GLP3
GLP-1 / GIP / glucagon, triple agonistA managed weight program, structured check-ins, nutrition guidance, and dose titration set with your consultant, not a dropdown.
Mean body-weight change at 48 weeks on the highest dose, the largest reported in the class. <em>N Engl J Med</em>, 2023. Full reference →
Who this is for
Adults with obesity, significant overweight with complications, or fatty liver disease, where a genuine metabolic indication exists. Candidacy is decided with your consultant against your history and labs, never by a checkout flow.
How the program works
Your consultant goes through your goals, history, and whether this therapy is appropriate. If it isn't, you'll hear that instead.
An at-home blood draw establishes your baseline. Your pen ships cold-chain once your program is agreed.
Dose steps up every four weeks as tolerated, with a video review at each step and messaging in between.
Repeat labs against your baseline. Together you decide: continue, adjust, or taper off with a plan.
Common questions
In the phase 2 trial, weight loss was progressive across 48 weeks and had not plateaued at study end. Your consultant tracks your response at every review, and expectations are set against your baseline, not someone else's before-and-after.
Your program is quoted in full after your consultation, before anything is supplied. There is no set program price because there is no off-the-shelf product: dose, duration and monitoring differ per patient.
Receptor count. Semaglutide is a GLP-1 receptor agonist. Tirzepatide adds GIP, making it a dual agonist. GLP3 adds glucagon on top of both, making it a triple agonist. The published Phase 2 data for each is not directly comparable across trials with different designs.
No. It is investigational. Phase 2 trial data has been published in obesity and type 2 diabetes, but it has not completed the approval process, and nothing on this page should be read as a recommendation to use it.
Not through us. The assessment is the point: an investigational triple agonist is not something to start on the strength of a web page.
Three receptors, one peptide
The most extensively characterised pathway in the incretin class. GLP-1 receptor engagement drives glucose-dependent insulin secretion, modulates gastric emptying, and acts on central appetite signalling. Forms the mechanistic backbone of every approved and investigational incretin compound.
Glucose-dependent insulinotropic polypeptide receptor activation. Preclinical research indicates GIP agonism contributes to lipid metabolism in adipose tissue and insulin sensitivity at effects not consistently observed with GLP-1 alone. Tirzepatide established the dual GLP-1/GIP architecture commercially; GLP3 retains it.
The mechanistic distinction that sets GLP3 apart in its class. Glucagon receptor activation increases hepatic glucose output in isolation, but combined with GLP-1 and GIP co-agonism the insulinotropic effects offset the glycemic impact while hepatic fat metabolism and thermogenic energy expenditure effects are preserved.
In vitro pharmacology characterised by Coskun and colleagues (Cell Metab, 2022;34(9):1234-1247) reports that LY3437943 shows balanced glucagon and GLP-1 receptor activity with relatively greater GIP receptor activity, providing the ratio that underpins the compound’s downstream metabolic profile in published trials.
GLP3 is also searched as LY3437943, Reta, Triple agonist.
- Coskun T, et al. LY3437943, a novel triple GIP/GLP-1/glucagon receptor agonist. Cell Metab. 2022;34(9):1234-1247.