In humans<unk>  is rapidly and almost completely absorbed and totally metabolised via the liver. Peak plasma levels occur 0.3 to 2 hours after oral administration. The bioavailability increases during the first week of therapy from 60% to 80% and more. The elimination half-life is around 2 hours. It is moderately bound to plasma proteins, especially albumin. However, the short disposition half life somewhat increases after repeated dosing;<unk>  has an intermediate elimination half life for systemic clearance and an intermediate volume of distribution. Despite its short half-life the pharmacodynamic action of a single dose persists for approximately 16 hours. The drug is almost completely metabolized in the liver; it is a substrate of CYP2C19 and an inhibitor of CYP2C19, CYP2D6 and CYP1A2. Less than 1 percent of the drug is excreted unchanged; 92 percent of the metabolised drug is excreted within the first 12 hours. The main metabolites are the N-oxide Ro 12-5637 formed via morpholine N-oxidation and lactam derivative Ro 12-8095 formed via morpholine C-oxidation; active metabolites are found only in trace amounts. The unchanged drug (less than 1%) as well as the metabolites are excreted renally (in urine). The main degradation pathway of<unk>  is oxidation. About 44 percent of the drug is lost due to the first pass effect through the liver. Age and renal function do not affect the pharmacokinetics of<unk> . However, patients with significantly reduced liver function require dose reductions due to the significant slowing of metabolism of<unk> . Food slows the absorption but does not affect the bioavailability of<unk> . Steady state concentrations are established after one week. It has been suggested that changes in dose should not be made with a gap of less than a week.<unk>  has good penetration across the blood brain barrier with peak plasma levels within the central nervous system occurring 2 hours after administration.
Moclobemide
Torasemide
Altretamine
Bumetanide
Yohimbine
Brimonidine
Clonidine
Amiloride