Systematic (IUPAC) name
Clinical data
Pregnancy cat.
  • ?
Legal status
  • Withdrawn worldwide
Routes Oral
Pharmacokinetic data
Bioavailability ?
Metabolism ?
Half-life 8.4 +/- 2.0 hours (parent compound)
19.4 +/- 3.6 hours (norzimelidine)[1]
Excretion ?
CAS number  N 60525-15-7 (anhydrous dihydrochloride), 61129-30-4 (dihydrochloride monohydrate)
ATC code N06
PubChem CID 5365247[3]
ChemSpider  YesY
Chemical data
Formula C16H17BrN2 
Mol. mass 317.224

Zimelidine (Zimeldine, Normud, Zelmid) was the first selective serotonin reuptake inhibitor (SSRI) antidepressant to be marketed. It is a pyridylallylamine, and is structurally different from other antidepressants.

Zimelidine was developed in the late 1970s and early 1980s by Arvid Carlsson, who was then working for the Swedish company Astra AB. It was discovered following a search for drugs with structures similar to brompheniramine (it is a derivative of brompheniramine), an antihistamine with antidepressant activity. Zimelidine was first sold in 1982.[4]

While zilmelidine had a very favorable safety profile, within a year and a half of its introduction, rare case reports of Guillain-Barré syndrome emerged that appeared to be caused by the drug, prompting its manufacturer to withdraw it from the market.[4][5] After its withdrawal, it was succeeded by fluvoxamine and fluoxetine (derived from the antihistamine diphenhydramine) in that order, and the other SSRIs.


  • Mechanism of action 1
  • Other uses 2
  • Side effects 3
  • Interactions 4
  • Dosage 5
  • See also 6
  • References 7

Mechanism of action

The mode of action is a strong reuptake inhibition of serotonin from the synaptic cleft. Postsynaptic receptors are not acted upon.

Other uses

Zimelidine was reported by Montplaisir and Godbout to be very effective for cataplexy in 1986, back when this was usually controlled by tricyclic antidepressants, which often had anticholinergic effects.[6] Zimelidine was able to improve cataplexy without causing daytime sleepiness.[6]

Side effects

Most often reported were:



The former doses were 200 to 400 mg daily in outpatients and up to 600mg in inpatients.

See also


  1. ^ Caille G, Kouassi E, de Montigny C. (1986). "Pharmacokinetic study of zimelidine using a new GLC method". Clinical Pharmacokinetics 8 (6): 530–40.  
  2. ^ Pubchem record
  3. ^ Pubchem record
  4. ^ a b Fagius J, et al. Guillain-Barré syndrome following zimeldine treatment J Neurol Neurosurg Psychiatry. 1985 Jan;48(1):65-9.
  5. ^ Arvid Carlsson. Review: A Paradigm Shift in Brain Research Science 2 November 2001: Vol. 294 no. 5544 pp. 1021-1024
  6. ^ a b Godbout R, Montplaisir J. (1986). "The effect of zimelidine, a serotonin-reuptake blocker, on cataplexy and daytime sleepiness of narcoleptic patients". Clinical Neuropharmacology 9 (1): 46–51.