Aripiprazole

Abstract

Oral aripiprazole (Abilify®) is an atypical antipsychotic agent that is approved worldwide for use in adult patients with schizophrenia. It is a quinolinone derivative that has a unique receptor binding profile as it exhibits both partial agonist activity at dopamine D(2) receptors and serotonin 5-HT(1A) receptors and antagonist activity at 5-HT(2A) receptors. In several well designed, randomized, clinical trials of 4-6 weeks duration, aripiprazole provided symptomatic control for patients with acute, relapsing schizophrenia or schizoaffective disorder. Furthermore, following 26 weeks' treatment, the time to relapse was significantly longer for patients with chronic, stabilized schizophrenia receiving aripiprazole compared with those receiving placebo. Using a variety of efficacy outcomes, aripiprazole showed a mixed response when evaluated against other antipsychotic agents in randomized clinical trials. Longer-term data showed that improvements in remission rates and response rates favoured aripiprazole over haloperidol, although, the time to failure to maintain a response was not significantly different between the treatment arms. On the other hand, improvements in positive and negative symptom scores mostly favoured olanzapine over aripiprazole, although, the time to all-cause treatment discontinuation was not significantly different between the two treatments. Several open-label, switching trials showed that aripiprazole provided continued control of symptoms in patients with schizophrenia or schizoaffective disorder. Using a variety of efficacy outcomes or quality-of-life scores, longer-term treatment generally favoured patients switched to receive aripiprazole compared with standard-of-care oral antipsychotics. Aripiprazole was generally well tolerated in patients with schizophrenia. In particular, its use seems to be associated with a lower incidence of extrapyramidal symptoms than haloperidol and fewer weight-gain issues than olanzapine. Aripiprazole also showed a favourable cardiovascular tolerability profile and its use was associated with a reduced risk of metabolic syndrome than placebo or olanzapine. As a consequence, aripiprazole may provide a more cost-effective treatment option compared with other atypical antipsychotics. In conclusion, oral aripiprazole provides an effective and well tolerated treatment alternative for the acute and long-term management of patients with schizophrenia.

Retrospective Study of Japanese Patients with Schizophrenia Treated with Aripiprazole

“…Consequently, reducing the incidence of glucose- and lipid-related side effects could lead to reduction in use of other drugs to counter these side effects and a huge reduction in the risk of developing other diseases. Studies by Croxtall [26] and Ganguli et al [27] support this study's results indicating that aripiprazole as having a low risk of metabolic syndrome.…”

Aripiprazole Lauroxil

“…Dehydro-aripiprazole accounted for approximately 38% of the aripiprazole exposure after aripiprazole lauroxil administration, which is comparable with what has been reported for oral aripiprazole. 21 …”

Repeated aripiprazole treatment causes dopamine D2 receptor up-regulation and dopamine supersensitivity in young rats

“…In clinical terms, adult humans respond well to aripiprazole, as it has an excellent side-effect profile (for reviews, see Stip and Tourjman, 2010; Croxtall, 2012). Even so, the response of younger patients to any pharmacotherapy cannot be deduced from observing adults, especially since children and adolescents are more prone to tolerability issues (Correll and Carlson, 2006).…”

“…Aripiprazole is purported to reduce both positive and negative symptoms, while exhibiting a good side-effect profile (for reviews, see Stip and Tourjman, 2010; Croxtall, 2012). Although aripiprazole is most typically categorized as a dopamine (DA) D2 partial agonist or as a functionally selective D2 ligand (Burris et al, 2002; Urban et al, 2007; Koener et al, 2012), this compound is also a partial agonist at serotonin 5-HT 1A receptors (Jordan et al, 2002; Shapiro et al, 2003), a full antagonist at 5-HT 2A receptors (Jordan et al, 2004), and it alters the expression of GABAergic binding sites and glutamatergic transporters (Segnitz et al, 2011; Peselmann et al, 2013).…”