[D-Ala2]-GIP (human)
Purity: ≥95%
Biological Activity
[D-Ala2]-GIP (human) is a highly potent GIP receptor agonist (EC50 = 630 ± 119 pM). Displays equivalent cAMP stimulating properties and improved resistance to enzymatic degradation compared to native GIP (Cat. No. 2084) in cells expressing wild type GIP receptor. Improves glucose tolerance, insulin release and cognitive function in various animal models of obesity and diabetes. Displays neuroprotective effects in an MPTP model of PD.Technical Data
(Modifications: Ala-2 = D-Ala)
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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Prolonged GIP receptor activation improves cognitive function, hippocampal synaptic plasticity and glucose homeostasis in high-fat fed mice.
Porter et al.
Eur.J.Pharmacol., 2011;650:688 -
Dipeptidyl peptidase IV-resistant [D-Ala2]glucose-dependent Insotropic polypeptide (GIP) improves glucose tolerance in normal and obese diabetic rats.
Hinke et al.
Diabetes., 2002;51:652 -
Effect of D-Ala2GIP, a stable GIP receptor agonist on MPTP-induced neuronal impairments in mice.
Verma et al.
Eur.J.Pharmacol., 2017;804:38
Product Datasheets
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Citations for [D-Ala2]-GIP (human)
The citations listed below are publications that use Tocris products. Selected citations for [D-Ala2]-GIP (human) include:
2 Citations: Showing 1 - 2
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A brainstem circuit for nausea suppression.
Authors: Frank Et al.
Cell Rep 2022;39:110953
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Chronic glucose-dependent insulinotropic polypeptide receptor (GIPR) agonism desensitizes adipocyte GIPR activity mimicking functional GIPR antagonism.
Authors: Bin Et al.
Nat Commun 2020;11:4981
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