Liraglutide
approvedAlso known as: Victoza, Saxenda, NN2211
**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 administration. It activates GLP-1 receptors in pancreatic beta cells, enhancing glucose-dependent insulin secretion, suppressing glucagon release, and slowing gastric emptying. Central GLP-1 receptor activation in the hypothalamus reduces appetite and food intake, contributing to weight loss. **Key Research Findings** The LEAD (Liraglutide Effect and Action in Diabetes) clinical trial program demonstrated significant reductions in HbA1c (0.8–1.5%) and fasting plasma glucose in type 2 diabetes patients, with weight loss of 2–3 kg versus placebo. The SCALE (Satiety and Clinical Adiposity—Liraglutide Evidence) trials in obesity showed mean weight loss of 8.4% of baseline body weight over 56 weeks with 3.0 mg liraglutide, compared to 2.8% with placebo. Cardiovascular outcome trials (LEADER) reported a 13% reduction in major adverse cardiovascular events (MACE) in high-risk patients. Common adverse effects include nausea, vomiting, and diarrhea, with rare risks of pancreatitis and gallbladder disease. **Clinical Relevance** Liraglutide is FDA-approved for type 2 diabetes (Victoza, 1.2–1.8 mg/day) and chronic weight management (Saxenda, 3.0 mg/day) in adults with BMI ≥30 kg/m² or ≥27 kg/m² with weight-related comorbidities. It is contraindicated in patients with medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2. As a first-line GLP-1 receptor agonist, it offers dual glycemic and weight benefits, with cardiovascular protection in high-risk populations. For research purposes only — not medical advice.
Key data
C172H265N43O51Research & studies
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 improved myocardial function and reduced myocardial apoptosis, hypertrophy, and interstitial fibrosis in DCM rats (P < 0.05).; In neonatal rat cardiomyocytes, liraglutide alleviated mitochondrial morphological and functional damage, oxidative stress, mitophagic defects, and cell apoptosis (P < 0.05).; Liraglutide's protective effects were mediated by enhanced mitophagy via the AMPK-Parkin signaling pathway, as evidenced by reversal with compound C treatment.
Liraglutide attenuated DOX-induced cardiac dysfunction and cardiomyocyte ferroptosis in vivo and in vitro.; Liraglutide restored DOX-impaired STAT3 phosphorylation and nuclear translocation, enhancing GPX4 transcription; STAT3 knockdown abolished protection.; Liraglutide upregulated DHHC7, rescuing DOX-suppressed STAT3 palmitoylation; DHHC7 knockdown and palmitoylation inhibition abrogated its effects.; Cardiomyocyte-specific DHHC7 overexpression replicated liraglutide's cardioprotection against DOX-induced ferroptosis and dysfunction.
Liraglutide reduced endometrial inflammation, collagen fibrosis, and EMT in IUA rats and human organoid IUA models.; NF-κB phosphorylation was up-regulated in the IUA model group and reversed by liraglutide treatment.; SuperPred analysis predicted NF-κB as a direct target of liraglutide, confirmed by cellular thermal shift assay.; Interfering with liraglutide's targeting of NF-κB in human endometrial organoids attenuated its effects on inflammation, fibrosis, and EMT.
Liraglutide exhibited high affinity and direct binding ability to TTR.; In ATTRv mice, liraglutide significantly decreased TTR protein content in brain compared with placebo.; Cardiovascular prognosis measures (plasma BNP, cardiac Cola1 and TGF-β1 expression, and cardiac pathological changes) were statistically comparable between liraglutide and placebo.; Liraglutide did not improve cardiovascular outcomes in ATTRv mice compared to placebo.
Liraglutide relieved RIRI and ferroptosis in vivo and inhibited renal I/R-induced METs both in vivo and in vitro.; F4/80 and citrullinated histone H3 (citH3) were highly co-localized after RIRI, and liraglutide attenuated this co-localization.; Liraglutide enhanced M2 markers and suppressed M1 markers, decreased STAT1 phosphorylation, and increased STAT3 and STAT6 phosphorylation.; STAT3/6 inhibition reversed liraglutide-inhibited M1 polarization, extracellular traps, and ferroptosis.
Frequently asked questions
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 5,695 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).
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