Semaglutide acetate is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer [1] [2] [3] [4] [5].
In Vivo, This product is not intended for oral administration. For animal studies, subcutaneous or intraperitoneal injection is recommended. Oral squamous cell carcinoma (OSCC) xenograft model Semaglutide (3 μmol/kg; subcutaneous injection; 3 times a week; 3 weeks) acetate significantly inhibits the growth of tumor volume in nude mouse oral squamous cell carcinoma (OSCC) xenograft model, downregulates proliferation markers Ki67 and PCNA, upregulates pro-apoptotic protein Bax and downregulates anti-apoptotic protein Bcl-xL, and induces tumor cell apoptosis by activating the P38 MAPK pathway[3]. Chronic MPTP-induced Parkinson's disease model Semaglutide (25 nmol/kg; intraperitoneal injection; once every 2 days; 30 days) acetate improves the chronic MPTP-induced Parkinson's disease model in mice and its motor dysfunction, increases the number of nigral tyrosine (TH)-positive neurons, reduces α-synuclein aggregation and glial activation, and reduces the level of oxidative stress marker 4-HNE[4]. Metabolic dysfunction-associated fatty liver disease (MASLD) model Semaglutide (25 μg/kg/week + 100 μg/kg/week; subcutaneous injection; once a week; 11 weeks) acetate reduces body weight, blood glucose and serum liver enzymes (ALT, AST, AP), reduces hepatic triglyceride deposition, improves hepatic steatosis and hepatocyte ballooning, and downregulates the de novo lipogenesis markers Acaca and Scd1 in the mouse metabolic dysfunction-associated fatty liver disease (MASLD) model[5].
In Vitro, 1. Anti-Aβ25-35 injury experiment: Semaglutide acetate (1-100 nM; 24 h) significantly increases the survival rate of SH-SY5Y cells, increases the expression of autophagy-related proteins such as LC3II, Atg7, Beclin-1 and P62, inhibits Bax and upregulated Bcl-2, and protectes neurons by enhancing autophagy, inhibiting apoptosis[1][2]. 2. Oral squamous cell carcinoma (OSCC) cell experiment: Semaglutide acetate (5-40 μM; 48 h) dose-dependently inhibits the proliferation, migration and invasion of Cal27 and HSC4 cells, upregulates E-cadherin and downregulates Vimentin, activates the P38 MAPK signaling pathway (increased p-P38 expression), and induces cell apoptosis[3].
References:
[1]. Chang YF, et al. Semaglutide-mediated protection against Aβ correlated with enhancement of autophagy and inhibition of apotosis. J Clin Neurosci. 2020 Nov;81:234-239.
[2]. Liu DX, et al. Semaglutide Protects against 6-OHDA Toxicity by Enhancing Autophagy and Inhibiting Oxidative Stress. Parkinsons Dis. 2022 Jul 13;2022:6813017.
[3]. Wang C, et al. Semaglutide, a glucagon-like peptide-1 receptor agonist, inhibits oral squamous cell carcinoma growth through P38 MAPK signaling pathway. J Cancer Res Clin Oncol. 2025 Mar 7;151(3):103.
[4]. Zhang L, et al. Semaglutide is Neuroprotective and Reduces α-Synuclein Levels in the Chronic MPTP Mouse Model of Parkinson's Disease. J Parkinsons Dis. 2019;9(1):157-171.
[5]. Soto-Catalán M, et al. Semaglutide Improves Liver Steatosis and De Novo Lipogenesis Markers in Obese and Type-2-Diabetic Mice with Metabolic-Dysfunction-Associated Steatotic Liver Disease. Int J Mol Sci. 2024 Mar 4;25(5):2961.
[6]. Stephen T Buckley, et al. Transcellular stomach absorption of a derivatized glucagon-like peptide-1 receptor agonist. Sci Transl Med. 2018 Nov 14;10(467):eaar7047.
In Vivo, This product is not intended for oral administration. For animal studies, subcutaneous or intraperitoneal injection is recommended. Oral squamous cell carcinoma (OSCC) xenograft model Semaglutide (3 μmol/kg; subcutaneous injection; 3 times a week; 3 weeks) acetate significantly inhibits the growth of tumor volume in nude mouse oral squamous cell carcinoma (OSCC) xenograft model, downregulates proliferation markers Ki67 and PCNA, upregulates pro-apoptotic protein Bax and downregulates anti-apoptotic protein Bcl-xL, and induces tumor cell apoptosis by activating the P38 MAPK pathway[3]. Chronic MPTP-induced Parkinson's disease model Semaglutide (25 nmol/kg; intraperitoneal injection; once every 2 days; 30 days) acetate improves the chronic MPTP-induced Parkinson's disease model in mice and its motor dysfunction, increases the number of nigral tyrosine (TH)-positive neurons, reduces α-synuclein aggregation and glial activation, and reduces the level of oxidative stress marker 4-HNE[4]. Metabolic dysfunction-associated fatty liver disease (MASLD) model Semaglutide (25 μg/kg/week + 100 μg/kg/week; subcutaneous injection; once a week; 11 weeks) acetate reduces body weight, blood glucose and serum liver enzymes (ALT, AST, AP), reduces hepatic triglyceride deposition, improves hepatic steatosis and hepatocyte ballooning, and downregulates the de novo lipogenesis markers Acaca and Scd1 in the mouse metabolic dysfunction-associated fatty liver disease (MASLD) model[5].
In Vitro, 1. Anti-Aβ25-35 injury experiment: Semaglutide acetate (1-100 nM; 24 h) significantly increases the survival rate of SH-SY5Y cells, increases the expression of autophagy-related proteins such as LC3II, Atg7, Beclin-1 and P62, inhibits Bax and upregulated Bcl-2, and protectes neurons by enhancing autophagy, inhibiting apoptosis[1][2]. 2. Oral squamous cell carcinoma (OSCC) cell experiment: Semaglutide acetate (5-40 μM; 48 h) dose-dependently inhibits the proliferation, migration and invasion of Cal27 and HSC4 cells, upregulates E-cadherin and downregulates Vimentin, activates the P38 MAPK signaling pathway (increased p-P38 expression), and induces cell apoptosis[3].
References:
[1]. Chang YF, et al. Semaglutide-mediated protection against Aβ correlated with enhancement of autophagy and inhibition of apotosis. J Clin Neurosci. 2020 Nov;81:234-239.
[2]. Liu DX, et al. Semaglutide Protects against 6-OHDA Toxicity by Enhancing Autophagy and Inhibiting Oxidative Stress. Parkinsons Dis. 2022 Jul 13;2022:6813017.
[3]. Wang C, et al. Semaglutide, a glucagon-like peptide-1 receptor agonist, inhibits oral squamous cell carcinoma growth through P38 MAPK signaling pathway. J Cancer Res Clin Oncol. 2025 Mar 7;151(3):103.
[4]. Zhang L, et al. Semaglutide is Neuroprotective and Reduces α-Synuclein Levels in the Chronic MPTP Mouse Model of Parkinson's Disease. J Parkinsons Dis. 2019;9(1):157-171.
[5]. Soto-Catalán M, et al. Semaglutide Improves Liver Steatosis and De Novo Lipogenesis Markers in Obese and Type-2-Diabetic Mice with Metabolic-Dysfunction-Associated Steatotic Liver Disease. Int J Mol Sci. 2024 Mar 4;25(5):2961.
[6]. Stephen T Buckley, et al. Transcellular stomach absorption of a derivatized glucagon-like peptide-1 receptor agonist. Sci Transl Med. 2018 Nov 14;10(467):eaar7047.