subcutaneous use require different concentrations and carrier solutions. The Peptide Calculator handles unit math. Note: topical GHK-Cu is not reconstituted the same way as subcutaneous peptides — always research application-specific protocols.
Peptides with primary research focus on mitochondrial structure, function, and energy production. The mitochondria produce ~90% of cellular ATP — their integrity determines cellular energy capacity, and mitochondrial dysfunction is increasingly understood as a central mechanism of aging. This is among the most active research frontiers in longevity biology.
A Szeto-Schiller tetrapeptide that concentrates ~1,000-fold in the inner mitochondrial membrane, where it binds cardiolipin — the structural lipid essential to electron transport chain integrity. Studied for mitochondrial cristae protection, ATP production restoration, and reduction of reactive oxygen species. One of the most advanced mitochondria-targeted peptides in clinical development — multiple Phase II/III trials in heart failure, renal disease, and aging.
Encoded within the 12S ribosomal RNA gene of the mitochondrial genome — not the nuclear genome — making it unique among known peptides. Functions as a mitochondrial hormone-like signal that regulates nuclear gene expression in response to metabolic stress. Studied for AMPK activation, glucose metabolism, exercise-mimicking effects, and age-related metabolic decline reversal in preclinical models.
Peptide-conjugated forms of Coenzyme Q10 (ubiquinone/ubiquinol) under research investigation for improved mitochondrial membrane targeting and bioavailability. Standard CoQ10 has poor oral bioavailability (~10%). Peptide conjugation strategies aim to direct it to the inner mitochondrial membrane — the site of electron transport. Research is in early stages. Standalone CoQ10 (not conjugated) has extensive clinical evidence for mitochondrial disease and statin-induced myopathy.
These two compounds address different aspects of mitochondrial biology — SS-31 targets structural integrity (cardiolipin/cristae), while MOTS-c targets metabolic signaling (AMPK/energy sensing). Check interaction data in the Interaction Checker.
Discuss these compounds with fellow researchers. Protocol design, dosing observations, interaction questions, literature reviews. The Biohacker Hub is the community space for everything on this page — evidence-based discussion only.
Every compound in this library is profiled strictly for research and educational purposes. No compound on this site is intended for human or veterinary use, clinical or diagnostic applications, or therapeutic use of any kind.