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Key Documents

SML2836

Sigma-Aldrich

Lixisenatide

≥95% (HPLC)

Synonyme(s) :

(Des-Pro38)-Exendin-4-(Lys)6 amide, AVE0010, HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPSKKKKKK-NH2, His-Gly-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Leu-Ser-Lys-Gln-Met-Glu-Glu-Glu-Ala-Val-Arg-Leu-Phe-Ile-Glu-Trp-Leu-Lys-Asn-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Ser-Lys-Lys-Lys-Lys-Lys-Lys-NH2, ZP10, ZP10A

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About This Item

Formule empirique (notation de Hill):
C215H347N61O65S
Numéro CAS:
320367-13-3
Poids moléculaire :
4858.49
Code UNSPSC :
51111800
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Pureté

≥95% (HPLC)

Forme

lyophilized powder

Couleur

white to beige

Température de stockage

−20°C

Actions biochimiques/physiologiques

Lixisenatide (AVE0010, ZP10A) is a C-terminal amidated synthetic glucagon-like peptide-1 receptor (GLP-1R) agonist peptide whose sequence corresponds to Pro38 deleted exendin-4 with a C-terminal extension by six Lys residues. Lixisenatide exhibits 4-times higher human GLP-1R affinity than GLP-1(7-36) amide and dispalys in vivo therapeutic efficacy in murine and rat models of type 2 diabetes, as well as rat models of dox-induced renal fibrosis, global cerebral I/R injury, abdominal aortic aneurysm (AAA) and Aβ25-35 toxicity.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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Consulter la Bibliothèque de documents

Preclinical pharmacology of the new GLP-1 receptor agonist AVE0010.
U Werner
Annales d'endocrinologie, 69(2), 164-165 (2008-04-18)
Qini Zhao et al.
Artificial cells, nanomedicine, and biotechnology, 47(1), 2325-2332 (2019-06-09)
Increased free fatty acids (FFA) are one of the risk factors for type 2 diabetes. FFA also contribute to endothelial dysfunction in both the prediabetes and diabetes conditions. Therefore, FFA are an important link between diabetes and endothelial dysfunction. In
N-F Guo et al.
European review for medical and pharmacological sciences, 23(9), 4017-4026 (2019-05-23)
The aim of this study was to investigate whether Lixisenatide, NF-kB/TNF-α, and TGF-β/Smad pathways exert clear regulatory roles in doxorubicin-induced renal fibrosis in rats, and to explore the possible underlying mechanism. 30 rats were randomly assigned into the sham group
Ángela Vinué et al.
Diabetologia, 60(9), 1801-1812 (2017-06-14)
Recent clinical studies indicate that glucagon-like peptide-1 (GLP-1) analogues prevent acute cardiovascular events in type 2 diabetes mellitus but their mechanisms remain unknown. In the present study, the impact of GLP-1 analogues and their potential underlying molecular mechanisms in insulin
Julie Charpentier et al.
American journal of physiology. Gastrointestinal and liver physiology, 315(5), G671-G684 (2018-08-03)
Endogenous glucagon-like peptide-1 (GLP-1) regulates glucose-induced insulin secretion through both direct β-cell-dependent and indirect gut-brain axis-dependent pathways. However, little is known about the mode of action of the GLP-1 receptor agonist lixisenatide. We studied the effects of lixisenatide (intraperitoneal injection)
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