Mechanism of action The mechanism of action of<unk>  has not currently been established. Its effect is thought to be localized to the central nervous system rather than a direct effect on skeletal muscles. It has no effect on the motor end plate or the peripheral nerve fiber. The efficacy of the medication is likely related to its sedative effect. Alternatively,<unk>  may act via inhibition of acetylcholinesterase, similarly to carbamate. Pharmacokinetics In healthy individuals, the plasma clearance of<unk>  ranges between 0.20 and 0.80 L/h/kg. The mean plasma elimination half-life ranges between 1 and 2 hours, and the plasma protein binding ranges between 46% and 50%. The elimination half-life was longer in the elderly, those with kidney problems, and those with liver problems. Metabolism<unk>  is the carbamate derivative of guaifenesin, but does not produce guaifenesin as a metabolite, because the carbamate bond is not hydrolyzed metabolically; its metabolism is by Phase I ring hydroxylation and O-demethylation, followed by Phase II conjugation. All the major metabolites are unhydrolyzed carbamates. Small amounts of unchanged<unk>  are also excreted in the urine.
Methocarbamol
Flutemetamol 
Perampanel
Felbamate
Cenobamate
Amivantamab
Tirapazamine
Difebarbamate