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In short, those who sleep 7/8 hours suffer more fat loss than those who sleep less

Wat a load of shait study

Key potency comparisons (human receptor cAMP EC₅₀ in comparable cell-based assays; lower EC₅₀ = stronger/more potent activation) • Pemvidutide → GCGR EC₅₀ ≈ 42 pM (balanced 1:1 with GLP-1R ≈ 39 pM). This is near-native glucagon potency and the highest GCGR potency reported for any advanced clinical candidate. • Survodutide (BI 456906) → GCGR EC₅₀ ≈ 0.52 nM (520 pM); GLP-1R ≈ 0.33 nM (≈ 1.6:1 GLP-1R bias). • Retatrutide (LY3437943, triple GLP-1/GIP/glucagon) → GCGR EC₅₀ ≈ 5.79 nM (≈ 2.9-fold less potent than native glucagon); much weaker GCGR component. • Cotadutide (MEDI0382) → Typically reported as ≈5-fold GLP-1R bias; absolute GCGR potency is in the low-nM range in most assays (weaker than pemvidutide). • Mazdutide (IBI362) → GCGR Ki ≈ 17.7 nM (lower affinity than the others). Pemvidutide’s exceptionally high GCGR potency (balanced with strong GLP-1R activity) drives its pronounced effects on energy expenditure, lipolysis, and hepatic fat reduction while the GLP-1R component offsets potential hyperglycemia—making it the “strongest” pure glucagon activator in the class. No marketed GLP-1RA (semaglutide, tirzepatide, etc.) has meaningful GCGR activity. Other early-stage or discontinued dual/triple agonists (e.g., efinopegdutide, NN1706, DA-1726) generally show lower or more biased GCGR potency than pemvidutide in available data. Potency values can vary slightly by assay conditions, but the rank order is consistent across publications.

In a nutshell greatest Glucagon activation was from Pemvidutide Most fat loss and liver fat loss was also from Pemvidutide even more so than Retatrutide.