BENZOQUINOLINE INHIBITORS OF VESICULAR MONOAMINE TRANSPORTER 2

1 . A method of treating Parkinson's disease levodopa-induced dyskinesia in a subject in need thereof, comprising administering a therapeutically effective amount of a compound that is

or a pharmaceutically acceptable salt thereof,

wherein each position represented as D has deuterium enrichment of no less than about 10%.

2 . The method of claim 1 , further comprising administering an additional therapeutic agent.

3 . The method of claim 2 , wherein said additional therapeutic agent is a dopamine precursor, DOPA decarboxylase inhibitor, catechol-O-methyl transferase (COMT) inhibitor, dopamine receptor agonist, neuroprotective agent, NMDA antagonist, or anti-psychotic.

4 . The method of claim 3 , wherein said dopamine precursor is levodopa.

5 . The method of claim 3 , wherein said DOPA decarboxylase inhibitor is carbidopa.

6 . The method of claim 3 , wherein said catechol-O-methyl transferase (COMT) inhibitor is entacapone or tolcapone.

7 . The method of claim 3 , wherein said dopamine receptor agonist is apomorphine, bromocriptine, ropinirole, or pramipexole.

8 . The method of claim 3 , wherein said neuroprotective agent is selegeline or riluzole.

9 . The method of claim 3 , wherein said NMDA antagonist is amantidine.

10 . The method of claim 3 , wherein said anti-psychotic is clozapine.

11 . The method of claim 1 , wherein said treatment results in at least one clinical effect which is:

improved Unified Parkinson's Disease Rating Scale scores;

improved Abnormal Involuntary Movement Scale scores;

improved Goetz Dyskinesia Rating Scale scores;

improved Unified Dyskinesia Rating Scale scores;

improved PDQ-39 Parkinson's Disease Questionnaire scores; or

improved Global Primate Dyskinesia Rating Scale scores.

12 . The method of claim 1 , wherein said treatment results in at least one effect which is:

decreased inter-individual variation in plasma levels of said compound or a metabolite thereof as compared to the non-isotopically enriched compound;

increased average plasma levels of said compound per dosage unit thereof as compared to the non-isotopically enriched compound;

decreased average plasma levels of at least one metabolite of said compound per dosage unit thereof as compared to the non-isotopically enriched compound;

increased average plasma levels of at least one metabolite of said compound per dosage unit thereof as compared to the non-isotopically enriched compound; or

an improved clinical effect during the treatment in said subject per dosage unit thereof as compared to the non-isotopically enriched compound.

13 . The method of claim 1 , wherein the method reduces a deleterious change in a diagnostic hepatobiliary function endpoint, as compared to the corresponding non-isotopically enriched compound.

14 . The method of claim 13 , wherein the diagnostic hepatobiliary function endpoint is alanine aminotransferase (“ALT”), serum glutamic-pyruvic transaminase (“SGPT”), aspartate aminotransferase (“AST,” “SGOT”), ALT/AST ratios, serum aldolase, alkaline phosphatase (“ALP”), ammonia levels, bilirubin, gamma-glutamyl transpeptidase (“GGTP,” “γ-GTP,” “GGT”), leucine aminopeptidase (“LAP”), liver biopsy, liver ultrasonography, liver nuclear scan, 5′-nucleotidase, or blood protein.