Retatrutide
Stylized molecular signature · scaled by MW
~6 days in humans (≈144 h, range 108–168 h across phase 1b/2 trials). Long t½ driven by a C20 fatty-diacid albumin-binding linker — not PEGylation. Urva et al., Lancet 2022.
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How it’s studied.
A 39-amino-acid synthetic peptide that is a triple agonist of GLP-1, GIP, and glucagon receptors. In research literature, retatrutide is studied for concurrent incretin signaling, lipolysis through the glucagon arm, and hepatic glucose modulation. Published clinical trials report substantial body weight reductions of 24–30% over 48–68 weeks alongside improvements in liver fat and cardiovascular markers.
Retatrutide is a 39-amino-acid linear synthetic peptide developed as the first triple agonist of GLP-1, GIP, and glucagon receptors. The fatty-acid linker enables albumin binding and a ~6-day plasma half-life. It represents one of the most extensively studied next-generation incretin compounds in metabolic research.
- 01
Triple-agonist receptor binding research
- 02
Metabolic pharmacology studies
- 03
Body weight regulation research
- 04
Hepatic fat reduction studies
Reported in literature: 0.5–12 mg weekly titration (clinical research, not for human use)
Verify each value in primary literature.
Pre-filled defaults for Retatrutide.
- Concentration
- 2.50mg/mL
- Draw on U-100
- 480units
- Volume / dose
- 4.800mL
- Doses / vial
- 0
Assumes 27-gauge insulin syringe, U-100 markings. Verify before use.
Open in calculatorCo-factors and supporting compounds.
Sparse literatureCompounds identified in published research as sharing pathways with Retatrutide, or studied alongside it in trials. Reference material only — not a recommendation, not medical advice. Citations link to PubMed.
Dietary protein (and resistance training)
Whole-food proteinRapid pharmacologic weight loss reduces both fat mass and lean mass; protein intake is the primary nutritional input that supports muscle protein synthesis
Retatrutide-specific co-factor literature is essentially absent as of mid-2026 (phase 2 trials completed 2023-2024, phase 3 ongoing). The closest applicable evidence is the GLP-1/GIP/glucagon receptor agonist class signal: pharmacologic weight loss is accompanied by meaningful losses of lean body mass, reported at 15-40% of total weight lost in narrative reviews of GLP-1 RA outcomes. Protein intake and resistance training are the most commonly described mitigation strategies in this literature. Retatrutide produced 24% weight reduction at 48 weeks in the Jastreboff phase 2 trial, the largest magnitude in the class to date, so the lean-mass concern extrapolates directly. Studied alongside the drug class, not yet alongside retatrutide specifically.
Vitamin D3 (cholecalciferol)
CholecalciferolReduced caloric intake during incretin-induced satiety lowers dietary vitamin D; concurrent bone mineral density decline during weight loss compounds the deficiency signal
Vitamin D deficiency is the most commonly reported micronutrient abnormality in GLP-1 RA users in a 2026 narrative review (~7.5% at 6 months, ~13.6% at 12 months), and retatrutide as a triple incretin agonist shares the appetite-suppression and reduced caloric intake pathway driving that signal. Vitamin D deficiency is separately associated with reduced bone mineral density during rapid weight loss, which observational data has flagged for GLP-1 RAs without diabetes. Studied alongside the drug class through deficiency surveillance rather than head-to-head supplementation RCTs in retatrutide-treated populations.
Retatrutide-specific cofactor literature is genuinely sparse — the molecule completed phase 2 in 2023 and phase 3 (TRIUMPH-1, TRIUMPH-2) was still ongoing in mid-2026. All cofactor evidence here is extrapolated from the GLP-1 RA class (semaglutide, tirzepatide, liraglutide). Consider as provisional until retatrutide-specific micronutrient surveillance data appears.