Survodutide 10mg

▎Survodutide Structure

▎Survodutide Research

Molecular Background

Survodutide (BI 456906) is a synthetic 29-amino-acid acylated peptide investigated as a dual glucagon receptor (GCGR) and glucagon-like peptide-1 receptor (GLP-1R) agonist. PubChem lists Survodutide under CID 168429725, with the molecular formula C192H289N47O61 and a molecular weight of approximately 4232 g/mol.[7]

Research Progress

Elita Yuliantie and colleagues used cAMP assays to compare Survodutide with the endogenous peptides GLP-1, glucagon (GCG), and oxyntomodulin (Oxy), and determined cryo-electron microscopy structures of Survodutide bound to GCGR and GLP-1R complexes. The authors described Survodutide as a 29-amino-acid peptide derived from glucagon, with selected substitutions from GLP-1 and exendin-4, additional sequence modifications, and the non-natural amino acid Ac4c at position 2. In the reported cAMP assays, Survodutide showed lower potency than native GLP-1 at GLP-1R and lower potency than native glucagon at GCGR, while its activity was within the range reported for the dual agonist oxyntomodulin. The structural analysis showed a peptide-binding orientation similar to other peptide agonists and identified contacts associated with the modified residues. The study also examined a non-acylated analogue and reported higher in vitro potency after removal of the linker and fatty-diacid modification. These findings were presented as a conference abstract and should be interpreted within that evidence level.[2]

Leo Thomas and colleagues evaluated a series of dual GCGR/GLP-1R agonists using CHO-K1 cells expressing human GCGR or GLP-1R, MIN6 cells, primary rat hepatocytes, and several mouse models. Acute in vivo target engagement was assessed using oral glucose-tolerance measurements for GLP-1R-related activity and plasma FGF21 together with hepatic NNMT mRNA expression for GCGR-related activity. From 19 dual agonists, Survodutide, BI 456908, and BI 456897 were selected for further profiling. In diet-induced obese mice, the authors reported changes in body weight and body-fat measurements after repeated exposure, while studies in db/db mice reported changes in glycated hemoglobin for Survodutide and BI 456908. The investigators also reported correlations between in vitro receptor potency and the selected in vivo biomarkers. These findings were generated in preclinical cell and mouse systems and remain specific to the experimental doses and models used in the publication.[3]

Fig1. Body-weight, body-fat, liver, plasma, and oral-glucose-tolerance measurements reported for Survodutide, BI 456908, and BI 456897 in diet-induced obese mice.[3]
The source figure shows repeated-dose body-weight measurements together with body-fat mass, liver triglycerides, plasma ALT, FGF21, hepatic NNMT mRNA expression, and oral glucose-tolerance data. Group definitions, doses, statistical methods, and complete experimental procedures are reported in the original publication.[3]

F. Briand and colleagues used a free-choice diet-induced obese and dyslipidemic hamster model to compare Survodutide, semaglutide, and vehicle over 5 weeks. The authors measured body weight, intake of standard chow, high-fat/high-cholesterol chow, plain water and fructose-enriched water, as well as plasma insulin, HOMA-IR, triglycerides, and cholesterol fractions. They reported different food- and fluid-intake patterns between the two peptide study groups and differences in plasma lipid measurements, including lower total cholesterol and LDL-cholesterol in the Survodutide group compared with vehicle. This work was published as a conference abstract and describes outcomes in a hamster model rather than clinical observations.[4]

Jasmine Swagel and colleagues examined Survodutide in male NZO/HILtJ mice maintained at thermoneutral temperature (30°C), a condition intended to reduce the cold-stress-related energy expenditure seen in mice housed near 22°C. After 2 weeks of Survodutide or vehicle exposure, the authors reported differences in body weight, food intake, fat mass, lean mass, and blood glucose. Indirect calorimetry showed that energy expenditure was lower, rather than higher, in the Survodutide group under the thermoneutral conditions used. This study was reported as a conference abstract and highlights the influence of housing temperature on interpretation of metabolic findings in mouse models.[5]
Alexander Hamilton and colleagues studied Survodutide in female obese and diabetic db/db C57BKS mice with uninephrectomy and ReninAAV-mediated hypertension. After 10 weeks of Survodutide or vehicle exposure, the authors evaluated blood and urine biochemistry, histological markers of glomerulosclerosis, tubular injury and inflammation, and quantitative three-dimensional imaging of the pancreas and kidneys. They reported differences in body weight, glycemic measurements, pancreatic islet-volume distribution, albuminuria, renal hypertrophy, glomerular morphology, inflammatory markers, liver weight, and circulating amino acids. Reduced plasma alanine was interpreted as evidence of hepatic glucagon-receptor engagement. These findings were obtained in an advanced diabetic-kidney-disease mouse model.[6]

The source figure includes urinary albumin-creatinine ratio, urine albumin and creatinine, plasma renin, cystatin C, urea, 3-hydroxybutyrate, albumin, beta-2 microglobulin, NGAL, KIM-1, clusterin, osteopontin, and MCP-1 measurements. Group sizes, statistical methods, and complete experimental conditions are reported in the original publication.[6]

Research Limitations

The studies summarized above use substantially different preclinical systems, including receptor assays, diet-induced obese mice, db/db mice, thermoneutral NZO/HILtJ mice, obese hamsters, and a hypertension-accelerated diabetic-kidney-disease model. Results from these systems are not directly interchangeable, and species, ambient temperature, diet, disease model, exposure schedule, receptor balance, and selected endpoints can materially affect the observations reported. The thermoneutral mouse study is particularly relevant because Survodutide was associated with lower energy expenditure at 30°C, indicating that metabolic responses should not be reduced to a single assumption that GCGR activation necessarily increases energy expenditure in every experimental setting.[3-6]

Several of the cited sources are conference abstracts rather than full-length peer-reviewed reports, including the structural study, hamster study, and thermoneutral mouse study.[2,4,5] Their available methodological and replication detail is therefore more limited. Survodutide also remains an investigational substance; the FDA Global Substance Registration System assigns it the UNII 2ALA66NS64, but FDA expressly notes that assignment of a UNII does not imply regulatory review or approval.[8]

COCER Peptides presents Survodutide solely for laboratory research and analytical use. It is not intended for human or veterinary use. This COCER Peptides material is not an FDA-approved drug product. The research described above summarizes findings reported in third-party publications and is not a statement of clinical efficacy, safety, diagnosis, treatment, prevention, or an instruction for use.

▎Relevant Citations

References

[1] Kushner P R, Michos E D. Cardiovascular Effects of Glucagon Receptor Signaling Alone and Combined With Glucagon-Like Peptide-1 Receptor Signaling in Multiagonists: A Narrative Review With a Translational Focus[J]. Journal of the American Heart Association, 2026,15(15).

DOI:10.1161/jaha.126.049727.

[2] Yuliantie E, Trinh P N H, Bumbak F, et al. 1974-LB: The Molecular Basis of Survodutide (BI456906) Glucagon/GLP-1 Receptor Dual Agonism[J]. Diabetes, 2025,74(Suppl_1):1974-LB.

DOI:10.2337/db25-1974-lb.

[3] Thomas L, Martel E, Rist W, et al. The dual GCGR/GLP‐1R agonist survodutide: Biomarkers and pharmacological profiling for clinical candidate selection[J]. Diabetes, Obesity and Diabetes, 2024,26(6):2368-2378.

DOI:10.1111/dom.15551.

[4] Briand F, Augustin R, Bleymehl K, et al. 7279 Survodutide and Semaglutide Both Induce Weight Loss but Show Different Effects on Food Preference and Dyslipidemia in the Free Choice Diet-induced Obese Hamster Model[J]. Journal of the Endocrine Society, 2024,8(Suppl_1):bvae163.034.

DOI:10.1210/jendso/bvae163.034.

[5] Swagel J, Olkkola S, Eschete K A, et al. 2168-LB: Metabolic and Physiological Effects of Survodutide in Polygenic Type 2 Diabetic Mice (NZO/HILtJ) under Thermoneutral Conditions[J]. Diabetes, 2025,74(Suppl_1):2168-LB.

DOI:10.2337/db25-2168-lb.

[6] Hamilton A, Thisted L, Ougaard M, et al. Nephroprotective Effects of the Dual GCGR/GLP-1R Agonist Survodutide in Hypertension-Accelerated Diabetic Kidney Disease[J]. Diabetes, Obesity and Diabetes, 2026. Advance online publication.

DOI:10.1111/dom.71387.

[7] NCBI PubChem. Survodutide, CID 168429725.

[8] FDA GSRS. Survodutide, UNII 2ALA66NS64.

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