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Zimelidine

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Zimelidine
200px
Systematic (IUPAC) name
(Z)-3-(4-Bromophenyl)-N,N-dimethyl-3-(pyridin-3-yl)prop-2-en-1-amine
Clinical data
  •  ?
  • Withdrawn worldwide
Oral
Pharmacokinetic data
Bioavailability ?
Metabolism ?
Half-life 8.4 +/- 2.0 hours (parent compound)
19.4 +/- 3.6 hours (norzimelidine)[1]
Excretion ?
Identifiers
56775-88-3 7pxN 60525-15-7 (anhydrous dihydrochloride), 61129-30-4 (dihydrochloride monohydrate)
N06AB02
PubChem [2] CID 5365247[2]
DrugBank DB04832 7pxY
ChemSpider 4517305 7pxY
UNII 3J928617DW 7pxY
ChEMBL CHEMBL37744 7pxY
Chemical data
Formula C16H17BrN2
317.224
 14pxN (what is this?)  (verify)

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.[3]

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

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:

Interactions

See also

References

  1. ^ Caille G, Kouassi E, de Montigny C. (1986). "Pharmacokinetic study of zimelidine using a new GLC method". Clinical Pharmacokinetics 8 (6): 530–40. PMID 6228368. doi:10.2165/00003088-198308060-00004. 
  2. ^ Pubchem record
  3. ^ Barondes, Samuel H. Better Than Prozac. p. 39–40. 
  4. ^ a b Fagius, J; Osterman, P. O.; Sidén, A; Wiholm, B. E. (1985). "Guillain-Barré syndrome following zimeldine treatment". Journal of Neurology, Neurosurgery, and Psychiatry 48 (1): 65–69. PMC 1028185. doi:10.1136/jnnp.48.1.65. 
  5. ^ Carlsson, A (2001). "A paradigm shift in brain research". Science 294 (5544): 1021–4. Bibcode:2001Sci...294.1021C. PMID 11691978. doi:10.1126/science.1066969. 
  6. ^ a b Godbout R, Montplaisir J.; Montplaisir (1986). "The effect of zimelidine, a serotonin-reuptake blocker, on cataplexy and daytime sleepiness of narcoleptic patients". Clinical Neuropharmacology 9 (1): 46–51. PMID 2950994. doi:10.1097/00002826-198602000-00004.