
Avexitide
CAS No. 133514-43-9
Avexitide( Exendin (9-39) | Exendin-3 (9-39) amide )
Catalog No. M23488 CAS No. 133514-43-9
Avexitide (Exendin (9-39)) is a specific and competitive antagonist of glucagon-like peptide-1 (GLP-1) receptor.
Purity : >98% (HPLC)






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Biological Information
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Product NameAvexitide
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NoteResearch use only, not for human use.
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Brief DescriptionAvexitide (Exendin (9-39)) is a specific and competitive antagonist of glucagon-like peptide-1 (GLP-1) receptor.
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DescriptionAvexitide (Exendin (9-39)) is a specific and competitive antagonist of glucagon-like peptide-1 (GLP-1) receptor.
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In VitroGLP-1 plays a role in the control of fasting glucose. Avexitide (Exendin (9-39)), a truncated form of the GLP-1 agonist exendin-4, is a specific GLP-1 receptor antagonist.
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In VivoContinuous subcutaneous infusion of Avexitide (Exendin (9-39)) significantly raises fasting blood glucose levels in SUR-1 -/- mice without affecting glucose tolerance.
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SynonymsExendin (9-39) | Exendin-3 (9-39) amide
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PathwayGPCR/G Protein
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TargetGlucagon Receptor
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RecptorGLP-1
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Research Area——
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Indication——
Chemical Information
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CAS Number133514-43-9
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Formula Weight3369.76
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Molecular FormulaC149H234N40O47S
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Purity>98% (HPLC)
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SolubilityH2O : 49 mg/mL (14.54 mM; Need ultrasonic)
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SMILESCC[C@H](C)[C@@H](C(N[C@@H](CCC(O)=O)C(N[C@@H](Cc1c[nH]c2c1cccc2)C(N[C@@H](CC(C)C)C(N[C@@H](CCCCN)C(N[C@@H](CC(N)=O)C(NCC(NCC(N(CCC1)[C@@H]1C(N[C@@H](CO)C(N[C@@H](CO)C(NCC(N[C@@H](C)C(N(CCC1)[C@@H]1C(N(CCC1)[C@@H]1C(N(CCC1)[C@@H]1C(N[C@@H](CO)C(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)NC([C@H](Cc1ccccc1)NC([C@H](CC(C)C)NC([C@H](CCCNC(N)=N)NC([C@H](C(C)C)NC([C@H](C)NC([C@H](CCC(O)=O)NC([C@H](CCC(O)=O)NC([C@H](CCC(O)=O)NC([C@H](CCSC)NC([C@H](CCC(N)=O)NC([C@H](CCCCN)NC([C@H](CO)NC([C@H](CC(C)C)NC([C@H](CC(O)=O)N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O
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Chemical Name——
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
1.Calabria AC, et al. GLP-1 receptor antagonist exendin-(9-39) elevates fasting blood glucose levels in congenital hyperinsulinism owing to inactivating mutations in the ATP-sensitive K+ channel. Diabetes. 2012 Oct;61(10):2585-91.
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