Longevity Peptides in Australia: Research Guide 2026

Modern longevity research is organised around the Hallmarks of Ageing framework, first proposed by López-Otín et al. in 2013 and updated in 2023 to 12 hallmarks. Each hallmark represents a biological process that deteriorates with age and contributes to the aged phenotype:

• Genomic instability, accumulation of DNA damage
• Telomere attrition, shortening of chromosome-protective telomeres
• Epigenetic alterations, changes in gene expression patterns
• Loss of proteostasis, failure of protein quality control systems
• Deregulated nutrient sensing, dysregulation of mTOR, AMPK, sirtuins
• Mitochondrial dysfunction, decline in mitochondrial bioenergetics
• Cellular senescence, accumulation of pro-inflammatory senescent cells
• Stem cell exhaustion, depletion of regenerative capacity
• Altered intercellular communication, chronic inflammation, hormonal dysregulation
• Disabled macroautophagy, microbiome disturbance, chronic inflammation (2023 additions)

Research-grade longevity compounds are generally studied for their effects on one or more of these hallmarks. The peptides and small molecules discussed below each target different parts of this framework.

Epitalon (also Epithalan, sequence Ala-Glu-Asp-Gly) is a synthetic tetrapeptide derived from the pineal peptide Epithalamin, developed by Vladimir Khavinson and colleagues at the St. Petersburg Institute of Bioregulation and Gerontology over 40+ years of research.

Epitalon addresses the telomere attrition hallmark: its most cited mechanism is telomerase (TERT) activation. In vitro studies have shown Epitalon treatment of human fetal fibroblasts increased telomerase activity and extended replicative lifespan beyond the Hayflick limit. Animal studies have reported lifespan extension of 11–16% in drosophila and smaller effects in rodents.

Additional researched mechanisms include:

• Restoration of nocturnal melatonin secretion in aged animals (pineal-melatonin axis)
• Normalisation of circadian rhythms
• Antioxidant effects via melatonin-mediated pathways
• Reduced markers of oxidative stress in animal models

Epitalon occupies an unusual position: extensive literature from a single research group with limited independent replication. It is a subject of ongoing interest in longevity research communities for its telomerase-activation hypothesis.

OzPeps stocks research-grade Epitalon 10mg → · Full Epitalon research guide →

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA Type-c) is a 16-amino acid peptide encoded within the mitochondrial genome, one of the few biologically active peptides of mitochondrial origin. It was first characterised in 2015 by Lee et al. at USC.

MOTS-c addresses the mitochondrial dysfunction hallmark. Its primary mechanisms include:

• AMPK activation, stimulating cellular energy sensing and metabolic adaptation
• Folate and methionine cycle modulation, affecting one-carbon metabolism
• Mitochondrial stress response, nuclear translocation under stress conditions
• Anti-inflammatory signalling, inhibition of NF-κB pathway

Research in aged rodents has shown MOTS-c improves insulin sensitivity, exercise capacity, and metabolic parameters. A 2021 study showed MOTS-c levels decline with age in humans but increase with exercise, placing it in the context of exercise-mimetic research.

MOTS-c 10mg → · MOTS-c 40mg → · Full MOTS-c research guide →

SS-31 (also known as Elamipretide, MTP-131, or Bendavia) is a tetrapeptide developed by Hazel Szeto at Cornell. It is highly lipophilic and selectively concentrates in the inner mitochondrial membrane, where it binds cardiolipin, a phospholipid critical to the electron transport chain.

SS-31 addresses both mitochondrial dysfunction and genomic instability (via reduction of mitochondrial ROS). Its mechanisms include:

• Cardiolipin binding, stabilising cristae structure and electron transport chain supercomplexes
• Reduction of mitochondrial reactive oxygen species (ROS)
• Preservation of ATP production under stress conditions
• Protection against ischaemia-reperfusion injury in multiple organ models

SS-31 has advanced to human clinical trials for heart failure (CADUCEUS trial, PROGRESS-HF trial) and age-related mitochondrial dysfunction. It is one of the most clinically advanced mitochondria-targeted peptides.

SS-31 10mg → · SS-31 50mg →

GHK-Cu (copper(II) tripeptide Gly-His-Lys) is an endogenous tripeptide that chelates copper(II) ions. It was first isolated from human plasma and is present in urine, saliva, and tissue. Plasma GHK-Cu levels decline significantly with age, approximately 200 ng/mL at age 20 to 80 ng/mL at age 60.

GHK-Cu addresses multiple hallmarks including altered intercellular communication and epigenetic alterations. Research has documented:

• Gene expression modulation, activation of wound healing, anti-inflammatory, and antioxidant pathways
• Collagen, elastin, and glycosaminoglycan synthesis stimulation
• Neuroprotective effects via BDNF and nerve growth factor upregulation
• Anti-inflammatory activity (downregulation of TNF-α, TGF-β)
• Skin fibroblast and keratinocyte proliferation in vitro

GHK-Cu 50mg → · GHK-Cu 100mg →

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme essential to cellular metabolism and a required substrate for sirtuins (SIRT1–7) and PARP enzymes, two major longevity-associated enzyme families. NAD+ levels decline approximately 50% between age 40 and 60 in most tissues.

NAD+ supplementation research addresses the deregulated nutrient sensing hallmark (via sirtuin activation) and genomic instability (via PARP-mediated DNA repair). Key research findings:

• Sirtuin activation, sirtuins are NAD+-dependent deacylases that regulate gene expression, DNA repair, mitochondrial biogenesis, and inflammation
• PARP activation, NAD+ fuels PARP enzymes required for DNA strand break repair; PARP hyperactivation in aged cells depletes NAD+, creating a vicious cycle
• Muscle function, oral NAD+ precursors (NMN, NR) have shown improved muscle function and endurance in aged mice; human trials ongoing
• Neurological models, NAD+ supplementation shows neuroprotective effects in multiple neurodegeneration models

NAD+ 100mg → · NAD+ 500mg →

Given that ageing is multifactorial, longevity research increasingly investigates combinations of compounds targeting different hallmarks simultaneously. Common research combinations and their rationale:

• Epitalon + NAD+, telomere maintenance (Epitalon) + NAD+ metabolic restoration; complementary mechanisms across different hallmarks
• MOTS-c + SS-31, dual mitochondrial approach; MOTS-c for AMPK/metabolic signalling, SS-31 for cardiolipin/ETC protection
• GHK-Cu + BPC-157, tissue regeneration focus; GHK-Cu for extracellular matrix and gene expression, BPC-157 for angiogenesis and wound healing
• Epitalon + MOTS-c + NAD+, broad longevity stack addressing telomere, mitochondrial, and nutrient-sensing hallmarks

See also: Epitalon full research guide →

All longevity compounds listed in this guide are supplied by OzPeps strictly for in-vitro laboratory and scientific research use only, not for human or animal administration. Products are sourced from suppliers with verified supplier Certificate of Analysis (COA).

For a detailed overview of the Australian regulatory framework for research compounds: Are Research Peptides Legal in Australia? →