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Research guide

What each peptide is and what has been studied

A summary of the published scientific literature on each compound in our catalogue: what it is, how it acts at molecular level and which research lines exist, with the references so you can check them yourself.

Scientific, descriptive information. It does not indicate doses, protocols or effects in people or animals and is not medical advice. All products are for research use only (RUO).
Coenzyme

NAD+

Mostly preclinical evidence

What it is

Nicotinamide adenine dinucleotide: a coenzyme present in every cell that carries electrons in redox reactions (NAD+/NADH).

Studied mechanism

Takes part in energy production (glycolysis, Krebs cycle, respiratory chain) and is a substrate for enzymes such as sirtuins, PARPs (DNA repair) and CD38.

Research lines

  • Energy metabolism and mitochondrial function.
  • DNA repair and cellular stress response.
  • Age-related decline of NAD+ levels in several tissues, and the role of its precursors (NR, NMN) in ageing models.

State of the evidence

Widely studied endogenous molecule. Much of the intervention data comes from cell and animal models.

Key references

  • Covarrubias AJ et al. NAD+ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol. 2021. PubMed ↗
Mitochondrial peptide

MOTS-c

Mostly preclinical evidence

What it is

16-amino-acid peptide encoded in mitochondrial DNA (12S rRNA gene). It belongs to the so-called mitochondrial-derived peptides.

Studied mechanism

In cell and mouse models it acts on the folate-methionine cycle and activates AMPK; under metabolic stress it moves to the nucleus and modulates gene expression.

Research lines

  • Glucose homeostasis and insulin sensitivity in high-fat-diet mice.
  • Mitochondria-to-nucleus communication.
  • Response to exercise and ageing in animal models.

State of the evidence

Young field (described in 2015). Evidence comes mainly from rodents and cells.

Key references

  • Lee C et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015. PubMed ↗
  • Kim KH et al. The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress. Cell Metab. 2018. PubMed ↗
Small molecule (NNMT inhibitor)

5-Amino-1MQ

Mostly preclinical evidence

What it is

Quinolinium derivative that inhibits the enzyme nicotinamide N-methyltransferase (NNMT). It is not a peptide: it is a small, membrane-permeable molecule.

Studied mechanism

NNMT methylates nicotinamide using SAM as the donor. Inhibiting it changes nicotinamide/NAD+ availability and the cell’s methylation potential.

Research lines

  • Adipocyte metabolism and fat accumulation in cells and in high-fat-diet mice.
  • NNMT as a target in metabolic and oncology research.

State of the evidence

Published data limited to cell and mouse models. No known clinical trials.

Key references

  • Neelakantan H et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2017. PubMed ↗
Synthetic tetrapeptide

Epithalon

Mostly preclinical evidence

What it is

Ala-Glu-Asp-Gly tetrapeptide developed from epithalamin, a pineal gland extract, by the research group of Vladimir Khavinson.

Studied mechanism

In human cell cultures, induction of telomerase activity and telomere elongation has been described.

Research lines

  • Telomerase and telomere length in cell cultures.
  • Neuroendocrine regulation and circadian rhythms in animal models.

State of the evidence

Most studies come from a single research group and there is little independent replication.

Key references

  • Khavinson VKh et al. Effect of epithalon on telomerase activity and telomere length in human somatic cells. Bull Exp Biol Med. 2003. PubMed ↗
Mitochondria-targeted tetrapeptide

SS-31

Some early clinical trials

What it is

Tetrapeptide (D-Arg-Dmt-Lys-Phe-NH2), also known as elamipretide or MTP-131, that concentrates in the inner mitochondrial membrane.

Studied mechanism

Binds cardiolipin, a phospholipid of the inner mitochondrial membrane, and in preclinical models helps preserve cristae structure and respiratory chain efficiency.

Research lines

  • Oxidative stress and ischaemia-reperfusion injury in animal models.
  • Mitochondrial function in heart, muscle and kidney in ageing models.
  • Clinical trials in mitochondrial diseases with mixed results.

State of the evidence

It has been evaluated in clinical trials by a pharmaceutical developer. The material on this site is for research use only.

Key references

  • Szeto HH. First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. Br J Pharmacol. 2014. PubMed ↗
GHRH analogue

CJC-1295 (no DAC)

Some early clinical trials

What it is

Synthetic 29-amino-acid analogue of growth hormone-releasing hormone (GHRH). The “no DAC” version (also called Mod GRF 1-29) lacks the albumin-binding affinity complex.

Studied mechanism

Acts on the pituitary GHRH receptor. Without DAC it has a short half-life of tens of minutes; the DAC variant, studied in humans, has a half-life of days.

Research lines

  • Pituitary signalling and the GH/IGF-1 axis in animal models.
  • Pharmacokinetics of short- and long-acting GHRH analogues.

State of the evidence

Not an approved medicine. Human studies mostly concern the DAC variant.

Key references

  • Teichman SL et al. Prolonged stimulation of growth hormone and IGF-I secretion by CJC-1295, a long-acting analog of GHRH, in healthy adults. J Clin Endocrinol Metab. 2006. PubMed ↗
GH secretagogue (ghrelin agonist)

Ipamorelin

Some early clinical trials

What it is

Synthetic pentapeptide that acts as an agonist of the growth hormone secretagogue receptor (GHS-R1a, the ghrelin receptor).

Studied mechanism

Stimulates growth hormone release from the pituitary. Early studies described it as more selective than other secretagogues, with little effect on ACTH and cortisol.

Research lines

  • GHS-R1a receptor selectivity compared with other secretagogues.
  • Gastrointestinal motility and post-operative ileus in animal models.

State of the evidence

Not an approved medicine. The most cited studies are preclinical and early phase.

Key references

  • Raun K et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998. PubMed ↗
Copper tripeptide

GHK-Cu

Some early clinical trials

What it is

Complex of the tripeptide glycyl-L-histidyl-L-lysine with copper(II). It was originally identified in human plasma and its concentration declines with age.

Studied mechanism

Acts as a copper carrier and modulates the expression of genes related to extracellular matrix remodelling, collagen and the antioxidant response.

Research lines

  • Wound healing and collagen and glycosaminoglycan synthesis in vitro and in animals.
  • Large-scale gene expression analysis (Connectivity Map).
  • Extracellular matrix and hair follicle in in-vitro cell models.

State of the evidence

Endogenous molecule described in human plasma. Data on its action in animal models are mostly preclinical.

Key references

  • Pickart L, Margolina A. Regenerative and protective actions of the GHK-Cu peptide in the light of the new gene data. Int J Mol Sci. 2018. PubMed ↗
GIP / GLP-1 / glucagon triple agonist

Retatrutide

Advanced clinical development

What it is

Modified peptide in development (code LY3437943) that activates the GIP, GLP-1 and glucagon receptors at the same time.

Studied mechanism

The combined action on the three incretin-glucagon receptors is studied for its effects on energy expenditure and glucose and lipid metabolism.

Research lines

  • Affinity and activity at the three receptors in binding assays.
  • Phase 2 and phase 3 clinical trials sponsored by the developer.

State of the evidence

Investigational drug, not approved. The material on this site is for in-vitro studies only and is not equivalent to any medicine.

Key references

  • Jastreboff AM et al. Triple-hormone-receptor agonist retatrutide for obesity — a phase 2 trial. N Engl J Med. 2023. PubMed ↗
Pentadecapeptide (KLOW component)

BPC-157

Mostly preclinical evidence

What it is

Synthetic 15-amino-acid fragment derived from a protective protein of gastric juice (Body Protection Compound).

Studied mechanism

In rodents, actions on angiogenesis, nitric oxide signalling and growth factors involved in tissue repair have been described.

Research lines

  • Tendon, muscle and gastrointestinal mucosa repair in rodent models.

State of the evidence

Most studies come from a single group and human data are very scarce. It is on the World Anti-Doping Agency prohibited list.

Key references

  • Sikiric P et al. Brain-gut axis and pentadecapeptide BPC 157: theoretical and practical implications. Curr Neuropharmacol. 2016. PubMed ↗
Thymosin β4 fragment (KLOW component)

TB-500

Mostly preclinical evidence

What it is

Synthetic fragment of thymosin β4, a 43-amino-acid protein that sequesters monomeric actin. The fragment corresponds to the actin-binding region.

Studied mechanism

Thymosin β4 is involved in cell migration, angiogenesis and tissue repair through actin cytoskeleton dynamics.

Research lines

  • Corneal and skin wound healing in animal models.
  • Cardiac repair after ischaemia in rodents.

State of the evidence

Clinical trials were done with full-length thymosin β4, not with this fragment. It is on the World Anti-Doping Agency prohibited list.

Key references

  • Goldstein AL et al. Thymosin β4: a multi-functional regenerative peptide. Basic properties and clinical applications. Expert Opin Biol Ther. 2012. PubMed ↗
Tripeptide (KLOW component)

KPV

Mostly preclinical evidence

What it is

Lys-Pro-Val tripeptide, the C-terminal fragment of the hormone α-MSH.

Studied mechanism

In intestinal epithelial cells it enters through the PepT1 transporter and reduces inflammatory signalling (NF-κB and MAPK).

Research lines

  • Intestinal inflammation in mouse colitis models.

State of the evidence

Published data limited to cell cultures and mice.

Key references

  • Dalmasso G et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008. PubMed ↗

References are peer-reviewed articles; links search the title in PubMed. That a compound has been studied does not mean it is safe or effective outside that research context, and most of the data in this list are preclinical.

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