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GLP-3 (RT) vs GLP-2 Tirz
Both compounds are incretin-based metabolic research compounds. GLP-2 Tirz targets dual incretin pathways. GLP-3(RT) adds a third receptor arm — a multi-receptor research compound with stronger metabolic-marker signals in published preclinical literature.
GLP-3 (RT)
GLP-3(RT) (LY3437943) is a synthetic unimolecular triple agonist that simultaneously activates glucagon-like peptide-1 receptors (GLP-1R), glucose-dependent insulinotropic polypeptide receptors (GIPR), and glucagon receptors (GcgR). GLP-1R agonism suppresses appetite via hypothalamic satiety signaling, slows gastric emptying, and potentiates glucose-stimulated insulin secretion. GIPR agonism augments incretin-mediated insulin release and may directly potentiate GLP-1 anorectic effects through central and peripheral synergy. The addition of glucagon receptor agonism distinguishes GLP-3(RT) from dual GLP-1/GIP agents: GcgR activation increases hepatic glucose output, elevates resting energy expenditure via brown adipose tissue thermogenesis, promotes hepatic lipid oxidation, and suppresses appetite through independent CNS circuits. Preclinical data in diet-induced obese rodents showed that the triple agonist combination produced substantially greater weight reduction than any dual-agonist pair, suggesting non-redundant mechanistic contributions. The compound is currently in Phase 3 (TRIUMPH program) following compelling Phase 2 results.
GLP-2 Tirz
Tirzepatide (LY3298176) is a synthetic dual agonist peptide that activates both the glucagon-like peptide-1 receptor (GLP-1R) and the glucose-dependent insulinotropic polypeptide receptor (GIPR). Structurally, it is a 39-amino acid peptide based on the native GIP sequence with modifications enabling GLP-1R activation, coupled to a C18 fatty diacid chain via a linker for albumin binding that extends plasma half-life to approximately 5 days, enabling once-weekly dosing. GLP-1R agonism reduces appetite through hypothalamic and brainstem satiety pathways, slows gastric emptying, and augments glucose-stimulated insulin release from pancreatic beta cells while suppressing glucagon. GIPR agonism complements this by further potentiating insulin secretion in a glucose-dependent manner and may modulate adipocyte lipid metabolism, reduce glucagon secretion, and enhance the anorectic effects of GLP-1R signaling through central GIPR circuits in the hypothalamus and area postrema. Tirzepatide received FDA approval for type 2 diabetes (Mounjaro, May 2022) and obesity (Zepbound, November 2023), representing the first approved dual GLP-1/GIP agonist.
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