The name of the company has been changed from Laurel Organics Limited to Kimia Biosciences Limited with effect from 04-01-2019 pursuant to the Scheme of Arrangement for Amalgamation of Kimia Biosciences Limited-Transferor Company-with Laurel Organics Limited -Transferee Company-as per the approval and Order of Honrable NCLT Chandigarh.
logo
+91-11-4706 3600
info@kimiabiosciences.com

Levosulpiride

LEVOSULIPRIDE

 

General Information:

Levosulpiride [RV 12309, L-sulpiride, levosulpride, Dislep® 25, Levopride®, Levopraid®] is a potent dopamine D2 receptor blocker that was originated by RavizzaFarmaceutici (now AbbVie). Levosulpiride is the levo enantiomer of sulpiride. The levo enantiomer shows better/similar pharmacological actions and lower incidence of toxic effects than both dextro as well as the racemic forms of the drug. Levosulpiride is marketed in Italy and South Korea, and is possibly available elsewhere in Europe and Asia. Levosulpiride does not appear to be available in North America. Levosulpiride is available as 25mg tablets, drops and in ampoules for parenteral administration. Generic versions of levosulpiride also appear to be available in some countries. Levosulpiride is primarily indicated in conditions like Anxiety, Depression, Gastro-esophageal reflux disease, Irritable bowel syndrome, Schizophrenia, Tourette's syndrome, dyspeptic syndrome, essential cephalgia, and can also be given in adjunctive therapy as an alternative drug of choice in Peptic ulcer, Vertigo.

Therapeutic Category:

Levosulipride falls under the Anti –Psychotic drugs category.

 

Primary Characterstics:

IUPAC Name:


N-[[(2S)-1-ethylpyrrolidin-2-yl]methyl]-2-methoxy-5-sulfamoylbenzamide

Molecular           Formula:
C15H23N3O4S

 

Molecular Weight:

341.4 g/mol

Molecular Structure:

 

Mechanism of Action:

Levosulpride is an atypical antipsychotic agent that blocks the presynaptic dopaminergic D2 receptors.1 Like its parent compound, levosulpiride shows antagonism at D3 and D2 receptors present presynaptically as well as postsynaptically in the rat striatum or nucleus accumbens2 . The preferential binding of the presynaptic dopamine receptors decreases the synthesis and release of dopamine at low doses whereas it causes postsynaptic D2 receptor antagonism at higher dose. This receptor profile of the drug along with its limbic selectivity explains its effectiveness in the management of both positive and negative symptoms of schizophrenia