Mecanismo de acción

TIRZ simultaneously engages two incretin receptors that play complementary roles in metabolic regulation. GIP receptor activation on pancreatic beta cells potentiates glucose-dependent insulin secretion, while agonism at the second incretin receptor reduces glucagon secretion and slows gastric emptying. Receptor-pharmacology studies compare the signaling profile of dual engagement against single-receptor agonists at the level of cAMP accumulation and beta-arrestin recruitment in cell-based assays.

The GIP receptor component is also expressed on adipocytes, where cell-culture studies report effects on lipid handling and lipolytic signaling. The C20 fatty diacid modification enables non-covalent albumin binding, resulting in a half-life of approximately 5 days that supports once-weekly administration.

Aplicaciones de investigación

• → Engineered as a dual agonist engaging both the GIP receptor and a second incretin receptor, each a class B G-protein-coupled receptor
• → Two alpha-aminoisobutyric acid residues at positions 2 and 13 are studied as substitutions conferring resistance to proteolytic degradation
• → A C20 fatty diacid conjugated at Lys20 enables albumin binding, extending circulating half-life in published pharmacokinetic models
• → Investigated in receptor-pharmacology work for biased signaling at the incretin receptor relative to single-receptor agonists
• → Used as an analytical reference standard in LC-MS and HPLC characterization of multi-agonist peptides

Validación analítica

TIRZ is verified via LC-MS and HPLC analysis. Each lot is tested for identity, purity (≥99% target), and endotoxin levels. Full certificate of analysis is available upon request.