<unk>  is used as adjunct to diet and exercise to treat type 2 diabetes. In the European Union, its use is limited to complementing insulin therapy. As of 2017 it is unclear if they affect a person's risk of death. It is provided in an autoinjector containing fourteen doses and is injected subcutaneously.<unk>  should not be used for people who have problems with stomach emptying.<unk>  delays emptying of the stomach, which may change how quickly other drugs that are taken by mouth take effect.<unk>  in neurodegenerative diseases Results from a research work which was done by McClean PL et al. demonstrated that the GLP-1 receptor agonists liraglutide and<unk>  which are on the market as treatments for type 2 diabetes show promise as potential drug treatments of Alzheimer disease AD.<unk>  was equally effective at a lower dose compared to liraglutide in some of the measured parameters after ten weeks of daily intraperitoneal injections with liraglutide (2.5 or 25 nmol/kg) or<unk>  (1 or 10 nmol/kg) or saline of APP/PS1 mice at an age when amyloid plaques had already formed. When analyzing synaptic plasticity in the hippocampus, LTP was strongly increased in APP/PS1 mice by either drug, with more effectiveness accomplished with<unk> . The reduction of synapse numbers seen in APP/PS1 mice was prevented by the two drugs. The amyloid plaque load and dense-core Congo red positive plaque load in the cortex were reduced by both drugs at all doses. The chronic inflammation response (microglial activation) was also reduced by all treatments Cai HY et al. demonstrated in a study that<unk>  could reduce amyloid plaques, neurofibrillary tangles and neuroinflammation in the hippocampi of 12-month-old APP/PS1/tau female mice; activation of PKA-CREB signaling pathway and inhibition of p38-MAPK might be the important mechanisms in the neuroprotective function of<unk> . So,<unk>  might have the potential to be developed as a novel therapy for AD Liu Wet al found an interesting results when comparing exendin-4 (10 nmol/kg), liraglutide (25 nmol/kg) and<unk>  (10 nmol/kg), it was found that exendin-4 showed no protective effects at the dose chosen, while both liraglutide and<unk>  showed effects in preventing the MPTP-induced motor impairment (Rotarod, open-field locomotion, catalepsy test), reduction in tyrosine hydroxylase (TH) levels (dopamine synthesis) in the substantia nigra and basal ganglia, a reduction of the pro-apoptotic signaling molecule BAX and an increase in the anti-apoptotic signaling molecule B-cell lymphoma-2. The previous results demonstrate that both liraglutide and<unk>  are superior to exendin-4, and both drugs show promise as a novel treatment of Parkinson disease Another study done by Kerry Hunter et al. profiled the GLP-1 receptor agonists liraglutide and<unk> . The kinetics of crossing the blood brain barrier (BBB), activation of the GLP-1R by measuring cAMP levels, and physiological effects in the brain on neuronal stem cell proliferation and neurogenesis were evaluated. Both drugs were able to cross the BBB.<unk>  crossed the BBB at all doses tested (2.5, 25, or 250 nmol/kg ip.) when measured 30 min post-injection and at 2.5-25 nmol/kg ip. 3 h post-injection.<unk>  also enhanced neurogenesis in the brain. Liraglutide crossed the BBB at 25 and 250 nmol/kg ip. but no increase was detectable at 2.5 nmol/kg ip. 30 min post-injection, and at 250 nmol/kg ip. at 3 h post-injection. Liraglutide and<unk>  enhanced cAMP levels in the brain, with<unk>  being more effective. The previous results suggest that these novel incretin analogues cross the BBB showing physiological activity and neurogenesis in the brain, which makes them good candidates to be used as a treatment of neurodegenerative diseases.
Lixisenatide
Linaclotide
Pramlintide
Tirzepatide
Glibenclamide
Canagliflozin
Linagliptin
Eluxadoline