Ex4-SAP (GLP-1-SAP) [IT-90, KIT-90]

a tool for eliminating cells that express GLP-1R; targeted via exendin-4, eliminated via saporin

SKU: IT-90 Category: Quantity: Individual 25 ug, Individual 100 ug, Individual 250 ug, Individual 1 mg, Kit w/controls 25 ug, Kit w/controls 100 ug, Kit w/controls 250 ug | Conjugate: streptavidin-saporin | Usage: eliminates cells |

Exenatide is a synthetic version of exendin-4, a hormone found in the saliva of the Gila monster.  It displays biological properties similar to human glucagon-like peptide-1 (GLP-1), a regulator of glucose metabolism and insulin secretion. Exenatide is a 39-amino-acid peptide that enhances glucose-dependent insulin secretion by the pancreatic beta-cell, suppresses inappropriately elevated glucagon secretion, slows gastric emptying, presents a subtle yet prolonged effect to reduce appetite and promote satiety via hypothalamic receptors, and reduces liver fat content. Exenatide demonstrates a 50% greater half-life than native GLP-1 in vivo and is DPP-4 resistant.

Ex4-SAP is a bonded conjugate of exendin-4 peptide, a glucagon-like peptide-1 (GLP-1) agonist and the secondary conjugate Streptavidin-ZAP (IT-27) containing the ribosome-inactivating protein, saporin. It eliminates cells expressing the GLP-1 receptor.

Ex4-SAP-SAP is available individually (Cat. #IT-90) or as a kit (Cat. #KIT-90) which includes Ex4-SAP and Blank-Streptavidin-SAP (Cat. #IT-27B).

keywords: exenatide, exenatide-4, Ex4-SAP, GLP-1-SAP, Exenatide-4-SAP, glucagon, insulin, GLP-1 receptor, GLP-1 agonist, human glucagon-like-peptide, exendin, exendin-4, satiety, diabetes, pancreas, beta-cell, appetite, gastric emptying, glucose, satiety, hypothalamic receptor, glia monster, DPP-4, liver fat, metabolism, streptavidin, saporin, eating, appetite, brain, neuroscience

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View Data Sheet

The deletion of glucagon-like peptide-1 receptors expressing neurons in the dorsomedial hypothalamic nucleus disrupts the diurnal feeding pattern and induces hyperphagia and obesity

Maejima Y, Yokota S, Shimizu M, Horita S, Kobayashi D, Hazama A, Shimomura K (2021) The deletion of glucagon-like peptide-1 receptors expressing neurons in the dorsomedial hypothalamic nucleus disrupts the diurnal feeding pattern and induces hyperphagia and obesity. Nutr Metab (Lond) 18(1):58. doi: 10.1186/s12986-021-00582-z

Summary: Feeding rhythm disruption contributes to the development of obesity. GLP-1 receptors (GLP-1R) are expressed in the dorsomedial hypothalamic nucleus (DMH) which are known to be associated with thermogenesis and circadian rhythm development. These findings suggest that GLP-1R expressing neurons in the DMH may mediate feeding termination.

Usage: Exenatide-SAP targets GLP-1R expressing cells. Injections of 0.1 μg/0.5 μl Ex4-SAP or 0.1 μg/0.5 μl Blank-SAP (control) were administered into the DMH.

Related Products: Ex4-SAP (GLP-1-SAP) (Cat. #IT-90), Blank-SAP (Cat. #IT-21)

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Saporin (Cat. #PR-01)

Blank-Streptavidin-SAP (Cat. #IT-27B)

Neuroscience

Cytotoxicity Assay for Targeted Toxins in vitro

Concentration Calculation Explained: Convert molarity to mg/ml and mg/ml to molarity

Preparing and Interpreting Cytotoxicity Data in vitro


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