Fluvoxamine Chemische Eigenschaften,Einsatz,Produktion Methoden
Chemische Eigenschaften
Colourless Oil
History
The development of Fluvoxamine began in the 1970s, led by a research team at the Belgian pharmaceutical company Solvay. As the first successfully commercialized selective serotonin reuptake inhibitor (SSRI), fluvoxamine was designed and synthesized to exert its antidepressant effect by highly selectively inhibiting the presynaptic serotonin transporter, while exhibiting a higher safety profile compared to tricyclic antidepressants. This compound received its first clinical approval and market launch in Switzerland in 1983, marking the beginning of the SSRI era. Leading researchers in psychopharmacology, including C. M. van Hout, systematically elucidated the pharmacological properties and clinical efficacy of fluvoxamine. With the expansion of its clinical applications, fluvoxamine has also established a therapeutic role in indications such as obsessive-compulsive disorder, and during the COVID-19 pandemic, its re-evaluation as a potential immunomodulator sparked renewed research interest, reflecting its evolution from a classic antidepressant to a multi-purpose psychopharmacological drug.
Allgemeine Beschreibung
The E-isomer of fluvoxamine (Luvox) can fold after protonation to the β-arylamine–like grouping. Here,the “extra” hydrophobic group is aliphatic.
Hazard
A poison.
Mechanism of action
Fluvoxamine is a highly selective inhibitor of 5-HT reuptake at the presynaptic membrane. Potency data from
in vitro affinity studies suggest that fluvoxamine is less potent than the other SSRIs (e.g., paroxetine,
sertraline, and citalopram). Its mechanism of action is similar to that of the other SSRIs. Fluvoxamine appears
to have little or no effect on the reuptake of NE or dopamine. In vitro studies have demonstrated that
fluvoxamine possesses virtually no affinity for other neuroreceptors. Its onset of action is similar to the other
SSRIs (2–4 weeks).
Pharmakokinetik
Fluvoxamine is well absorbed, with a bioavailability of approximately 50%, probably because of first-pass
metabolism. At steady-state doses, fluvoxamine demonstrates nonlinear pharmacokinetics over a
dosage range of 100 to 300 mg/day, which results in higher plasma concentrations at higher doses than
would be predicted by lower-dose kinetics (single dose, 15 hours; multiple dosing, 22 hours). Food does not
significantly affect oral bioavailability. The mean apparent volume of distribution for fluvoxamine reflects its
lipophilic nature, extensive tissue distribution, and protein binding. Fluvoxamine is distributed into breast
milk. Fluvoxamine is preferentially metabolized by CYP2D6 in the liver by O-demethylation to its alcohol
metabolite, which subsequently is oxidized to a carboxylic acid. Oxidative deamination and nine other
metabolites have been identified, none of which shows significant pharmacological activity.
Clinical Use
Fluvoxamine is approved for use in obsessive-compulsive disorders.
Nebenwirkungen
The adverse effects for fluvoxamine include symptoms of drowsiness, nausea or vomiting, abdominal pain,
tremors, sinus bradycardia, and mild anticholinergic symptoms. Toxic doses could produce seizures and
severe bradycardia.
Arzneimittelwechselwirkung
In vitro studies have shown fluvoxamine to be a potent inhibitor of CYP1A2, to inhibit CYP3A4 and CYP2C19,
and to weakly inhibit CYP2D6. The bioavailability of fluvoxamine is significantly decreased in smokers
compared with nonsmokers, possibly because of induction of CYP1A metabolism of fluvoxamine. Therefore,
interactions with drugs that inhibit CYP1A2 also should be considered (e.g., theophylline and caffeine).
Fluvoxamine Upstream-Materialien And Downstream Produkte
Upstream-Materialien
Downstream Produkte
