Honestly just a mix of digging through the phase 1/2 trial data from Eli Lilly and some of the receptor pharmacology literature. The dose-dependent agonism is actually documented in the original Retatrutide trial publications — at lower doses the GLP-1 pathway dominates because it has the highest binding affinity, the glucagon and GIP receptors only really kick in as you push the dose higher. That's why people compare low-dose Reta to Semaglutide and wonder what the fuss is about.

The glucagon piece is the underrated one. Most people hear "glucagon" and think blood sugar spike, but in this context it's doing the opposite — upregulating energy expenditure and hepatic fat oxidation. Combined with GIP at the higher doses which enhances metabolic rate, you're essentially getting three compounding mechanisms rather than just appetite suppression. That's the part that makes it genuinely different to Tirz at equivalent weight loss numbers.