Talk:Levomepromazine

Sedative neuroleptic non plus ultra.
I just wanted to mention that levomepromazine is considered by the most experts known to me to be the most sedative neuroleptic among all. In a sedative/neuroleptic-naive patient, doses as low as 2,5 - 7,5 mg orally are so strongly sedative, that it can be used as hypnotic, or rather hypnagogic.--84.163.87.66 08:10, 28 April 2007 (UTC)

Structure/stereochemistry.
I would also like to stress, that the drug levomepromazine is a pure enantiomer, as the name already suggests: it is the (R)-enantiomer of the racemate mepromazine (formerly the L-isomer, hence the name levomepromazine). The structure and IUPAC name of the compound in the drugbox are those of the racemic mepromazine; correct IUPAC name of levomepromazine is (R)-, or (2R)-3-(2-Methoxyphenothiazine-10-yl-)-N,N,2-trimethylpropanamine. Structure can be seen here: http://img207.imageshack.us/img207/830/levomepromazinepl5.png Usually, oral tablets of levomepromazine contain the drug as hydrogenmaleate salt, liquid galenics (such as drops/oral solution/syrup and injections) contain the levomepromazine as hydrochloride salt.--84.163.87.66 08:42, 28 April 2007 (UTC)

(Adjuvant) use in agitated depression.
Quote: "It should never be used in the treatment of agitated depressions because this drug increases agitation through the side effect of akathisia." Though levomepromazine is nowadays seldom used, it was and ocassionaly is (at least in Europe) used also as an adjunct in seriously agitated depressive patients. The argument that it worsens the agitation through akathisia is questionable, because every antipsychotic can cause akathisia, and quite some are used in agitated depressive patients nevertheless. Levomepromazine is also not nearly as "bad" in causing akathisia as some less-sedative highly potent antipsychotics, e.g. haloperidol, pimozide or perphenazine. I could provide sources for the potential use of levomepromazine in agitated depression, but these are not in english (some in german). Yet levomepromazine, with advent of atypicals in the last two decades, lost much of its clinical importance even in central Europe, where it was for decades one of the most important sedative low potency antipsychotics. I therefore am not going to challenge its role in the treatment of MDD exhaustively, instead just attenuating the categorical point of this assertion (that it should never be used...; it was and sometimes still is, along with the invalidity of argumentation with akathisia, see above.). Cheers, --Spiperon (talk) 22:01, 8 January 2009 (UTC)

Affinities
It has different antagonist affinity at different receptors: - D2/D3/D4 > D1/D5; - alpha-1 >> alpha-2 adrenergic; - 5-HT2x > 5-HT1x.

More research needed. 69.196.8.13 (talk) 21:13, 1 November 2016 (UTC)

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