Semaglutide Acetate is a GLP-1R agonist (EC50=6.2 pM) with long-acting, selective, competitive, and oral efficacy. Semaglutide acetate can be used in the study of type 2 diabetes.

GLP1:0.38 nM (Ki)

METHODS: SH-SY5Y cells were treated with Semaglutide acetate (0, 1, 10, and 100 nM) for 24 hours, and cell viability was measured using MTT assay.
RESULTS: Semaglutide acetate significantly increased the survival rate of SH-SY5Y cells. [1]
METHODS: SH-SY5Y cells were treated with Semaglutide acetate for 48 hours, and target protein expression was detected using Western Blot.
RESULTS: Semaglutide acetate increased the expression of autophagy-related proteins such as LC3II, Atg7, Beclin-1, and P62, inhibited Bax and up-regulated Bcl-2, thereby protecting nerve cells by enhancing autophagy and inhibiting apoptosis. [2]
METHODS: Oral squamous cell carcinoma (OSCC) cells were treated with Semaglutide acetate (5-40 μM) for 48 hours, and target protein expression was detected using Western Blot.
RESULTS: Semaglutide acetate up-regulated E-cadherin and down-regulated Vimentin, activated P38 MAPK signaling pathway (p-P38 expression increased), and induced cell apoptosis. [3]

METHODS: To study the antitumor activity of Semaglutide Acetate, Semaglutide (3 μmol/kg) was subcutaneously injected into nude mice with oral squamous cell carcinoma (OSCC) transplanted tumors for 3 weeks per week for 3 consecutive weeks.
RESULTS: Semaglutide Acetate significantly inhibited the growth of oral squamous cell carcinoma (OSCC) xenografts in nude mice, down-regulated the proliferation markers Ki67 and PCNA, up-regulated the pro-apoptotic protein Bax and down-regulated the anti-apoptotic protein Bcl-xL. Tumor cell apoptosis was induced by activation of P38 MAPK pathway. [3]
METHODS: To investigate the effect of Semaglutide Acetate on Parkinson's disease, a mouse model of chronic MPTP-induced Parkinson's disease was induced by intraperitoneal injection of Semaglutide (25 nmol/kg) every 2 days for 30 consecutive days.
RESULTS: Semaglutide Acetate improved chronic MPTP-induced Parkinson's disease and motor dysfunction in mice. Semaglutide acetate increased the number of tyrosine (TH) -positive neurons in the substantia nigra, reduced α-synuclein aggregation and glial cell activation, and decreased the level of oxidative stress marker 4-HNE. [4]
METHODS: To study the effect of Semaglutide Acetate on fatty liver disease, metabolic dysfunction associated fatty liver disease (MASLD) mice were subcutaneously injected with Semaglutide (25 μg/kg, 100 μg/kg) once a week for 11 weeks.
RESULTS: Semaglutide Acetate reduced body weight, blood glucose, serum liver enzymes (ALT, AST, and AP), reduced intrahepatic triglyceride deposition, ameliorated hepatic steatosis and hepatocyte balloon-like degeneration, and down-regulated de novo lipogenesis markers Acaca and Scd1. [5]