NNZ-2566: A Gly–Pro–Glu analogue with neuroprotective efficacy in a rat model of acute focal stroke

@article{Bickerdike2009NNZ2566AG,
  title={NNZ-2566: A Gly–Pro–Glu analogue with neuroprotective efficacy in a rat model of acute focal stroke},
  author={Michael J. Bickerdike and Gregory B. Thomas and David C Batchelor and Ernest S. Sirimanne and Wing Leong and Hai Lin and Frank Sieg and Ji-Yue Wen and Margaret A. Brimble and Paul W. R. Harris and Peter D. Gluckman},
  journal={Journal of the Neurological Sciences},
  year={2009},
  volume={278},
  pages={85-90}
}
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GPE and GPE analogues as promising neuroprotective agents.
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This review will focus on structural modifications performed on the GPE molecule in order to obtain bioactive analogues with increased pharmacokinetic profile useful for the treatment of central nervous system injures and neurodegenerative disorders.
The role for IGF-1-derived small neuropeptides as a therapeutic target for neurological disorders
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These small neuropeptides provide effective neuroprotection by offering an improved pharmacokinetic profile and more practical route of administration compared with IGF-1 administration.
Neuroprotection with Glycine-2-Methylproline-Glutamate (G-2MePE) after hypoxic-ischemic brain injury in adult rats
TLDR
Neuroprotection with G-2MePE after hypoxic-ischemic brain injury in adult rats is associated with reduced neuronal necrosis, apoptosis, modulated inflammatory responses and augmented astrocytosis.
NNZ-2566, a Glypromate Analog, Attenuates Brain Ischemia-Induced Non-Convulsive Seizures in Rats
TLDR
Results indicate that NNZ-2566 possesses a unique therapeutic potential as a safe prophylactic agent that synergistically provides neuroprotection and reduces injury-induced seizures.
Mechanism of Action for NNZ-2566 Anti-inflammatory Effects Following PBBI Involves Upregulation of Immunomodulator ATF3
TLDR
Results demonstrating that the anti-inflammatory and neuroprotective drug NNZ-2566 increase both mRNA and protein levels of ATF3 in multiple cell types provide a cellular mechanism for NNZ -2566 modulation of neuroinflammation following PBBI are demonstrated.
IGF‐1 derived small neuropeptides and analogues: a novel strategy for the development of pharmaceuticals for neurological conditions
TLDR
The research suggests that small neuropeptides have advantages over growth factors in the treatment of brain injury, and that modified neuropePTides designed to overcome the limitations of their endogenous counterparts represent a novel strategy of pharmaceutical discovery for neurological disorders.
NNZ-2566, a Novel Analog of (1–3) IGF-1, as a Potential Therapeutic Agent for Fragile X Syndrome
TLDR
NNZ-2566, a synthetic analog of a naturally occurring neurotrophic peptide derived from insulin-like growth factor-1 (IGF-1), was administered to fmr1 knockout mice and implicate the IGF-1 molecular pathway in the pathogenesis of FXS.
Insulin‐Like Growth Factor ‐1 (IGF‐1) Derived Neuropeptides, a Novel Strategy for the Development of Pharmaceuticals for Managing Ischemic Brain Injury
  • J. Guan
  • Biology, Medicine
    CNS neuroscience & therapeutics
  • 2011
TLDR
Glycine‐proline‐glutamate (GPE) is naturally cleaved from the IGF‐1 N‐terminal and is also neuroprotective after ischemic injury, thus providing a potential novel strategy of drug discovery for management of neurological disorders.
Pharmacokinetics and neurotropic effects of cyclo-L-prolylglycine and its modified analogues
TLDR
CPG shows neuroprotective activity in ischemic-hypoxic and other brain injuries, in addition, it has a complex of other pharmacological effects and therefore CPG can be considered not only as a potential drug, but also as a basic structure for the development of new neurotropic drugs.
Design, Synthesis, and Biological Evaluation of Hybrid Glypromate Analogues Using 2-Azanorbornane as a Prolyl and Pipecolyl Surrogate.
Neurodegenerative disorders of the central nervous system are a class of heterogeneous pathologies affecting millions of people worldwide and represent a global health burden in developed and…
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References

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Neuroprotective effects of Gly-Pro-Glu, the N-terminal tripeptide of IGF-1, in the hippocampus in vitro.
TLDR
A neuroprotective role for GPE tripeptide is reported, with enhanced survival of the CA1-2 hippocampal neurons following an excitotoxic insult in vitro, which could lead to new strategies to reduce neuronal death after injury and in disease.
Neuroprotective effects of the N-terminal tripeptide of IGF-1, glycine-proline-glutamate, in the immature rat brain after hypoxic–ischemic injury
Neuroprotective effects of the N-terminal tripeptide of insulin-like growth factor-1, glycine-proline-glutamate (GPE) following intravenous infusion in hypoxic–ischemic adult rats
Delayed Peripheral Administration of a GPE Analogue Induces Astrogliosis and Angiogenesis and Reduces Inflammation and Brain Injury following Hypoxia-Ischemia in the Neonatal Rat
TLDR
This study indicates that peripheral administration of G-2mPE, starting 2 h after a hypoxic-ischemic insult, reduces the degree of brain injury in the immature rat brain.
Pharmacokinetics of glycine-proline-glutamate, the N-terminal tripeptide of insulin-like growth factor-1, in rats.
Central penetration and stability of N-terminal tripeptide of insulin-like growth factor-I, glycine-proline-glutamate in adult rat
Identification of Gly-Pro-Glu (GPE), the aminoterminal tripeptide of insulin-like growth factor 1 which is truncated in brain, as a novel neuroactive peptide.
N-terminal tripeptide of IGF-1 (GPE) prevents the loss of TH positive neurons after 6-OHDA induced nigral lesion in rats
Delayed treatment with AM-36, a novel neuroprotective agent, reduces neuronal damage after endothelin-1-induced middle cerebral artery occlusion in conscious rats.
TLDR
AM-36 potently protects against both neuronal damage and functional deficits even when administered up to 180 minutes after induction of stroke, which suggests that AM-36 may have great promise in the acute treatment of human stroke.
Effects of IGF-1, truncated IGF-1 and the tripeptide Gly-Pro-Glu on acetylcholine release from parietal cortex of rat brain.
TLDR
The mechanism of action behind GPEs enhancement of cholinergic transmission is still unknown and the possible underlying mechanisms of action of GPE in theCholinergic synapse were investigated.
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