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    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Kurzfassung: GLP-1 is an incretin hormone with broad pharmacological potential. GLP-1 receptor agonists (GLP-1RAs) are successfully in clinical use for T2D and obesity. Several GLP-1-based therapies are in clinical evaluation for treating metabolic diseases. Supaglutide (supa), a novel GLP-1RA, is in late-stage development for T2D. The efficacy and safety of supa is being investigated in 297 patients with newly diagnosed T2D inadequately controlled with diet and exercise in this randomized, double-blind, placebo-controlled phase 3 clinical trial (NCT04994288). Supa treatment resulted in a statistically and clinically significant reduction from baseline in HbA1c at Week 24 of -1.73% and -2.15% with 1 and 3 mg QW dosing, respectively (p & lt;0.001). Body weight was decreased by 0.97% and 3.14% from baseline in the supa 1 and 3 mg groups, respectively, with a significant difference for supa 3 mg versus 1 mg group (p & lt;0.001). Supa also significantly improved glucose excursion, and increased meal-stimulated insulin and C-peptide secretion as determined by MMTT, suggesting improved glucose tolerance and enhanced β-cell function. The most common TEAEs with supa were GI symptoms, such as nausea, vomiting, diarrhea and decreased appetite, mostly in mild or moderate severity. Our data showed that supa improved glycemic and metabolic control and was well tolerated in T2D, suggesting supa as a novel alternative therapy for T2D and metabolic disorders. Disclosure Q.Wang: None. F.Bian: None. Y.Wang: None. X.Shi: None. Q.Li: None. X.Su: None. K.Wang: None. G.Yuan: None. L.Li: None. H.Ling: None. X.Hu: None. Y.Zhou: None. Y.Wang: None. N.Zhao: None. Y.Yang: None. J.Ma: None. Y.Li: None. D.Zhu: None. W.Wang: None. G.Tong: None. W.Jia: None. L.Li: None. Z.Cheng: None. Y.Lu: None. B.Shi: None.
    Materialart: Online-Ressource
    ISSN: 0012-1797
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2023
    ZDB Id: 1501252-9
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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