Drug class
Anticonvulsant - Functionalized Amino Acid
The drug class descriptor "Anticonvulsant - Functionalized Amino Acid" designates a chemical and therapeutic subclass of antiepileptic agents structurally derived from D-serine, prototyped by lacosamide. Read more about Anticonvulsant - Functionalized Amino Acid
49 drugs in this class 46 manufacturers
Drugs in Anticonvulsant - Functionalized Amino Acid
VIMPAT (lacosamide)
VIMPAT (lacosamide)
VIMPAT (lacosamide)
MOTPOLY XR (lacosamide)
LACOSAMIDE
LACOSAMIDE
LACOSAMIDE
LACOSAMIDE
The drug class descriptor "Anticonvulsant - Functionalized Amino Acid" designates a chemical and therapeutic subclass of antiepileptic agents structurally derived from D-serine, prototyped by lacosamide.
Agents in this class exert their primary therapeutic effect by selectively enhancing the slow inactivation of voltage-gated sodium channels, thereby stabilizing hyperexcitable neuronal membranes and curbing repetitive, high-frequency neuronal firing without disrupting physiological fast inactivation.
Clinically, these agents are indicated for the management of epilepsy, specifically as monotherapy or adjunctive therapy for partial-onset seizures and primary generalized tonic-clonic seizures.
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fda.gov
The drug class descriptor "Anticonvulsant - Functionalized Amino Acid" designates a chemical and therapeutic subclass of antiepileptic agents structurally derived from D-serine, prototyped by lacosamide
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nih.gov
The drug class descriptor "Anticonvulsant - Functionalized Amino Acid" designates a chemical and therapeutic subclass of antiepileptic agents structurally derived from D-serine, prototyped by lacosamide Agents in this class exert their primary therapeutic effect by selectively enhancing the slow inactivation of voltage-gated sodium channels, thereby stabilizing hyperexcitable neuronal membranes and curbing repetitive, high-frequency neuronal firing without disrupting physiological fast inactivat...
-
nih.gov
Agents in this class exert their primary therapeutic effect by selectively enhancing the slow inactivation of voltage-gated sodium channels, thereby stabilizing hyperexcitable neuronal membranes and curbing repetitive, high-frequency neuronal firing without disrupting physiological fast inactivation
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