Liraglutide

Tirzepatide 10 and 15 mg achieved significantly greater percentage weight reduction than liraglutide (by 4.85% and 6.26%, respectively) and semaglutide (by 4.85% and 6.26%, respectively).; Tirzepatide 10 and 15 mg also significantly reduced waist circumference compared with liraglutide (by 11.79 cm and 12.30 cm) and semaglutide (by 4.81 cm and 5.32 cm).; All tirzepatide doses significantly improved triglycerides and diastolic blood pressure versus liraglutide, with generally comparable effects on other metabolic parameters.; Safety profiles were comparable among tirzepatide, liraglutide, and semaglutide.

Liraglutide significantly accelerates wound closure in diabetic mouse models (db/db and streptozotocin-induced).; Improved healing effects are abrogated in Dock5 keratinocyte-specific knockout mice.; Liraglutide directly binds to Myo1c at arginine 93, enhancing Myo1c/Dock5 interaction.; Liraglutide promotes keratinocyte proliferation, migration, and adhesion via the Myo1c/Dock5 pathway.

Liraglutide robustly activates GLP-1R-positive neurons in the lateral septum.; Chemogenetic activation of LSGLP-1R neurons dramatically suppresses feeding.; Knockdown of GLP-1 receptors in the LS, but not hypothalamus, attenuates liraglutide's anorectic and weight-lowering effects.; Synaptic inactivation of LSGLP-1R neurons diminishes liraglutide's anorexic effects.

Empagliflozin and liraglutide significantly improved diastolic function, cardiomyocyte hypertrophy, cardiac fibrosis, and exercise tolerance in HFpEF mice.; Combination therapy showed no synergistic benefit over monotherapy.; Both drugs restored Erbb4 expression in a specific myocyte subcluster, as identified by snRNA-seq, and the Erbb4 pathway was essential for their actions.; Beneficial effects diminished after 1 week of drug withdrawal, and in vitro experiments linked Erbb4 to palmitic acid- or high glucose-induced PKC/ERK1/2 phosphorylation changes.

Liraglutide significantly decreased AAD incidence and mortality in Ang II-infused APOE (-/-) mice.; Liraglutide inhibited M1 macrophage polarization through GLP-1R activation.; The protective mechanism involved suppression of CXCL3 expression via the PI3K/AKT signaling pathway.; M1 macrophage polarization and GLP-1R expression were increased in aortas of AAD patients and mouse models.

Liraglutide improved glucose metabolism and ameliorated liver tissue damage in T2DM-associated NAFLD mice.; Transcriptomic analysis revealed liraglutide regulates lipid metabolism via AMPK and ACC signaling.; Liraglutide suppressed ferroptosis, and a ferroptosis inhibitor rescued liver cell viability under high glucose conditions.; AMPK inhibitor compound C blocked liraglutide's suppression of ferroptosis, confirming the pathway's role.

What is Liraglutide?

**Mechanism of Action** Liraglutide is a once-daily acylated glucagon-like peptide-1 (GLP-1) receptor agonist with 97% sequence homology to endogenous GLP-1. Its fatty acid side chain enables non-covalent binding to albumin, extending the half-life to approximately 13 hours and allowing once-daily subcutaneous administ

How does Liraglutide work?

Once-daily acylated GLP-1 receptor agonist for type 2 diabetes and chronic weight management.

What is the research status of Liraglutide?

Liraglutide is currently classified as approved, with 5,582 research references on record. This is for research purposes only and is not medical advice.

What is the half-life of Liraglutide?

The reported half-life of Liraglutide is ~13 hours.

What is the molecular weight of Liraglutide?

Liraglutide has a molecular weight of approximately 3751 g/mol (formula C172H265N43O51).