Zimelidine: A new antidepressant?

Cox, John; Moore, G. E.; Evans, Larry

doi:10.1016/0364-7722(78)90095-4

Cited by 18 publications

(6 citation statements)

References 11 publications

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“…Alaproclate is even more selective than zimelidine in 5-HT uptake inhibition (Lindberg et aI., 1978;Carlsson and Lindqvist, 1978) and causes no sedation at doses which inhibit uptake in animals (unpublished observations). Furthermore, neither zimelidine (Hall and Ogren, submitted for publication; Cox et al, 1978; Xberg and Holmberg, t979) nor alaproclate (Hall and Ogren, submitted for publication) have significant anticholinergic or adrenolytic properties, which is in keeping with the second and third hypotheses above. The tetracyclic compound, mianserin, also has a different pharmacological profile from the tricyclics.…”

Section: Discussionmentioning

confidence: 57%

“…Zimelidine, a bicyclic compound, which has recently been shown to be an effective antidepressant (Cox et al, 1978;dberg and Holmberg, 1979;Coppen et al, 1979), and its main metabolite, norzimelidine, are both selective and potent inhibitors of 5-HT uptake (Ross et al, 1976;Ross and Renyi, 1977). Zimelidine, at doses markedly inhibiting 5-HT uptake, does not cause significant sedation in mice (Ross et al, 1976) and none of the aforementioned clinical trials have reported sedative side-effects--thus differentiating zimelidine from the tertiary amine tricyclics.…”

Section: Discussionmentioning

confidence: 95%

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Antidepressant drugs and ethanol: Behavioral and pharmacokinetic interactions in mice

1980

J. Neural Transmission

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The interactions between ethanol and antidepressant drugs (both tricyclics and newer non-tricyclics) were studied in mice. The ability of these drugs to enhance the sedative effects of ethanol at two different doses (3.2 and 4.0 g/kg) was measured. The percentage of mice losing the righting-reflex was used for the lower dose, and the duration of ethanol-induced sleep was used at the higher dose. The relative order of potency was amitriptyline greater than or equal to imipramine > maprotiline = mianserin > desipramine greater than or equal to chlorimipramine > iprindole greater than or equal to alaproclate > norzimelidine greater than or equal to zimelidine. Amitriptyline (60 mg/kg) caused death in all mice when combined with 4.0 g/kg ethanol. Clinically established antidepressants which enhanced ethanol sedation only at doses considerably above therapeutic levels were zimelidine and iprindole. The relative potency of the antidepressants to enhance ethanol sedation is correlated with their inherent sedative properties which are in turn related to their ability to block central 5-HT, alpha-NA, muscarinic and H1-receptors. Amitriptyline (20 mg/kg) was found to increase ethanol plasma levels to 202, 167 and 132% of control values at 30, 60 and 90 min after ethanol administration, respectively. Desipramine, mianserin and alaproclate also increased ethanol plasma levels initially, but to a lesser extent. These findings suggest that in addition to their sedative effect, several antidepressants, particularly amitriptyline, are likely to interact with ethanol by increasing its concentration in plasma.

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 95%

Antidepressant drugs and ethanol: Behavioral and pharmacokinetic interactions in mice

1980

J. Neural Transmission

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“…Blood pressures were all within the normal range. ECGs showed the minor changes reported by Cox et al (1978).…”

Section: Resultsmentioning

confidence: 68%

The treatment of phobic anxiety by zimelidine

Evans

Moore

1981

Acta Psychiatr Scand

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Seven patients who were diagnosed as suffering from phobic anxiety were treated with a new antidepressant which causes relatively selective inhibition of serotonin uptake. This compound, zimelidine, was given for five weeks in doses of up to 300 mg per day. One patient dropped out of the study. Of the remaining six patients all but one made an improvement, which in most cases is thought to have been a drug effect. One patient relapsed some months following treatment and responded again to treatment with zimelidine having failed to respond to other psychotropic drugs.

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“…Normal, therapeutic plasma concentrations of zimelidine range from 0.02 to 0.25 mg/L (1,4-9). However, as with tricyclic antidepressants, individual variations do occur with zimelidine concentrations with steady-state plasma levels having been reported up to 0.8 m g / L (4,8). There is very little information in the literature on overdosage of zimelidine.…”

Section: R E S U L T S a N D Discussion Smentioning

confidence: 99%

Zimelidine Distribution in a Sudden Death*

Semple

1984

Journal of Analytical Toxicology

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The occurrence of zimelidine, a new experimental antidepressant, in a sudden death is presented. Tissues were extracted with n-butyl chloride. Quantitation was done by capillary gas chromatography with a nitrogen/phosphorus detector. Drug confirmation was obtained by gas chromatography and mass spectrometry. Blood concentrations of zimelidine and its metabolite norzimelidine were 0.71 and 2.2 mg/L respectively. Concentrations of the drug and metabolite are also given for the urine, liver, bile, and brain.

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Zimelidine: A new antidepressant?

Cited by 18 publications

References 11 publications

Antidepressant drugs and ethanol: Behavioral and pharmacokinetic interactions in mice

Antidepressant drugs and ethanol: Behavioral and pharmacokinetic interactions in mice

The treatment of phobic anxiety by zimelidine

Zimelidine Distribution in a Sudden Death*

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