Semaglutide

Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver) . Semaglutide 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 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].

910463-68-2

12352209

H302, H315, H319, H335

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-sugar/lipid metabolism

Cancer; Metabolic Disease; Neurological Disease

https://www.medchemexpress.com/Semaglutide.html

99.84

DMSO : 5 mg/mL (ultrasonic) |H2O : 3.85 mg/mL (ultrasonic; adjust pH to 1 with 1 M HCl)

O=C(O)CNC([C@H](CCCNC(N)=N)NC(CNC([C@H](CCCNC(N)=N)NC([C@H](C(C)C)NC([C@H](CC(C)C)NC([C@H](CC1=CNC2=C1C=CC=C2)NC([C@H](C)NC([C@H]([C@@H](C)CC)NC([C@H](CC3=CC=CC=C3)NC([C@H](CCC(O)=O)NC([C@H](CCCCNC(COCCOCCNC(COCCOCCNC(CC[C@@H](C(O)=O)NC(CCCCCCCCCCCCCCCCC(O)=O)=O)=O)=O)=O)NC([C@H](C)NC([C@H](C)NC([C@H](CCC(N)=O)NC(CNC([C@H](CCC(O)=O)NC([C@H](CC(C)C)NC([C@H](CC4=CC=C(O)C=C4)NC([C@H](CO)NC([C@H](CO)NC([C@H](C(C)C)NC([C@H](CC(O)=O)NC([C@H](CO)NC([C@H]([C@H](O)C)NC([C@H](CC5=CC=CC=C5)NC([C@H]([C@H](O)C)NC(CNC([C@H](CCC(O)=O)NC(C(NC([C@H](CC6=CNC=N6)N)=O)(C)C)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O

C187H291N45O59

4113.58

H302, H315, H319, H335

[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

Launched