Explore our research guides for every peptide in the Vytol catalogue. Mechanisms, published data and handling protocols all in one place.
Retatrutide (LY3437943) is a synthetic triple hormone receptor agonist developed by Eli Lilly, engineered to simultaneously activate GIP, GLP-1 and glucagon receptors within a single peptide molecule. Unlike semaglutide which targets GLP-1 only, and tirzepatide which targets GLP-1 and GIP, retatrutide adds glucagon receptor agonism as a third pathway — a mechanism published research suggests significantly augments metabolic activity beyond dual agonism alone. GLP-1 and GIP agonism drives increased insulin secretion and satiety signalling, while glucagon receptor agonism increases energy expenditure and lipolysis in published preclinical and clinical research models.
Tirzepatide (LY3298176) is a synthetic dual hormone receptor agonist developed by Eli Lilly, engineered to simultaneously activate GIP and GLP-1 receptors within a single peptide molecule. Unlike semaglutide which targets GLP-1 receptors only, tirzepatide adds GIP receptor agonism as a second pathway — a mechanism published research suggests enhances metabolic activity beyond single receptor agonism alone. GLP-1 agonism drives increased insulin secretion, reduced appetite and delayed gastric emptying, while GIP receptor agonism further enhances insulin secretion and improves insulin sensitivity in published clinical research models.
GHK-Cu (copper peptide glycyl-L-histidyl-L-lysine) is a naturally occurring tripeptide-copper complex first isolated from human plasma in 1973 by Loren Pickart. Studied extensively in published laboratory settings, GHK-Cu has demonstrated a remarkable capacity to interact with a broad range of biological pathways — most notably collagen synthesis, dermal fibroblast activity, angiogenesis signalling and cellular regeneration models. Published fibroblast research models have demonstrated up to a 70% increase in collagen synthesis when treated with GHK-Cu, and bioinformatics analyses have identified over 4,000 human genes modulated by the compound — a significant subset linked to tissue repair and skin regeneration signalling pathways.
BPC-157 (Body Protection Compound-157) is a synthetic pentadecapeptide comprising 15 amino acids, derived from a protein sequence found in human gastric juice. First studied by Professor Predrag Sikiric and his team at the University of Zagreb in the 1990s, BPC-157 has since accumulated an extensive body of published laboratory research exploring its interactions with a broad range of biological pathways. In published in-vitro and animal model research settings, BPC-157 has been studied for its role in angiogenesis signalling, growth factor receptor interactions, nitric oxide pathway modulation and cellular migration models — making it one of the most widely studied gastroprotective peptides in published laboratory research history.
Melanotan 2 (MT-2) is a synthetic cyclic heptapeptide analogue of alpha-melanocyte stimulating hormone (alpha-MSH), first developed at the University of Arizona in the late 1980s by researchers seeking to study melanocortin receptor activation pathways. Engineered for greater potency and metabolic stability than naturally occurring alpha-MSH, Melanotan 2 has been classified in published research as a superpotent cyclic melanotropic peptide due to its high-affinity binding at melanocortin receptor subtypes MC1R through MC4R. Published laboratory research has explored its interactions with pigmentation signalling pathways, melanocyte stimulation models and photoprotection research applications across multiple in-vitro and animal model settings.
Nicotinamide adenine dinucleotide (NAD+) is a coenzyme for redox reactions, making it central to energy metabolism, and an essential cofactor for non-redox NAD+-dependent enzymes including sirtuins, CD38 and poly(ADP-ribose) polymerases. NAD+ can directly and indirectly influence many key cellular functions, including metabolic pathways, DNA repair, chromatin remodelling, cellular senescence and immune cell function. NAD+ concentrations in humans may be 10–80% lower with advancing age — a decline published research has linked causally to numerous ageing-associated conditions including cognitive decline, metabolic disease and sarcopenia.
