Clinical efficacy of XXXX - @entity935 antagonists relative to classic neuroleptics.

@entity1 @entity1088 @entity21886 @entity935 @entity22521 @entity1109 @entity161 @entity1431 @entity750 @entity1767 @entity1037 @entity1090
@entity750 - @entity935 antagonists (SDAs) offer the possibility of improved treatment of @entity161 compared with conventional neuroleptics and have superior safety profiles. Clinical trial data have so far been published for only three SDAs to date, namely, @entity1090 , @entity22521 , and @entity1037 . Of these, extensive data are available only for @entity1090 , showing that at doses of 4 to 16 mg/day, it is superior to @entity1767 at 10 to 20 mg/day. Furthermore, @entity1090 , 6 and 16 mg/day, significantly improved negative/symptoms, whereas 20 mg/day of @entity1767 was ineffective. @entity1090 also appears to cause fewer @entity1109 ( @entity1109 ) than @entity1767 , 10 or 20 mg/day. Similar advantages of @entity1090 over @entity21886 have also been found. A clinical trial of @entity22521 showed that, at 20 mg/day, it was equivalent to @entity1767 , 16 mg/day, and caused fewer @entity1109 . @entity1037 , a chemical derivative of @entity1088 , has also been shown to be superior to @entity1767 (10 to 20 mg/day) at doses of 7.5 to 17.5 mg/day. In addition, at doses of 12.5 to 17.5 mg/day, @entity1037 was found to have a significantly superior effect on negative symptoms over @entity1767 , 10 to 20 mg/day. Doses of up to 17.5 mg/day of @entity1037 also caused fewer @entity1109 than @entity1767 , 10 to 20 mg/day. There was no evidence of any @entity1431 in @entity1 treated with @entity1037 in this small study (N = 335). The low @entity1109 liability of these SDAs, combined with their efficacy, suggests that SDAs should become the mainstay of treatment for @entity161 .
