Research Library
What the science actually says.
This page summarises the current research context for each compound in our catalogue. We distinguish between preclinical findings, clinical trial data, and approved pharmaceutical use — because conflating them is how misinformation spreads.
All compounds are sold for laboratory research purposes only. Nothing on this page constitutes medical advice. Research summaries are provided for informational context and do not imply any claim about human health outcomes.
Mechanism of action
Retatrutide binds and activates three receptors: GLP-1 (reduces appetite and slows gastric emptying), GIP (potentiates insulin release and fat metabolism), and glucagon (increases energy expenditure and hepatic glucose output). The combined effect produces greater metabolic impact than single or dual agonism alone.
Research context
TRIUMPH-1 and TRIUMPH-2 phase 2 trials (2023) enrolled participants with obesity across 12-week and 48-week periods. At the 48-week mark, participants receiving the highest dose demonstrated a mean weight reduction of 24.2% — a figure not previously achieved by any pharmacological intervention in clinical trials. Retatrutide continues to progress through phase 3 trials.
Mechanism of action
Tirzepatide activates both GLP-1 and GIP receptors. GLP-1 agonism reduces appetite and slows gastric emptying; GIP agonism amplifies insulin secretion and acts on adipose tissue directly. The combination produces greater weight loss than GLP-1 agonism alone, which was the mechanism behind the previous generation of compounds.
Research context
The SURMOUNT-1 trial (NEJM, 2022) demonstrated mean weight loss of 20.9% at the highest dose over 72 weeks. Subsequent trials confirmed effects across populations with and without type 2 diabetes. Tirzepatide was FDA-approved as Mounjaro in 2022 and Zepbound in 2023.
Mechanism of action
BPC-157 is a synthetic pentadecapeptide derived from a protein found in gastric juice. It promotes angiogenesis, upregulates growth hormone receptors, and exerts cytoprotective effects on gut and tendon tissue. TB-500 (a fragment of Thymosin Beta 4) promotes actin regulation, cell migration into damaged tissue, and reduces inflammation. Together they address tissue repair through complementary pathways.
Research context
BPC-157 has been studied across rat models showing accelerated healing of tendon, ligament, muscle, and intestinal tissue. TB-500 research includes models of cardiac injury, neurological damage, and systemic inflammation. Neither has entered human clinical trials, and all evidence is preclinical.
Mechanism of action
GHK-Cu acts as a copper carrier, facilitating cellular uptake of copper ions required for enzymatic reactions including lysyl oxidase (collagen and elastin crosslinking) and superoxide dismutase (antioxidant). In vitro studies show upregulation of collagen, glycosaminoglycans, and decorin. It also appears to downregulate inflammatory cytokines and TGF-β1.
Research context
GHK-Cu has an unusually broad research base spanning 50+ years. Studies have examined effects on skin fibroblasts, wound healing models, hair follicle growth, and gene expression. Pickart et al. demonstrated stimulation of collagen synthesis in dermal fibroblasts. More recent work has examined its genomic effects, with GHK-Cu appearing to modulate 31% of pathways involved in human ageing according to microarray studies.
Mechanism of action
Semax increases BDNF (brain-derived neurotrophic factor) and NGF (nerve growth factor) expression. It appears to enhance dopaminergic and serotonergic activity in the prefrontal cortex, and to exhibit neuroprotective effects following ischaemic injury. Unlike ACTH itself, Semax has minimal adrenal effects, as the melanocortin-stimulating region has been modified.
Research context
Russian clinical literature describes use in ischaemic stroke recovery, optic nerve disease, and attention deficit conditions. Western preclinical work has focused on its effects on BDNF upregulation, memory consolidation in animal models, and neuroprotection following hypoxia. Limited English-language human trials exist — most clinical data originates from Russian-language publications.