Liraglutide
Acylated GLP-1 analog with 97% homology to native human GLP-1. The C16 fatty acid chain enables albumin binding, extending duration from the native peptide’s 2-minute half-life to 13 hours. Activates GLP-1 receptors in the pancreas (insulin secretion, glucagon suppression), hypothalamus (satiety), and gastrointestinal tract (delayed gastric emptying).
Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.
- fasting-glucose
- hba1c
- fasting-insulin
- homa-ir
- lipid-panel
- thyroid-panel
- alt
- ast
- creatinine
- medullary-thyroid-carcinoma
- men2-syndrome
- pancreatitis-history
- severe-gastroparesis
- PMID:25801582A Randomized, Controlled Trial of 3.0 mg of Liraglutide in Weight Management (SCALE Obesity) — N Engl J Med, 2015
- PMID:27295427Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes (LEADER) — N Engl J Med, 2016
- PMID:19221380Pharmacokinetics, pharmacodynamics, safety and tolerability of liraglutide — J Clin Pharmacol, 2009
Liraglutide is the first-generation proof of concept. Daily dosing at 3.0mg for obesity. ~8% body weight reduction in SCALE — meaningful in 2015, modest by 2024 standards. LEADER demonstrated cardiovascular benefit, which opened the door for semaglutide’s SELECT trial. The 13-hour half-life means daily injections, which means compliance friction, which means real-world results trail behind clinical data. Semaglutide displaced it for the same reason cypionate displaced propionate — pharmacokinetics that match human behavior. But liraglutide still has a role. It clears fast. If you develop pancreatitis or intolerable GI effects, you want the drug out of your system in 48 hours, not 5 weeks.
This is not medical advice
Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.
See Liraglutide in a protocol matched to you