Product Overview

GLP-1 S

GLP-1 S is a long-acting glucagon-like peptide-1 (GLP-1) receptor agonist approved for chronic weight management and glycemic control in adults with obesity or type 2 diabetes. It mimics endogenous GLP-1, acting on central and peripheral pathways to suppress appetite, delay gastric emptying, increase glucose-dependent insulin secretion, decrease glucagon release, and promote pancreatic β-cell growth.[1][2]

Efficacy for Weight Loss & Obesity Management

Indicated for adults with BMI ≥30 kg/m² or ≥25 kg/m² with a weight-related comorbidity.[3][2][4] In STEP 1 and STEP 3, mean weight loss at 68 weeks was 14.9% and 16.0%, respectively, vs 2.4% and 5.7% with placebo. Most participants achieved ≥10% loss, and over half achieved ≥15% loss.[1][5–7] Benefits are maintained with continued therapy; discontinuation often leads to weight regain, underscoring the need for long-term treatment.[1][5][7]

Glycemic Control & Cardiometabolic Benefits

  • Significant reductions in HbA1c and fasting glucose in type 2 diabetes.[8–11][2][5]
  • Lowers blood pressure, improves lipid profiles, and reduces inflammatory markers (e.g., CRP).[4][6]
  • Recommended by ADA and AGA as a first-line pharmacologic option for weight management in adults with obesity and/or type 2 diabetes.[11][2]

Cardiovascular & Renal Outcomes

  • Reduces MACE, cardiovascular mortality, and all-cause mortality in high-risk populations per large trials/meta-analyses.[12–15][4]
  • Kidney-protective effects; recommended for CKD with type 2 diabetes.[12][15][2]

Safety & Tolerability

  • Most common AEs are GI (nausea, vomiting, diarrhea); discontinuation rates similar to placebo in trials.[5–7]
  • Rapid weight loss may increase risk of gallstones/hepatobiliary disorders.[6]
  • No consistent link with increased cancer or psychiatric AEs confirmed.[7]
  • Low hypoglycemia risk as monotherapy.[8–10][2]

Clinical Considerations

  • Use alongside nutrition and physical-activity interventions.[1][2][6]
  • Plan for long-term therapy; counsel on potential weight regain after stopping.[1][5][7]
  • Individualize therapy based on comorbidities, preferences, and access.[2][7]

References

  1. Elmaleh-Sachs A, Schwartz JL, Bramante CT, et al. JAMA. 2023;330(20):2000-2015.
  2. Grunvald E, Shah R, Hernaez R, et al. AGA Guideline. Gastroenterology. 2022;163(5):1198-1225.
  3. FDA Orange Book.
  4. Joseph JJ, Deedwania P, Acharya T, et al. AHA Statement. Circulation. 2022;145(9):e722-e759.
  5. Bergmann NC, Davies MJ, Lingvay I, Knop FK. Diabetes Obes Metab. 2023;25(1):18-35.
  6. Wadden TA, Bailey TS, Billings LK, et al. STEP 3. JAMA. 2021;325(14):1403-1413.
  7. Ferrara F, Bazzani D, Crivelli B, et al. Naunyn-Schmiedeberg’s Arch Pharmacol. 2025.
  8. Blonde L, Fonseca V. Endocr Pract. 2018.
  9. Sheahan KH, Wahlberg EA, Gilbert MP. Postgrad Med J. 2020;96:156-161.
  10. Sharma D, Verma S, Vaidya S, et al. Biomed Pharmacother. 2018;108:952-962.
  11. ADA/EASD Consensus. Diabetes Care. 2022;45(11):2753-2786.
  12. Salama L, Sinn L. Am J Health-Syst Pharm. 2025.
  13. Sachinidis A, Nikolic D, Stoian AP, et al. Metabolism. 2020;111:154343.
  14. Drucker DJ. Diabetes. 2018;67(9):1710-1719.
  15. Galli M, Benenati S, Laudani C, et al. J Am Coll Cardiol. 2025.
  16. Knop FK, Aroda VR, do Vale RD, et al. OASIS-1. Lancet. 2023;402:705-719.

All information provided is for research purposes only.

ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.