Semaglutide.
Reconstituted: 2-8°C
Mechanism. Long-acting GLP-1 receptor agonist. Mimics endogenous glucagon-like peptide-1 to enhance glucose-dependent insulin secretion, suppress glucagon, slow gastric emptying, and reduce appetite via hypothalamic POMC pathway activation.
Trial data
- STEP-1 (NEJM 2021) — 68-week RCT, n=1,961 adults with overweight/obesity. Mean weight loss 14.9% with semaglutide 2.4mg weekly vs 2.4% placebo.
- STEP-3 (JAMA 2021) — semaglutide + intensive behavioral therapy = 16.0% weight reduction.
- SUSTAIN-6 — significant cardiovascular risk reduction in T2D patients.
- SELECT (2023) — 20% reduction in MACE in adults with established CV disease.
Tirzepatide.
Reconstituted: 2-8°C
Mechanism. Single-molecule dual agonist activating both GIP (glucose-dependent insulinotropic polypeptide) and GLP-1 receptors. Additive incretin signaling produces greater insulinotropic response and weight reduction than GLP-1 agonism alone.
Trial data
- SURMOUNT-1 (NEJM 2022) — 72-week RCT, n=2,539 adults without diabetes. Mean weight loss 20.9% at 15mg vs 3.1% placebo.
- SURMOUNT-2 — 15.7% weight reduction in T2D patients (vs 3.3% placebo).
- SURPASS series — superior glycaemic control vs semaglutide head-to-head.
Retatrutide.
Mechanism. Adds glucagon receptor agonism to dual incretin signaling. Glucagon co-agonism increases hepatic and adipose energy expenditure, complementing appetite suppression for amplified weight loss.
Trial data
- Phase 2 (NEJM 2023) — 48-week RCT in 338 adults. Mean weight loss 24.2% at 12mg.
- Highest weight reduction of any incretin-class agent to date.
- Phase 3 TRIUMPH trials ongoing.
Cagrilintide.
Mechanism. Selective amylin receptor agonist. Amylin is co-secreted with insulin and modulates satiety, gastric emptying, and glucagon. Combined with GLP-1 agonism (CagriSema), produces additive weight-loss effects in clinical trials.
BPC-157.
Mechanism. Stable gastric pentadecapeptide that has demonstrated cytoprotective, angiogenic, and reparative effects in preclinical models. Modulates nitric oxide signaling, VEGF expression, and growth-factor pathways. Mostly studied in animal models for tendon/ligament repair, gut mucosal healing, and post-surgical recovery.
Note: No human RCTs have been published as of 2026. All available data is preclinical.
TB-500.
Mechanism. Synthetic version of the active site region of Thymosin Beta-4, a naturally occurring 43-amino-acid peptide. Binds G-actin to regulate actin polymerization. Preclinical research suggests roles in wound healing, vascular endothelial cell proliferation, and tissue regeneration.
GHK-Cu.
Mechanism. Naturally occurring tripeptide with high affinity for copper(II). Modulates collagen synthesis, glycosaminoglycan production, ECM remodeling, and anti-oxidant pathways. Extensively studied in dermatology research for skin regeneration.
HGH (somatropin).
Mechanism. Recombinant 191-amino-acid polypeptide identical to endogenous human growth hormone. Binds GH receptor on hepatocytes and peripheral tissues to stimulate IGF-1 production, lipolysis, and protein anabolism. Established therapeutic use in growth hormone deficiency.