Midafotel: Difference between revisions
CSV import Tags: mobile edit mobile web edit |
CSV import |
||
| Line 28: | Line 28: | ||
[[Category:NMDA antagonists]] | [[Category:NMDA antagonists]] | ||
{{stub}} | {{stub}} | ||
<gallery caption="Midafotel"> | |||
File:CPPene.svg|Midafotel | |||
File:Midafotel-3D.png|Midafotel | |||
</gallery> | |||
Latest revision as of 01:01, 20 February 2025
Midafotel is a drug that was under development for the treatment of stroke and schizophrenia. It acts as an NMDA antagonist, specifically targeting the glutamate site. Midafotel was developed by Pfizer but its development was discontinued in 1998.
History[edit]
Midafotel was first synthesized by Pfizer in the 1990s as a potential treatment for stroke and schizophrenia. The drug was designed to act as an NMDA antagonist, blocking the action of glutamate at the NMDA receptor. This mechanism of action was thought to be beneficial in the treatment of stroke and schizophrenia, as overactivity of the NMDA receptor has been implicated in both conditions.
However, in 1998, Pfizer discontinued the development of Midafotel. The reasons for this decision are not publicly available, but it is likely that the drug did not meet the necessary safety and efficacy standards in clinical trials.
Mechanism of Action[edit]
Midafotel acts as an NMDA antagonist, specifically targeting the glutamate site. The NMDA receptor is a type of ionotropic glutamate receptor, and it plays a key role in synaptic plasticity and memory function. Overactivity of the NMDA receptor has been implicated in a number of neurological and psychiatric disorders, including stroke and schizophrenia.
By blocking the action of glutamate at the NMDA receptor, Midafotel was designed to reduce the overactivity of the receptor and thereby alleviate the symptoms of stroke and schizophrenia.
Clinical Trials[edit]
While the specific details of the clinical trials conducted on Midafotel are not publicly available, it is known that the drug was tested in both stroke and schizophrenia patients. However, the drug did not meet the necessary safety and efficacy standards, leading to the discontinuation of its development.
See Also[edit]
References[edit]
<references />
