Semaglutide TFA
Based on 3 publication(s) in Google Scholar
Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA 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 TFA 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.
For research use only. We do not sell to patients.
- Purity: 99.74%
- Formula: C187H291N45O59.xC2HF3O2
- Molecular Weight:4113.58 (free base)
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) Semaglutide TFA
MoreAll α-synuclein Isoforms
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Biological Activity
1. Anti-Aβ25-35 injury experiment:
Semaglutide TFA (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 TFA (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].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SH-SY5Y human neuroblastoma cells
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Concentration:0, 1, 10, 100 nM
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Incubation Time:24 h
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Result:Cell Viability: Significantly increased cell survival rate in a dose-dependent manner, reversing Aβ25-35-induced cytotoxicity.
WB (Western Blot): Upregulated autophagy markers (LC3II, Atg7, Beclin-1, P62) and anti-apoptotic protein Bcl-2, while downregulating pro-apoptotic protein Bax.
Oral squamous cell carcinoma (OSCC) xenograft model
Semaglutide (3 μmol/kg; subcutaneous injection; 3 times a week; 3 weeks) TFA 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) TFA 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) TFA 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].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude mice (male, 4-6 weeks old) with oral squamous cell carcinoma (OSCC) xenograft model[3]
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Dosage:3 μmol/kg Semaglutide
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Administration:Subcutaneous injection, 3 times weekly, for 3 weeks
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Result:Significantly reduced tumor volume and weight compared to the control group.
Decreased expression of proliferation markers (Ki67, PCNA) and mesenchymal marker Vimentin, while increasing epithelial marker E-cadherin.
Chemical Information
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Appearance Solid
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Molecular Weight 4113.58 (free base)
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Formula C187H291N45O59.xC2HF3O2
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Color White to off-white
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Sequence
His-{Aib}-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Val-Ser-Ser-Tyr-Leu-Glu-Gly-Gln-Ala-Ala-{C18 diacid-γ-Glu-(AEEA)2-Lys}-Glu-Phe-Ile-Ala-Trp-Leu-Val-Arg-Gly-Arg-Gly
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Sequence Shortening
H-{Aib}-EGTFTSDVSSYLEGQAA-{C18 diacid-γ-Glu-(AEEA)2-Lys}-EFIAWLVRGRG
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (3)
Solvent & Solubility
0.5 M NH4OH : 25 mg/mL (ultrasonic and warming and heat to 60°C)
For the following dissolution methods, please prepare the working solution directly:
It is recommended to prepare fresh solutions and use them promptly within a short period of time.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: PBS
Solubility: 2 mg/mL; Clear solution; Need ultrasonic and warming and heat to 60°C
Purity & Documentation
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Data Sheet (294 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
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. [Content Brief]
[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. [Content Brief]
[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. [Content Brief]
[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. [Content Brief]
[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. [Content Brief]
[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. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Semaglutide TFA Related Classifications
HY-114118A Related Classifications
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