Gavestinel: Difference between revisions

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'''Gavestinel''' (also known as '''GV150526''') is a [[pharmaceutical drug]] that was developed by [[GlaxoSmithKline]] for the treatment of [[stroke]]. It is a selective antagonist for the [[glycine]] site of the [[N-methyl-D-aspartate receptor]] (NMDAR), which is a major subtype of [[glutamate receptor]].
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== Gavestinel ==
[[File:Gavestinel.svg|thumb|right|Chemical structure of Gavestinel]]
'''Gavestinel''' is a chemical compound that acts as a selective antagonist of the [[NMDA receptor]], specifically targeting the [[glycine]] site of the receptor. It was investigated for its potential use in the treatment of [[stroke]] and other [[neurological disorders]].


== Mechanism of Action ==
== Mechanism of Action ==
Gavestinel works by selectively blocking the glycine site of the NMDAR. This site is crucial for the activation of the receptor. By blocking this site, Gavestinel prevents the excessive activation of the NMDAR, which is believed to be a major cause of neuronal death following a stroke.
Gavestinel functions by inhibiting the activity of the NMDA receptor, a type of [[glutamate receptor]] that plays a crucial role in [[synaptic plasticity]] and [[neurotransmission]]. By blocking the glycine site, Gavestinel reduces the excitotoxicity associated with excessive NMDA receptor activation, which is a common pathological feature in conditions such as stroke.


== Clinical Trials ==
== Clinical Development ==
Gavestinel has undergone several [[clinical trial]]s to assess its efficacy and safety in the treatment of stroke. In early phase trials, it showed promise in reducing the severity of stroke symptoms. However, in larger phase III trials, it failed to show a significant benefit over placebo.
Gavestinel was developed as a neuroprotective agent with the aim of reducing brain damage following an acute ischemic stroke. Despite promising preclinical results, clinical trials did not demonstrate significant efficacy in improving outcomes for stroke patients. As a result, its development for this indication was discontinued.


== Side Effects ==
== Pharmacokinetics ==
The most common side effects of Gavestinel include [[nausea]], [[vomiting]], and [[headache]]. In rare cases, it can cause serious side effects such as [[seizure]]s and [[hallucination]]s.
The pharmacokinetic profile of Gavestinel includes its absorption, distribution, metabolism, and excretion. It is known to cross the [[blood-brain barrier]], which is essential for its action on central nervous system targets. However, specific details on its half-life and metabolic pathways are less documented in the literature.


== Current Status ==
== Potential Applications ==
As of now, Gavestinel is not approved for use in any country. After the disappointing results of the phase III trials, GlaxoSmithKline decided to discontinue its development.
Although Gavestinel was not successful in clinical trials for stroke, its mechanism of action suggests potential applications in other neurological conditions where NMDA receptor-mediated excitotoxicity is implicated, such as [[traumatic brain injury]] and certain types of [[epilepsy]].


== See Also ==
== See Also ==
* [[NMDA receptor antagonist]]
* [[Excitotoxicity]]
* [[Neuroprotection]]
== Related Pages ==
* [[Stroke]]
* [[Stroke]]
* [[Glutamate receptor]]
* [[Glycine receptor]]
* [[Clinical trial]]
* [[Glutamate]]
 
[[Category:Pharmaceutical drugs]]
[[Category:Stroke]]
[[Category:GlaxoSmithKline]]


{{medicine-stub}}
[[Category:NMDA receptor antagonists]]
[[Category:Neuroprotective agents]]

Latest revision as of 04:01, 13 February 2025


Gavestinel[edit]

Chemical structure of Gavestinel

Gavestinel is a chemical compound that acts as a selective antagonist of the NMDA receptor, specifically targeting the glycine site of the receptor. It was investigated for its potential use in the treatment of stroke and other neurological disorders.

Mechanism of Action[edit]

Gavestinel functions by inhibiting the activity of the NMDA receptor, a type of glutamate receptor that plays a crucial role in synaptic plasticity and neurotransmission. By blocking the glycine site, Gavestinel reduces the excitotoxicity associated with excessive NMDA receptor activation, which is a common pathological feature in conditions such as stroke.

Clinical Development[edit]

Gavestinel was developed as a neuroprotective agent with the aim of reducing brain damage following an acute ischemic stroke. Despite promising preclinical results, clinical trials did not demonstrate significant efficacy in improving outcomes for stroke patients. As a result, its development for this indication was discontinued.

Pharmacokinetics[edit]

The pharmacokinetic profile of Gavestinel includes its absorption, distribution, metabolism, and excretion. It is known to cross the blood-brain barrier, which is essential for its action on central nervous system targets. However, specific details on its half-life and metabolic pathways are less documented in the literature.

Potential Applications[edit]

Although Gavestinel was not successful in clinical trials for stroke, its mechanism of action suggests potential applications in other neurological conditions where NMDA receptor-mediated excitotoxicity is implicated, such as traumatic brain injury and certain types of epilepsy.

See Also[edit]

Related Pages[edit]