Survodutide
Dual GLP-1 and glucagon receptor agonist. Unlike tirzepatide’s GIP/GLP-1 dual agonism, survodutide pairs GLP-1 with glucagon — prioritizing hepatic lipid mobilization and thermogenesis over incretin potentiation. Glucagon receptor activation in hepatocytes drives fatty acid oxidation and reduces hepatic steatosis directly. The GLP-1 component provides appetite suppression and glucose-dependent insulin secretion to offset glucagon-driven hyperglycemia.
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
- alt
- ast
- ggt
- triglycerides
- hs-crp
- creatinine
- egfr
- medullary-thyroid-carcinoma
- men2-syndrome
- pancreatitis-history
- severe-gastroparesis
- hepatic-impairment-severe
- PMID:37908901Survodutide for MASH — a randomised, double-blind, placebo-controlled, phase 2 trial — Lancet, 2024
- PMID:37078536Efficacy and safety of survodutide for overweight and obesity — Lancet Diabetes Endocrinol, 2024
Survodutide occupies a different niche than tirzepatide. Where tirzepatide maximizes incretin synergy through GIP, survodutide targets the liver directly through glucagon. The MASH data is the signal worth watching. Phase 2 showed significant reductions in liver fat content and fibrosis improvement — outcomes that matter beyond the scale. The obesity cohort showed ~19% body weight reduction at the highest dose. Competitive with semaglutide, trailing tirzepatide, but the hepatic angle gives it a distinct clinical identity. If phase 3 MASH data holds, this becomes a liver drug that also causes weight loss — a completely different regulatory and commercial positioning than the incretin-first compounds.
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 Survodutide in a protocol matched to you