Gavestinel
≥98%(HPLC)
- Product Code: 190919
CAS:
153436-38-5
| Molecular Weight: | 397.19 g./mol | Molecular Formula: | C₁₈H₁₁Cl₂N₂O₃Na |
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| Density: | Storage Condition: | -20°C, Sealed, Dry |
Product Description:
Gavestinel was developed as a neuroprotective agent targeting acute neurological conditions, particularly those involving excitotoxicity due to overactivation of the NMDA receptor. It acts as a competitive antagonist at the glycine binding site of the NMDA receptor, helping to reduce excessive glutamate signaling that can lead to neuronal damage.
Its primary investigated application was in the treatment of ischemic stroke, where it aimed to limit brain injury following interruption of blood flow. Clinical trials also explored its potential in traumatic brain injury and global cerebral ischemia, such as after cardiac arrest. By modulating NMDA receptor activity without completely blocking it, gavestinel sought to preserve essential neurotransmission while preventing neurotoxic effects.
Despite promising preclinical results showing reduced infarct size and improved neurological outcomes in animal models, gavestinel did not demonstrate significant efficacy in large-scale human clinical trials. As a result, its development was discontinued, and it is not used clinically. However, it remains a notable example in the study of glutamate antagonists and the challenges in translating neuroprotective strategies from bench to bedside.
Sizes / Availability / Pricing:
| Size | Availability | Price | Quantity |
|---|---|---|---|
| 0.005 G | 10-20 days | ฿16,270.00 |
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| 0.010 G | 10-20 days | ฿22,740.00 |
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Gavestinel
Gavestinel was developed as a neuroprotective agent targeting acute neurological conditions, particularly those involving excitotoxicity due to overactivation of the NMDA receptor. It acts as a competitive antagonist at the glycine binding site of the NMDA receptor, helping to reduce excessive glutamate signaling that can lead to neuronal damage.
Its primary investigated application was in the treatment of ischemic stroke, where it aimed to limit brain injury following interruption of blood flow. Clinical trials also explored its potential in traumatic brain injury and global cerebral ischemia, such as after cardiac arrest. By modulating NMDA receptor activity without completely blocking it, gavestinel sought to preserve essential neurotransmission while preventing neurotoxic effects.
Despite promising preclinical results showing reduced infarct size and improved neurological outcomes in animal models, gavestinel did not demonstrate significant efficacy in large-scale human clinical trials. As a result, its development was discontinued, and it is not used clinically. However, it remains a notable example in the study of glutamate antagonists and the challenges in translating neuroprotective strategies from bench to bedside.
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