Cariprazine, sold under the brand name Vraylar among others, is an atypical antipsychotic developed by Gedeon Richter,[8] which is used in the treatment of schizophrenia and bipolar disorder.

[15][6][16] Cariprazine consistently improved clinical severity across a spectrum of patients with bipolar disorder or schizophrenia - effectively reducing psychosis, anxiety, manic and depressive symptoms.

[6] Cariprazine does not appear to impact prolactin levels, and unlike many other antipsychotics, does not increase the QT interval on the electrocardiogram (ECG).

In short term clinical trials, extrapyramidal effects, sedation, akathisia, nausea, headache, dizziness, vomiting, insomnia, anxiety, and constipation were observed.

One review characterized the frequency of these events as "not greatly different from that seen in patient treated with placebo"[21] but a second called the incidence of movement-related disorders "rather high".

[22][23] Regarding these side effects, the label of cariprazine states, "The possibility of lenticular changes or cataracts cannot be excluded at this time.

[21] In monkey studies, the administration of increasing doses of cariprazine resulted in a dose-dependent and saturable reduction of specific binding.

[31][32][33] Moreover, partial agonists, through their limited response triggering, ironically often have the tendency to occupy near all targeted receptors at relatively low dosages of the drug.

[34][35] This Partial agonist activity induces, considered through two depicted schematas in pharmacology (either in determining their intrinsic value of activity making up the proportions of how much of a dose of this molecule binds to postsynaptic (dopamine)receptors to inactivate further exacerbating signalling through agonists with locking the receptor making it unavailable for other molecules and binding to the presynaptic site at autoreceptors in the synaptic cleft which triggers the transmitting with agonistic behaviour, or, binding independently to the site in the synaptic cleft inducing a certain response in relative to its agonist maximum potential to activate its relative receptor, then, depicted as percentage of intrinsic activity for this specific partial agonist) but with both needed to express just a "half-maximal response" (caught statistically in EC-responsecurves in a response-inhibited curve for maximal activation in graphes stretched on their longitudes, which it's due to their effect enabling tendency in time) to be able to compete successfully, relative to their dependent natural agonists (in case of antipsychotics dopamine) at full partial agonist concentrations where it happens to turn out luckily that atypical antipsychotics working as partial agonists (or the so-called third generation; e.g. aripiprazole, cariprazine and brexpiprazole) demonstrating near full "occupation" or concentration of them in the brain where then this idea of competing and inhibiting dopamin tends to work out (because the alone-giveable possibility what a neuroleptic per definition has to be to called by this name, needs to have an antipsychotic (or positive symptoms erasing effect), e.g. being moodstabilizing), where without the pharmacologic term of a partial agonist would just work out to exacerbate and activate receptors by an unsatisfying concentration of it in the brain.

[36][37][38][39][circular reference] Cariprazine has high oral bioavailability and can cross the blood brain barrier easily in humans because it is lipophilic.

In February 2022, AbbVie requested approval by the US Food and Drug Administration (FDA) for adjunctive treatment for major depressive disorder.