Anti-Exendin-4 ELISA Kit (DEIABL206)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
2x96T
Sample
serum, plasma
Species Reactivity
human
Intended Use
The Anti-Exendin-4 ELISA kit is a dual detection sandwich assay for the determination of antibodies against exendin-4 in serum and plasma samples. Assay employs acid charcoal pre-treatment of samples to improve drug tolerance. The assay is designed to detect all isotypes of immunoglobulins against exendin-4.
Storage
Store the unopened kit at 2-8°C.
Precision
Intra-assay precision (CV%): 5% - 11%. Inter-assay precision (CV%): 15%.
Detection Range
The drug tolerance is up to 100 ng/mL.
Detection Limit
107-188 ng/mL

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References


Exenatide Reverts the High-Fat-Diet-Induced Impairment of BDNF Signaling and Inflammatory Response in an Animal Model of Alzheimer's Disease

JOURNAL OF ALZHEIMERS DISEASE

Authors: Bomba, Manuela; Granzotto, Alberto; Castelli, Vanessa; Onofrj, Marco; Lattanzio, Rossano; Cimini, Annamaria; Sensi, Stefano L.

Alzheimer's disease (AD) is a multifactorial condition in which, along with amyloid-beta (A beta) and tau-related pathology, the synergistic activity of co-morbidity factors promote the onset and progression of the disease. Epidemiological evidence indicates that glucose intolerance, deficits in insulin secretion, or type-2 diabetes mellitus (T2DM) participate in increasing cognitive impairment or dementia risk. Insulin plays a pivotal role in the process as the hormone critically regulates brain functioning. GLP-1, the glucagon-like peptide 1, facilitates insulin signaling, regulates glucose homeostasis, and modulates synaptic plasticity. Exenatide is a synthetic GLP-1 analog employed in T2DM. However, exenatide has also been shown to affect the signaling of the brain-derived neurotrophic factor (BDNF), synaptic plasticity, and cognitive performances in animal models. In this study, we tested whether exenatide exerts neuroprotection in a preclinical AD model set to mimic the clinical complexity of the human disease. We investigated the effects of exenatide treatment in 3xTg-AD mice challenged with a high-fat diet (HFD). Endpoints of the study were variations in systemic metabolism, insulin and neurotrophic signaling, neuroinflammation, A beta and tau pathology, and cognitive performances. Results of the study indicate that exenatide reverts the adverse changes of BDNF signaling and the neuroinflammation status of 3xTg-AD mice undergoing HFD without affecting systemic metabolism or promoting changes in cognitive performances.

Antidiabetic Effect of Abextide, a Long-Acting Exendin-4 Analogue in Cynomolgus Monkeys

ADVANCED HEALTHCARE MATERIALS

Authors: Niu, Gang; Wang, Guohao; Lau, Joseph; Lang, Lixin; Jacobson, Orit; Ma, Ying; Kiesewetter, Dale O.; Zhang, Shaoliang; Chen, Xiaoyuan

Abextide, synthesized by conjugating an albumin-binding moiety-truncated Evans blue-to glucagon-like peptide 1 receptor (GLP-1R) agonist exendin-4, shows extended drug release and enhanced hypoglycemic effect in diabetic mice. The aim of this study is to evaluate the pharmacodynamics of Abextide in nonhuman primates. Two batches of elderly cynomolgus monkeys with naturally occurring diabetes are used for this study. During the whole experiment period, no abnormalities such as swelling at the injection site, lethargy, or hypoglycemia are observed in all animals. The monkeys in the Abextide group lose appetite after drug administration and then recover over time. In the single dose treatment, at day 1 and day 3 after treatment, decreased plasma glucose level is observed in the Abextide-treated group but not in placebo or Albiglutide-treated group. For monkeys that receive two doses of drug, the blood glucose level in all subjects in Abextide group decreases rapidly upon drug administration and return to a plateau by day 3. A similar pattern of response is seen after the second dose administration. The delayed drug release and hypoglycemic effect of Abextide make it potentially useful as an antidiabetic drug for weekly subcutaneous administration.

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