Semaglutide (acetate)

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].

1997361-85-9

AHPN

12352209

Apoptosis; Autophagy; Bcl-2 Family; GLP Receptor; Insulin Receptor; p38 MAPK; α-synuclein

Reference compound

Apoptosis; Autophagy; GPCR/G Protein; MAPK/ERK Pathway; Neuronal Signaling; Protein Tyrosine Kinase/RTK

Metabolism-protein/nucleotide metabolism

Cancer; Metabolic Disease; Neurological Disease

https://www.medchemexpress.com/semaglutide-acetate.html

99.92

DMSO : < 1 mg/mL (ultrasonic) |H2O : 23.81 mg/mL (ultrasonic; adjust pH to 8 with NH3·H2O) |H2O : 25 mg/mL (ultrasonic; adjust pH to 4 with CH3COOH)

O=C(CNC([C@@H](NC(CNC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC(CNC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC(CNC([C@@H](NC(C(C)(C)NC([C@@H](N)CC1=CNC=N1)=O)=O)CCC(O)=O)=O)=O)[C@@H](C)O)=O)CC2=CC=CC=C2)=O)[C@@H](C)O)=O)CO)=O)CC(O)=O)=O)C(C)C)=O)CO)=O)CO)=O)CC3=CC=C(C=C3)O)=O)CC(C)C)=O)CCC(O)=O)=O)=O)CCC(N)=O)=O)C)=O)C)=O)CCCCNC(COCCOCCNC(COCCOCCNC(CC[C@H](NC(CCCCCCCCCCCCCCCCC(O)=O)=O)C(O)=O)=O)=O)=O)=O)CCC(O)=O)=O)CC4=CC=CC=C4)=O)[C@H](CC)C)=O)C)=O)CC5=CNC6=C5C=CC=C6)=O)CC(C)C)=O)C(C)C)=O)CCCNC(N)=N)=O)=O)CCCNC(N)=N)=O)O.CC(O)=O.[x]

C187H291N45O59.xC2H4O2

4113.58 (free base)

[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.

Blue Ice

-80°C, 2 years; -20°C, 1 year (Powder, sealed storage, away from moisture)

Reference compound1