From Wikipedia, the free encyclopedia
Jump to: navigation, search


Why isn't there any mention of it's potential for extrapyramidal side effects

The reason there's no mention is because there's not any. The studies haven't found significant evidence of them. It's a dopamine receptor AGONIST. Technically, if it did what they think, it could be used to treat parkinsons. (talk) 03:23, 1 May 2009 (UTC)

hogwash. —Preceding unsigned comment added by (talk) 15:14, 15 May 2011 (UTC)

this is a misunderstanding of partial agonism. Partial agonists usually function as a competitive antagonist at the receptor site. A full agonist will exhibit 100% effect, while a partial agonist has <100% effect leading to a relative reduction in function despite being an agonist. Therefore, the partial effect exhibited by aripiprazole at the dopamine receptor sites(2-4 primarily) decrease the effect of dopamine and can cause parkinsonian types of side effects.

sure it can cause EPS. it's dose-related from 5%-16%

                            Pharm D at psych hospital


Surely weight gain is a side effect as with other atyp anti psy.??? 10:22, 26 September 2007 (UTC)

Can anyone find specific information about what this medication does?

ADHD instead of due to the calming effect it has although it is not licensed for ADHD treatment What specific kind of information are you looking for?

Search Google for aripiprazole and you will find more information than you may wish to digest.

This is just medical justifiation of many cases of mind control

Yes, I need this class of drug. Thanks for the info - I am going on a drug trial of this.

The statement that there are case reports of abilify inducing mania needs citations. Medline does not show any such case reports in my search, and I have never heard this. Abilify is used to treat mania. It can cause akathesia and states of agitation, which are not the same as mania, although may be confused with mania. It does not cause weight gain, unlike most of the other atypical agents. —Preceding unsigned comment added by Lizdoc (talkcontribs) 17:31, 14 February 2008 (UTC)

Anecdotal evidence[edit]

I know Wikipedia prohibits original research, but I know that I experienced tardive dyskinesia and insomnia after only about a week on this drug (prescribed for manic break). I was also taking an antibiotic that is metabolized by the liver, so I think that was blocking the pathway and may have strengthened the effect some. Is there any data to be had as to how common such reactions are among users of the drug, or is still too early? I was rather upset, to say the least, once I had recovered to find that I had been put on such an untried medication. Now I'm on Depakote, which seems to stabilize me without any significant side effects Evan Donovan 03:10, 25 March 2006 (UTC)

Anti-biotics commonly interact with many drugs.J. M. 02:25, 22 May 2006 (UTC)
What you was experiencig after a week of aripiprazole medication almost certainly was not tardive dyskinesia, unless you've been taking other antipsychotics before at least for some weeks (rather months or years); what it well could have been would be early extrapyramidal syndrome; in this cases, dystonia, dyskinesia, akathisia and the like are not uncommon. Insomnia could have been a side-effect of aripiprazole medication; and some antibiotics are certainly inhibiting microsomal metabolism of other drugs, aripiprazole included. Wish you all best with current therapy.--Spiperon 09:21, 4 May 2007 (UTC)

I would not consider this "original research" anymore maybe it is time some doc wrote an article on this so we can make it a fact. Oh i know this is not a "request page" but can someone clarify that MAJOR WARNING!!! message at the bottom of this page? its making me nervous.

I would just like to add that within one month of my starting Abilify, I started having severe restless leg syndrome. Just another side effect to look out for with this drug. —Preceding unsigned comment added by (talk) 16:31, 28 March 2008 (UTC)

I thought I would add that I had been on Abilify for a short while, but started having linguistic hallucinations (basically, auditory hallucinations, however as a polyglot I couldn't attach a specific language to any of the hallucinations, just random spontaneous hallucinations of meaning). I tried to offer my pen to a wall one time. It's probably important to note that this drug shouldn't be used for anyone without mood-stabilization issues in their depression. --Puellanivis (talk) 08:06, 16 December 2008 (UTC)

Abilify is a dopamine receptor AGONIST. What you guys are describing is basically impossible if you were normal. The person who says RLS, it's probably tremors - abilify increases motor activity (though dopamine), you're probably only noticing because when you go to sleep, dopamine levels RISE until you fall asleep. And the other person who says hallucinations - you're probably right. Hallucinations get worse on Abilify, but usually only after pre-treatment with a typical antipsychotic - a typical antipsychotic can upregulate dopamine up to 98% - check haloperidol, but I don't doubt someone will develop hallucinations after taking it normally. Anecdotally, I'm having some language difficulty on Abilify (I say the wrong words e.g. if they sound alike) and my attention is reduced to nothing - like from playing video games for an hour now I quit after five mins, but here's the catch - I have treatment resistant depression, and the medicine isn't working for that anyway.

Here's one link for agonism proof:

Risperidone to Abilify relieves Tardive Dyskinesia: (talk) 03:42, 1 May 2009 (UTC)

It is a partial and selective dopamine agonist, your sir are a tard. Anti-psychotics, typical or atypical, should be used with caution in anyone. Also raising dopamine lowers serotonin and raising serotonin lowers dopamine, so perhaps there is something to do with that if it actually was a true dopamine agonist (like cocaine or amphetamine) (talk) 19:36, 4 June 2009 (UTC)

This is a misunderstanding of pharmacology. Abilify is a partial agonist, meaning that is exhibits less effect on the receptors than does a full agonist, in this case dopamine. It is a competitive antagonist since they are both capable of exerting effect at the receptor site, which REDUCES the effects of dopamine. In parkinson's disease, there is a relative lack of dopamine receptors, using abilify would exacerbate the disease state by inhibiting dopamine activity. Hope that helps.

PharmD at a psychiatric hospital — Preceding unsigned comment added by (talk) 20:23, 16 August 2013 (UTC)


Please correct "miscle", etc under "Side Effects"

Tardive dysphrenia[edit]

I've included a link to the new wiki Tardive dysphrenia (under See Also), which I hope, must be of interest to this one. Cheers, LFrota.

Major Warning![edit]

Waring: This drug (even at low dosages) may cause liver failure/disease, high chlosterol, diabetes, and weight gain, etc.

This guy better be screwing around! ill rather die than to go trough this kinda fucked up stuff... oh and cholesterol is misspelled... can someone clarify this ASAP? (please?)

There's no evidence of those effects. (talk) 05:11, 1 May 2009 (UTC), I swear to fucking god you work for a pharma company, weight gain is common with dopamine changes because less dopamine = more eating (that is why amphetamine for example stops you eating since it is such a potent dopamine agonist), stop spewing shit out of your mouth. (talk) 19:38, 4 June 2009 (UTC)
This is a dopamine agonist too, dork. — Preceding unsigned comment added by (talk) 19:29, 5 November 2011 (UTC)
Nope, aripiprazole is technically a dopamine "partial" agonist. See: Tkadm30 (talk) 11:13, 26 March 2017 (UTC)

Not an azole[edit]

Who names these drugs? It's not an azole! Bloody pharmacologists.

neither are metronidazole or tinidazole. they're nitroimidazoles. proton pump inhibitors have -azole at the ending as well: pantoprazole, omeprazole, etc. there are differenct classes of antibiotics which end in -mycin: macrolides, lacosamides and aminoglycosides end in -mycin. — Preceding unsigned comment added by (talk) 10:08, 7 September 2015 (UTC)

New Indication for Major Depressive Disorder[edit]

On 11/16/2007, US FDA approved aripiprazole for use as adjunctive therapy for Major Depressive Disorder (unipolar depression).

For this purpose, it is usually prescribed at a much lower dose than for bipolar or schizophrenia (schiz= 10-15 mg/day, bipolar=15-30 mg/day, major depress=5-10 mg/day with starting dose of only 2 mg/day).

This is listed on FDA website:

and new FDA labeling info is here:,021713s013,21729s005,021866s005lbl.pdf

Crazymiddle (talk) 03:57, 22 November 2007 (UTC)

I've just been perscribed this drug at 5mg to replace the Seroquel I've been taking for the last 7 months after having gained 30 pounds in 7 months. But this doesn't seem to be any better when I read the side effects. Has anyone actually taken this drug and did you gain weight or not? What about the diabetes issue? —Preceding unsigned comment added by (talk) 20:19, 20 June 2008 (UTC)

I just recently started taking it and my appetite is way up, so I guess it can make you overweight. Not sure about the Diabetes, though. It seems likely that diabetes would be a product of increased appetite, thus making Apiprazole only the indirect cause.

3D structure[edit]

It would be nice to get a 3D representation of the aripiprazole molecule. Is their anyone out there that could add one?--Metalhead94 (talk) 18:02, 19 November 2008 (UTC)

Someone added one, but an animated one, which I find next to unusable, and removed the stick-and-balls one. I'm pretty sure I've seen click-for-animation images somewhere on Wikipedia. Is there a better way to have those than a static GIF linked to a spinning one? Pending that, I'll remove the animated GIF and restore the ball-and-stick one. The Crab Who Played With The Sea (talk) 08:32, 22 July 2013 (UTC)

Using Abilify for ADHD?[edit]

I know a woman who has gotten Abilify for her ADHD. Does anybody know if this is a known usage of Abilify? --Algotr (talk) 22:41, 29 April 2009 (UTC)

Abilify has been researched for ADHD, and while there's nothing really definitive, at least one pilot study in children with no comorbidities and two studies in children and adolescents with comorbid bipolar disorder have been done, with mixed results (two favorable, one unfavorable wrt reduction in ADHD symptoms). --Aurochs (Talk | Block)
I think that information should be in the article as well! --Algotr (talk) 18:32, 14 May 2009 (UTC)
So do I. I just need to get up off my lazy ass and finish writing the therapeutic uses section. --Aurochs (Talk | Block)

"Aripiprazole is at least as effective as haloperidol at reducing manic symptoms"[edit]

I find this statement pretty dubious. I can understand how it would be better tolerated, but, I highly doubt it is AT LEAST as effective as haloperidol. This isn't just my original research or POV either, I think most psychiatrists would agree, I don't see aripiprazole being very effective in cases that would require Haloperidol. Any feedback is welcome.--Metalhead94 (talk) 13:57, 10 July 2009 (UTC)

I was only following the abstract of the article I cited. I don't have access to the article itself, nor the training to determine whether or not it's reliable. If you're able to review the study and debunk it, be my guest. However, my understanding is that anecdata is not a reliable source as far as Wikipedia is concerned. --Aurochs (Talk | Block)
Okay, I just reviewed what I could of the article, and it appears that most of the authors were employed by either Brisol-Myers Squibb or Otsuka. That alone makes the abstract suspect, but it doesn't necessarily disprove the findings. If anybody can get me a copy of the article, I would be pleased to review the data to the best of my ability. In the meantime, I'm tagging it as a possibly unreliable source. --Aurochs (Talk | Block)
I agree. I generally am careful around studies funded by pharmacuetical companies themselves, as they often seem slightly biased, especially when it is the very company[ies] that market the drug. Thanks for the feedback.--Metalhead94 (talk) 19:29, 11 July 2009 (UTC)

drug studies are almost exclusively funded by the manufacturers of the medications. bias is searched for by peer-reviewers in the methods, statistics, exclusion and inclusion criteria etc to ensure that any bias on the part of the authors is recognized. articles which are determined to be biased are not usually published in the better journals (lancet, NEJM, or JAMA) and are then rejected outright, or the authors will have them published in less reputable journals. the term for this is the 'power' of a publication (publication power). — Preceding unsigned comment added by (talk) 11:49, 6 September 2015 (UTC)

Side effects: citation needed for sudden death claim under side effects section[edit]

I've marked that tidbit of info with a citation needed tag. If anyone can find a source that says Aripiprazole causes sudden death, go ahead and add it in because I can't seem to find one. -- (talk) 15:13, 11 February 2010 (UTC)


Where do they make and produce abilify? —Preceding unsigned comment added by Eupeyd (talkcontribs) 21:05, 24 March 2010 (UTC)


Why does the posted synthesis use a chemical weapon (mustard gas, in this case)? I mean it's great to find new applications for chemical weapons but I am somewhat skeptical that this is the correct synthetic pathway. That and it doesn't come up in any patent/research article related to synthesis of this drug. —Preceding unsigned comment added by (talk) 19:51, 19 May 2010 (UTC)

Use of Ki values[edit]

Is it really necessary to have a long list of numbers that are completely meaningless to the average reader, and easily found by anyone who does know what they mean? What's especially problematic is that there's only one source given for these numbers, even though different labs can come up with completely different values. There's no real assurance given in the text that these numbers closely approximate other published data. I just feel like aripiprazole's affinity for various receptors can be easily explained without getting so technical, and that anyone who wants more precise information (i.e. numbers) can follow the citations. --Aurochs (Talk | Block)

It's been over a month since I posted this, and nobody has responded. I'm going to go ahead and remove the list of values from the page. --Aurochs (Talk | Block) 00:31, 26 September 2011 (UTC)
It's an encyclopedia. Please put the table back. — Preceding unsigned comment added by (talk) 19:31, 5 November 2011 (UTC)
Exactly. It's an encyclopedia, not a technical reference. I do not expect to see long lists of data in any encyclopedia article. --Aurochs (Talk | Block)

Ki ratings are very useful in my opinion. — Preceding unsigned comment added by (talk) 10:05, 7 September 2015 (UTC)


It would be helpful to have a section entitled "Litigation" on this drug and many others. The best way to gauge the seriousness and pervasiveness of the side-effects for drugs like Abilify is to look at the lawsuits. Who is suing? Why? Have class actions been initiated? What are the characteristics of the Plaintiffs? What are the claims? Wrongful death? Loss of consortium? Serious bodily harm? Have doctors been sued as well as the drug companies? Have settlements been reached? If so, how much? Has a verdict been rendered? If so, where and for how much? Has the research that lead to the approval of this drug been subjected to scrutiny through the deposition process? If so, what were the results? Were admissions made? Etc. — Preceding unsigned comment added by (talk) 04:46, 29 May 2012 (UTC)

Binding Profile[edit]

There is an error there: aripiprazole is 5HT2A partial agonist, not parcial antagonist. Correcting it. Thank you. — Preceding unsigned comment added by (talk) 13:36, 13 May 2013 (UTC)

Ongoing Phase 3 trial[edit]

Is the currently ongoing phase 3 trial (efficacy and tolerability of aripiprazole depot IM injection for treatment of bipolar disorder I) worth mentioning in the wiki? Here's the link: I'd make that nicer... but I don't know how to do a link in wiki markup! Sorry... Havensfire (talk) 18:20, 22 June 2013 (UTC)

We do not typically mention ongoing trials unless they have been discussed in a secondary source (thus putting them into context). Doc James (talk · contribs · email) (if I write on your page reply on mine) 18:30, 22 June 2013 (UTC)

Chemical structure diagrams with no description[edit]

If I draft a description, can someone check for me that it's accurate? The Crab Who Played With The Sea (talk) 08:39, 22 July 2013 (UTC)


Some portions of the article say irritability associated with autism, and some just say autism. The drug is approved by the FDA for the former. It's misleading to only say autism, and I believe this should be changed. Thoughts? Archdiamond (talk) 17:09, 3 October 2013 (UTC)

Is this the same as saying that it treats symptoms? MaynardClark (talk) 14:46, 26 April 2014 (UTC)

no. Irritability isn't a core symptom of autism. (talk) 21:55, 22 November 2015 (UTC)

...Society and Culture...?[edit]

Society and Culture seems like a weird heading for the information it contains, but I'm having trouble coming up with a better one.Archdiamond (talk) 17:17, 3 October 2013 (UTC)

I agree, I was expecting more about how commercials advertising the drug have become the target of jokes. Seriously the list of side effects is comical. — Preceding unsigned comment added by (talk) 19:36, 4 July 2014 (UTC)

Diabetes etc.[edit]

The article mentions diabetic ketoacidosis as a side effect, but it doesn't say anywhere that Abilify can cause blood sugar problems that lead to diabetes. To me, saying diabetic ketoacidosis does not imply that. Thoughts? Archdiamond (talk) 17:19, 3 October 2013 (UTC) one published adverse effect is hyperglycemia which can lead to ketoacidosis if untreated. — Preceding unsigned comment added by (talk) 11:55, 6 September 2015 (UTC)

Removed large tract of uncited text added by good faith edit by IP, I've placed it below if anyone wants to restore it with citations[edit]

Misuse of Aripiprazole (Abilify)

Receptors are activated by agonists and blocked by antagonists. Upon binding to its receptors, an agonist will trigger a cascade of biochemical and/or physiological reactions. Each agonist has two characteristics: affinity and efficacy. Affinity is the reciprocal of dissociation constant. It indicates how tightly an agonist binds to its receptors. Efficacy was measured by the effectiveness of the response elicited by an agonist. A full agonist produces 100% response while an antagonist produces no response and blocks the activation of receptors by its agonists. A partial agonist, also called a partial antagonist, produces less than 100% but more than 0% response. It blocks a full agonist but can still produce partial response. It also can replace an antagonist and unblock the blockage by the antagonist. As a result, it will produce a partial response. Using a simple analogy, we may say a full agonist opens a door fully; a full antagonist keeps the door closed. A partial agonist will keep the door ajar.

Abilify is a partial agonist on the Dopamine D2 receptor site. It has been misused with full D2 antagonists, such as Risperdal, Zyprexa, Geodon, Haldol. It will attenuate the effects of a full D2 antagonist. It has been observed that Abilify worsened TD, similar to withdrawal TD, and exacerbation of psychosis in patients who were on a full antagonist and then started Abilify.

Partial agonists have used for various reasons. Subutex, a partial agonist on opioid mu receptors, is used for opioid withdrawal and addiction. If a patient has been on a full opioid agonist, the patient has to wait until moderate withdrawal symptoms occur before starting Subutex. If it is used too early, it can precipitate opioid withdrawal symptoms. Suboxone, a combination of Subutex and Naloxone, a full opioid antagonist, is used to prevent perenteral use of Subutex. When administered sublingually, due to its low bioavailability, Naloxone has minimal effects on Subutex activity, whereas when administered intramuscularly, Naloxone is able to block the partial agonist activity of Subutex. Chantix, a nicotinic acetylcholine receptor partial agonist, has been used for nicotine cessation. It produces partial activation of the nicotinic acetylcholine receptors so that a smoker will not have severe nicotine withdrawal symptoms and at the same time, the smoker will not be able to feel the full effects of nicotine as Chantix occupies the receptor and prevent nicotine from binding to the receptor. Acebutolol, a partial agonist on beta adrenergic receptor site, produces a lesser reduction in heart rate and cardiac output than does a full antagonist (propranolol or atenolol). It has been used on hypertensive patients with slow heart rate.

Abilify is also a 5-HT-2A receptor antagonist and can alleviate depressive symptoms. But it should not used when a patient is on a D2 antagonist or a D2 agonist.

In summary, Abilify interferes with full D2 antagonists or agonists. It should not be used with those medications. Economically, it is a waste of money. Pharmacologically, it does not make sense. Clinically, it is not a good practice.Wzrd1 (talk) 16:13, 16 October 2013 (UTC)

Off-Label Uses[edit]

Can the edit (inserted sentence) "Abilify is sometimes used to treat ADHD instead of due to the calming effect it has although it is not licensed for ADHD treatment" be rewritten as "Abilify is sometimes used of-label for ADHD because of its calming effect."? MaynardClark (talk) 14:46, 26 April 2014 (UTC)

That would be an off-label use. It'd require a citation, but we should first get some consensus here on including it. Anyone, is it a common off-label use for ADHD that would make it notable enough to include in the article?Wzrd1 (talk) 14:57, 26 April 2014 (UTC)

Edits of August 2014[edit]

@Jmh649: what can we do here to make this better? I am convinced that despite the limitations of these drugs and the excessive marketing that gave the whole industry yet another black eye, the statement that "there is tentative evidence that aripiprazole may be useful in schizophrenia" does not represent mainstream medical thought.

Cochrane in particular has seemed pretty inconsistent in their conclusions:

  • Comparing aripiprazole to placebo:
  • In 2006, based on 15 trials/7110 people comparing aripiprazole to placebo or a first gen antipsychotic, "Compared with placebo, aripiprazole significantly decreased relapse in both the short and medium term"
  • In 2011, based on 9 RCTs with 2585 people (comparisons to placebo only), this conclusion is softened by the same author to "Aripiprazole may be effective for the treatment of schizophrenia."
  • Comparing aripiprazole to other antipsychotics:
  • In 2006, based on 15 trials/7110 people comparing aripiprazole to placebo or a first gen antipsychotic, "Aripiprazole is not much different from typical antipsychotic drugs with respect to efficacy. However it presents significant advantages in terms of tolerability due to its favourable adverse effects profile."
  • In 2009, aripiprazole is compared to other atypicals (4 trials with 1404 participants). The article states "Aripiprazole may be somewhat less effective than olanzapine, but more tolerable in terms of metabolic effects and sedation. There is no evidence for a difference in efficacy compared to risperidone, but far better tolerability..."
  • In 2013, a non-Cochrane analysis by Leucht, concludes confidently that the efficacy of all of the 15 atypical and typical antipsychotics examined in their meta analysis is similar, and all are "substantially better" than placebo.
  • In 2014 and 2013 the Cochrane group publishes meta analyses comparing aripiprazole to other atypicals. Compared to the 2009 Cochrane meta analysis, the number of patients and trials has exploded to 17,244 and 174, but now every comparison is followed by the phrase "low level of evidence" or "very low level of evidence" complaining about the trial designs and endpoints, emphatically making clear that no comparison can be made with confidence. NOtably, one of the co-authors is Leucht, who reached very different conclusions in his separately published meta analysis in 2013 (above)

As the amount of data increased, the tentativeness of the conclusions only grew. Perhaps one aspect of this was the revelation of selective publication and increasing understanding of its impact, but even the earliest study states "We contacted relevant pharmaceutical companies, the FDA and authors of trials for additional information." Furthermore, dramatically different conclusions were reached in two studies co-authored by Leucht in the same year. That co-written with Cochrane collaborators was by far the more critical/skeptical.

I don't know the best way to approach this, but I am increasingly skeptical that meta analysis is much more than the writing of detailed editorials. The process of analysis is opaque and not readily evaluated by the reader. Different (and sometimes the same!) authors look at the same data and reach different conclusions by means that one cannot readily examine and critique for oneself.

And somehow, whatever mistakes are sometimes made by these agencies, the opinions of the FDA and the EMA needs to come into play. Ultimately, if the analysis is subject to the prejudices and pre-judgments of those doing the analysis, the more people involved in the analysis the better. And the regulatory opinions involve scores of people not two to eight.

I'm not trying to be difficult here, but if you have any thoughts on navigating this issue I would appreciate it. Somehow in following Cochrane, we've ended up with "may be useful" in the lede of an article about a drug that has been approved by regulatory agents on every continent, which is recommended by NICE, and which is prescribed millions of times each year by psychiatrists who are quite competent to judge whether or not a patient is psychotic and who are familiar with competing drugs. We set aside all of this and rely on a paper written by 6 analysts, one of whom expressed very different opinions in a separately published paper the same year written by 2 analysts, each of whom has fewer than 20 publications under their belt. It seems to me that this is not the best way, and if you have any thoughts on alternative approaches that would be acceptable to you, I'd be eager to hear them. Formerly 98 (talk) 19:44, 10 August 2014 (UTC)

Will take me a little time to review all this. Doc James (talk · contribs · email) (if I write on your page reply on mine) 05:18, 12 August 2014 (UTC)
Would changing to "Aripiprazole may be useful in schizophrenia" be good? Doc James (talk · contribs · email) (if I write on your page reply on mine) 05:49, 12 August 2014 (UTC)
Yes, I'm guilty of throwing a very long-winded, open-ended question about the nature of medical evidence at you. If you are interested in thinking about this and getting back to me at your leisure, that would be great. If not, I understand entirely. For now I'll leave it as is, and perhaps circle back in a week or two and see if I can do something better (and mutually acceptable) with it.
One thing that I found interesting in this case is that as time rolled by, the nature of the data did not change so much as did the Cochrane Group's interpretation of its significance and meaning. The p values favoring efficacy remain the same in the later studies, but the analysts now question the validity of the endpoints, the impact of the high dropout rates, and other trial features. Since this interpretation aspect is not derived mathematically, does the meta analysis in this case differ in evidence quality from any other review and its associated expression of opinion? The facts did not change much, but the interpretation changed dramatically.
Anyway, that's what I've been thinking about. If its interesting to you, I'd be interested in your thoughts. If I'm just being a data geek, kindly disregard this entire note. Formerly 98 (talk) 06:28, 12 August 2014 (UTC)Formerly 98 (talk) 06:18, 12 August 2014 (UTC)
Agree we need to add the positions of major guidelines. Am not home for a week yet. (talk) 15:54, 12 August 2014 (UTC)
@Jmh649: can you email me reference 9? I'm a little concerned that the prominence of the statement "there is tentative evidence of efficacy" is a little like a see-saw, with half a dozen Cochrane authors on one side sitting on the ground, and all of current treatment guidelines and clinical practice on the other side, up in the air. Formerly 98 (talk) 01:49, 24 August 2014 (UTC)
Okay let me try to get you a copy. IMO there is room for both the position of guidelines (which is often simply expert opinion) and the best available evidence. We have the same situation with electronic cigarettes. All the guidelines raise the concern of addiction in children yet their is tentative evidence of no concern. We do and should mention both. Doc James (talk · contribs · email) (if I write on your page reply on mine) 21:38, 24 August 2014 (UTC)

Which ref do you want? Doc James (talk · contribs · email) (if I write on your page reply on mine) 21:44, 24 August 2014 (UTC)

This is a bland statement that is not really needed "The efficacy of aripiprazole for the treatment of acute exacerbations of schizophrenia and for the prevention of relapses has been examined by several groups."
This "Overall, there is strong support for the efficacy of aripiprazole in the treatment of acute psychotic episodes. The Cochrane collaboration evaluated aripiprazole and 14 other anti-psychotics in 2013, concluding that aripiprazole on average produced a 43% reduction in symptoms. It was found to be more effective than asenapine, lurasidone, ziprasidone, and chlorpromazine, but less effective than amisulpride, olanzapine, and clozapine" has issues for a number of reasons. First of all the ref is not a Cochrane review but a lancet paper. Second most of the confidence intervals overlap and thus one cannot make the statement about one be better than the other that that was made.Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:14, 24 August 2014 (UTC)
Agree that I made several errors here. Formerly 98 (talk) 10:22, 25 August 2014 (UTC)

Cochrane reviews of antipsychotics[edit]

With much temptation to cherry pick, I did my best here to fairly pick some representative examples of how Cochrane findings translate to global summaries of antipsychotic effectiveness. My conclusion is that the latter correlate with the authorship much more so than with the findings, and thus should not be used. Formerly 98 (talk) 18:06, 24 August 2014 (UTC)

Ah... We should not use the global summaries of Cochrane reviews? Unclear why.Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:16, 24 August 2014 (UTC)
I've tried to make two points, Doc.
  • The added external validity of a meta analysis as I understand it comes from the fact that is is averaging across many studies. This is true for the data analysis, such as when they find that there is no statistically significant difference in relapse rate. But when they go on to opine about the adequacy of the trial design or the absence of secondary endpoints they feel should have been included, they are just opining like the author of any primary citation.
  • As seen below, they do not opine consistently. Therefore its not really high value information.
The first point is probably more relevant than the latter one.
I think it would be fair to respond to the information and comments that I posted and not simply do the "Ah, I don't see why" routine. Its a completely nonspecific response, and I think I've put in enough good faith effort here as an editor to deserve a real one, whatever our differences in opinion.
And with due respect for your expertise and role here (genuinely, that's not a wise ass remark), I think you missed the point on your edits. Every treatment guideline, as well as Cochrane, the FDA, and the EMA distinguishes between studies designed to show efficacy in acute psychotic episodes and as prophylactic maintenance therapy. That difference is as real as primary and secondary prevention with statins in heart disease. Its not really that complicated that our readers can't understand it, and you're eliminating as useful part of the description of treatment.
I certainly don't want to edit war with the head of the Wikipedia Medcine project. If you are not willing to compromise, would you do me a favor and post a RFc? (Specifically with regards to the material you changed in this article, not the broader philosphical question about sourcing). Thanks.
Formerly 98 (talk) 23:15, 24 August 2014 (UTC)
You have raised a few issues. Which would you like to have a RfC regarding? That we not summarize the global summaries of the Cochrane collaboration?
That we instead ask editors to look at the results ourselves and provide their own interpretations? I have added some concerns regarding your edits in the section above. Doc James (talk · contribs · email) (if I write on your page reply on mine) 23:36, 24 August 2014 (UTC)
I think I was a initially put off by the extent of the edits, and reacted without reading it as carefully as I should have. I apologize for this. Let me look some more and respond more thoughtfully. Formerly 98 (talk) 23:40, 24 August 2014 (UTC)
I am happy to debate improved wording / a compromise.
The "adequacy of the trial design or the absence of secondary endpoints" put the conclusions into perspective. The endpoints used separate clinically meaningful from non clinically meaningful statistically significant conclusions. Doc James (talk · contribs · email) (if I write on your page reply on mine) 23:36, 24 August 2014 (UTC)
Frankly I'm still a bit put off a bit by the phrase "may be useful" in the opening sentence. Cochrane says its equivalent to other antipsychotics, as do the major treatment guidelines, and ALL the treatment guidelines say to treat with an antipsychotic.
Nonetheless, I recognize that the current text probably already reflects some compromise on your part. Let me think about this overnight and see if I have anything new to say tomorrow. Thanks. Formerly 98 (talk) 23:49, 24 August 2014 (UTC)
I have used "may be" as there are concerns regarding what endpoints were looked at and the quality of the evidence. We now state that it decreases relapse in definitive terms and improves treatment compliance compared to placebo. Doc James (talk · contribs · email) (if I write on your page reply on mine) 23:52, 24 August 2014 (UTC)
Continuing this conversation with some concern that I may be viewed as quibbling, but this was exactly the subject of my broader comment above. The Cochrane authors had concerns about the adequacy of the endpoints and the quality of the evidence, but I did not see those concerns voiced elsewhere. Nor in most cases did other Cochrane authors express similar concerns (at least not to the extent of going to "may be useful") when encountering similar shortcomings in trials of other antipsychotics. So the concerns being expressed here have not been voiced by non-Cochrane authors regarding aripiprazole, nor have they been voiced by Cochrane authors in most cases when encountering similar data sets for non-aripiprazole antipsychotics.
So I'm inclined to think that this is undue weight given the opinion of 6 authors, and that the fact that the meta analysis itself is a secondary source does not give their opinion greater weight than those of the other 300 or so psychiatrists who have written on the subject of aripiprazole.
I'm not asking you to do anything right now except to consider this idea and the possibility that I'm not just being a shill or a general pain in the ass. I can certainly understand that I sometimes give that impression. :>) Formerly 98 (talk) 00:10, 25 August 2014 (UTC)
Interesting paper here. The authors were quite critical of the Cochrane methodology in schizophrenia trials, in particular their failure to follow pre-specified inclusion and exclusion criteria or to disclose that they had disregarded the protocol. For what its worth, they also concluded that the 2006 aripiprazole review probably overestimated aripiprazole's efficacy.
"We found Cochrane reviews varied in their stated approach to handling attrition. This means that some drugs could be judged conservatively, while others could be judged generously. Whether it is possible or desirable for the Cochrane Schizophrenia Group to prescribe how to deal with attrition is a matter for further debate. Reporting the specific proportion of data that are missing for each outcome could allow readers to have a greater understanding of the robustness of each finding."
Mostly these are older reviews, though the 2010 review on olanzapine might be used in the corresponding Wikipedia article. Formerly 98 (talk) 19:17, 25 August 2014 (UTC)

We could have a RfC. What wording are you wanting? Doc James (talk · contribs · email) (if I write on your page reply on mine) 00:30, 27 August 2014 (UTC)

Let me think about it. My primary goal was to influence your opinion about the overall question of the hierarchy of evidence if I could; this particular article was just the vehicle for that discussion. I'm trying to argue a fairly argue a fairly complicated position, and if I wasn't able to convince you, my chances of convincing people who on average spend much less time and energy thinking about the issues than yourself are likely to be poor.
I'm disappointed I wasn't able to change your mind, but thanks for engaging and taking the time to listen. I appreciate it. Formerly 98 (talk) 02:51, 27 August 2014 (UTC)
Drug Year Issues considered / Evidence quality Summary evaluation
Aripiprazole 2011 "Compared with placebo, aripiprazole significantly decreased relapse in both the short (n = 310, 1 RCT, RR 0.59 CI 0.45 to 0.77) and medium term (n = 310, 1 RCT, RR 0.66 CI 0.53 to 0.81). It also produced better compliance with study protocol (n = 2275, 8 RCTs, RR 0.74 CI 0.59 to 0.93)". "Unable to extract any usable data on death, service outcomes, general functioning, behaviour, engagement with services, satisfaction with treatment; economic outcomes or cognitive functioning". "There was high attrition" "May be effective"
Trifluperazine 2014 "Significant clinical improvement in clinical global state (Low quality evidence"), all other outcomes described as supported by low quality or very low quality evidence "An effective antipsychotic"
Chlorpromazine 2014 "Chlorpromazine provided a global improvement in a person's symptoms and functioning" but "The quality of evidence is very low". "No difference was found in relapse rates". "Chlorpromazine's global position as a 'benchmark' treatment for psychoses is not threatened by the findings of this review"
Pimozide 2013 "Only one study provided data for global state relapse, for which no difference between groups was noted ". No study provided data on imporvement in mental state or quality of life. "seven studies provided data for global state relapse at medium term, for which no difference was noted..another study demonstrated no difference in the presence of first-rank symptoms at medium term" "Although shortcomings in the data are evident, enough overall consistency over different outcomes and time scales is present to confirm that pimozide is a drug with efficacy similar to that of other, more commonly used antipsychotic drugs "
Fluphenazine 2013 "Results, based on this small selection of studies, suggested that there was no significant difference between oral fluphenazine and placebo for most outcomes, including global state and leaving the study early. Results did suggest a statistically significant effect favoring oral fluphenazine in the short term for levels of relapse (n = 38, 1 RCT, RR 0.25 CI 0.06-1.03) with levels of extrapyramidal adverse effects more frequent with oral fluphenazine" " It is indeed a potent antipsychotic"
Sulpride 2009 and 2012 "There were no data for many important outcomes such as general functioning, service use or adverse effects". Data quality "poor" "Sulpiride may be an effective antipsychotic drug"

Auditory hallucinations[edit]

I was prescribed Abilify for auditory hallucinations (music, both choral and instrumental, & unidentifiable shouting voices). It worked and I'm now off it, with no return of the hallucinations. (I am not nor have ever been diagnosed schizophrenic.) Since this use isn't mentioned in the article, I googled and found several "references" (admittedly not good ones) for this use:

On the other hand, there are claims that Abilify can cause auditory hallucinations.

If an acceptable reference can be found showing Abilify effective for getting rid of auditory hallucinations, this would be an important addition to this article. --Hordaland (talk) 15:30, 26 September 2014 (UTC)

Antipsychotic Medication[edit]

I'm pretty sure abilify is also a antipsychotic... might want to add that into the beginning section — Preceding unsigned comment added by Oddtruth (talkcontribs) 20:25, 30 October 2014 (UTC)

Most people don't know what atypical means... might want to claify what that is as mental health is a HUGE problem is the USA. I would say abilify is primarily a antipsychotic... not an partial dopamine agonist. Again most people don't understand what these large and complicated words mean. I'm not a doctor but wikipedia a huge FREE encylopedia. Even kids use it. I did when I was in high school. Adults too. aripiprazole is an antipsychotic that works by partial agonism of dopamine receptors. maybe that will clarify — Preceding unsigned comment added by (talk) 12:00, 6 September 2015 (UTC)

Uncertain benefit and Wikipedia's voice[edit]

I've taken the Cochrane conclusion that aripiprazole's utility in schizophrenia is unclear out of Wikipedia's voice and attibuted it to the source. There is not sufficient consensus among recognized reliable sources to make this statement in Wikipedia's voice. In fact, it is a minority opinion.

NICE and the British Association for Psychopharmacology recommend that all people being treated for psychosis recieve an antipsychotic both as acute and maintenance therapy. They further state that patients should be warned that acute treatment is less successful and that relapse is more likely if the drugs are not taken. The BAP further states that antipsychotic discontinuation is likely the most important cause of relapse. Lastly both groups state that the efficacy of different antipsychotic drugs is similar. These statements are incompatible with the hypothesis that these groups agree with Cochrane's assessment of aripiprazole as having questionable utility.

I've also removed the blanket statement in Wikipedia's voice of Cochrane's conclusions from the intro. Formerly 98 (talk) 02:13, 26 January 2015 (UTC)

There is issues with the quality of the evidence support the conclusions. Thus while recommended these recomendations are not based on that good of evidence. Doc James (talk · contribs · email) 02:23, 26 January 2015 (UTC)
I think your modification is a reasonable one. On one hand I don't think that these organizations would be explicitly guiding that patients should be warned against discontinuation if they bought into the Cochrane conclusions. But on the other my changes involve extrapolating from statements about antipsychotics in general to aripiprazole in particular, and are at least flirting with WP:SYNTHESIS. So I wouldn't have been surprised by a simple reversion. Overall I think the version as of your last edit captures the landscape of expert opinion pretty well.
Not the place to wander back into our longstanding debate over EBM, but I'm not sure that ideal quality, placebo-controlled RCTs are going to be achievable for every intervention, and I don't think perpetually expressing doubt over those for which such evidence is not available is helpful. I'd be willing to guess that there are no placebo controlled RCTs for interventions as simple as suturing large lacerations, or for thoroughly disinfecting the wound before doing so, but we take the sum of our observational data and connect the dots. I suspect that this is what NICE and BAP are doing here in light of the high dropout rates seen especially in the placebo arms of AP clinical trials (there is a whole literature on this subject).
That being said, the dropout rates in the aripiprazole trials seem higher than for most APs, which seems to fit with anecdotal statements that it is a less potent AP with fewer side effects than some others. So I can to some extent understand why Cochrane singled it out for low evidence quality.
I switched the statement in the lede from Wikipedia's voice to Cochranes. This seems reasonable to me but I'm not going to fight you over it if reverted based on the handful of sources that I am currently aware of that address the issues above. Thanks. Formerly 98 (talk) 12:48, 26 January 2015 (UTC)
we having the same tension here that we had at Oseltamivir. I think the medical consensus should get the most weight, and the evidence should follow. Can we do that here? I say the following with trepidation but will go ahead and say it. Everybody knows that the drugs we have for many psychiatric diseases are poor. but they are what we have. To the extent they are effective, they have to actually be taken -- compliance is a huge, huge issue with drugs for schizophrenia. Here is the really difficult part -- in my view, emphasizing the following: "A Cochrane review concluded that high dropout rates in clinical trials, and a lack of outcome data regarding general functioning, behavior, mortality, economic outcomes, or cognitive functioning make it difficult to definitively conclude that aripiprazole is useful for the prevention of relapse" is .... UNDUE. And to be frank, irresponsible of us. I am not saying we should hide anything, but we should definitely give the most weight to medical practice. We are an encyclopedia for the general public Please see how AFP handles the Cochrane review: Jytdog (talk) 14:16, 26 January 2015 (UTC)
see also this: which looks at the most recent independent clinical trial data, and confirms the practice guidelines (which acknowledge the uncertainties and the need to experiment, to find the most effective regimen) Jytdog (talk) 14:22, 26 January 2015 (UTC)

I've obviously harped on the issues around this article for some time, but I do think it represents an intersting case as to how we incorporate orthodox EBM into our thinking about interventions for which double blind, PBO controlled RCTs cannot be performed well. In the case of APs I was surprised to learn a year or so ago that the dropout rates in the PBO arms of AP trials are higher thsn in the active arms in spite of AP dide effects. So if dropout rates are typically 50% or more in the PBO arm, the problem is likely with the merhodology used to determine efficacy as much so as with the drugs. How do EBM advocates handle other interventions for which PBO controlled RCTs are not possible? The CDC in the case of Tamiflu accepted observationsl data, which shows that some reliable sources reject EBM advocate assertions that only double blind RCTs "count". The evidence for aripiprazoles efficacy is equivicol by orthodox EBM standards, but its not clear to me that those standards are universally accepted.Formerly 98 (talk) 15:45, 26 January 2015 (UTC)

I am fine with attributing the position of Cochrane. I am not okay with removing it. Glossing over the fact that the quality of evidence is poor is sort of paternalistic.
We at Wikipedia are not here to convince people to either take or not take medications. We give weight as per WP:MEDRS. Cochrane is a major notable position.
Many organizations and individuals, especially American ones prefer to do "something" when the evidence is not clear. Thus we give epinephrine for cardiac arrest. Trying to hide the fact that epinephrine is not supported by the evidence even though the AHA recommends it also not something I support. If you are doing something with poor evidence to support it you should at least realize this and definitely not try to hide it. Doc James (talk · contribs · email) 17:31, 26 January 2015 (UTC)

Well, that was a little harsh. I don't think anyone is trying to hide anything. The fact that others do not share your beliefs about the nature of medical knowledge is something that could and should be addressed in these discussions without impugning their good intent. I'm every bitas concerned about your approach as u are about mine.Formerly 98 (talk) 17:39, 26 January 2015 (UTC)

We have had many discussions regarding what qualifies as a high quality source. You two did not get support for your proposed changes at WP:MEDRS.
The AFP statement is a summary of the 2009 review. Doc James (talk · contribs · email) 17:49, 26 January 2015 (UTC)

"No offense intended" would have been a great response here. Formerly 98 (talk) 00:44, 27 January 2015 (UTC)

Hi DocJames. I realize you are busy and edit a lot, but am asking you to slow down here. Please I didn't ask to remove Cochrane, not at all. This is WEIGHT issue. As at tamiflu, I am asking that we give more weight to what the treatment guidelines, which speak clearly that the drug has an important place in treatment. We should definitely mention that the evidence for that practice is not strong, but that should come after, and with less weight. Shall i make an edit to show you what I mean - would you be open to seeing that? Jytdog (talk) 22:54, 26 January 2015 (UTC)
I hope we can all agree it is recommended but that the evidence is not good. That is also the way it is currently worded. Doc James (talk · contribs · email) 00:43, 27 January 2015 (UTC)
I don't mean to be catty in stating the obvious, but its not whether we think the evidence is weak but whether reliable sources think so, and whether there is unaminity in that viewpoint if the lede is to remain unchanged.
In spite of the comment here implying that I am trying to "hide" something, I've been extremely candid about what I see as the strengths and weaknesses of the argument that I've tried to put forth here that groups other than Cochrane do not see the evidence for aripiprazole's efficacy as a maintenence therapy as being weak. I see professional treatment guidelines as 1) strongly recommending maintenance therapy with an antipsychotic, and 2) stating that approved antipsychotics have equivalent efficacy, and 3) the warning to patients that they place themselves at high risk of relapse if they discontinue shows strong belief that the evidence for antipsychotic efficacy in relapse prevention is solid. Does tying these together to state that these same groups see solid evidence that aripiprazole is efficacious in this application represent WP:synthesis? Maybe we should seek outside opinion on this.
I remain concerned here that this article as currently constituted represents something close to a recommendation to people with schizophrenia that they don't need to take their maintenance meds seriously. I have never spoken to a psychiatrist in academia or private practice who would not pull his or her hair out at this suggestion, and am concerned about potential harms.
Lastly I would point out that the FDA approved the current label of aripiprazole in February 2014. According to that label, the efficacy of aripiprazole for the treatment of schizophrenia, including relapse prevention, has been established in "adequate and well-controlled clinical trials". The FDA is a WP:MEDRS compliant source, as is the EMA, and their opinions cannot be excluded simply because they disagree with Cochrane, as WP:NPOV requires that we include the opinions according to their prevalence in reliable sources. If Cochrane does not believe these trials were adequate, that is just another opinion that needs to be cited, not the voice of God.
Formerly 98 (talk) 00:52, 27 January 2015 (UTC)
And we now have it attributed which I am fine with. Doc James (talk · contribs · email) 05:05, 28 January 2015 (UTC)

Airpiprazole abilify injection contains[edit]

contains sodium hydroxide which is caustic soda in the other ingredients listed this is may cause weight loss in people or harm you are not given an injection leaflet like the tablet one. injection leaflet left behind by team worker.

Cochrane Review[edit]

The Cochrane Review referenced in the first paragraph is grossly misrepresented. I tried to delete but my edit was reverted. The passage in question was:

"According to a Cochrane review, evidence for the effectiveness of the oral form in schizophrenia is not very strong, as many people dropped out of the medication trials before they were completed."

The Cochrane review in question came to the conclusion that "Aripiprazole may be effective for the treatment of schizophrenia" because "Compared with placebo, aripiprazole significantly decreased relapse in both the short...and medium term." It also noted that "Aripiprazole has a lower risk of raised prolactin and prolongation of the QTc interval" compared with other antipsychotics which is to say that in some contexts it may be a superior medication. It did mention a high dropout rate, but in fact the drop out rate was lower in the aripiprazole group than in the control, so not only is saying that the "evidence for the effectiveness of the oral form in schizophrenia is not very strong" is not only original research (WP:OR), it's just wrong.

Let me know if anyone still objects to me removing this garbage.

Quodfui (talk) 23:58, 3 October 2015 (UTC)

Yes the review states "Despite the fact that 2585 people participated in nine randomised aripiprazole studies, we were unable to extract any usable data on death, service outcomes, general functioning, behaviour, engagement with services, satisfaction with treatment; economic outcomes or cognitive functioning. In general, study attrition was very large for all studies over four weeks' duration. There was high attrition in most of the included studies. Fewer people left the aripiprazole group compared with those in the placebo group"
So yes should be adjusted. But the evidence of benefit was not very strong as most relevant benefits were not looked at. And large number of people dropped out of the trials before they were completed. Doc James (talk · contribs · email) 06:49, 4 October 2015 (UTC)

External links modified[edit]

Hello fellow Wikipedians,

I have just modified one external link on Aripiprazole. Please take a moment to review my edit. If you have any questions, or need the bot to ignore the links, or the page altogether, please visit this simple FaQ for additional information. I made the following changes:

When you have finished reviewing my changes, please set the checked parameter below to true or failed to let others know (documentation at {{Sourcecheck}}).

You may set the |checked=, on this template, to true or failed to let other editors know you reviewed the change. If you find any errors, please use the tools below to fix them or call an editor by setting |needhelp= to your help request.

  • If you have discovered URLs which were erroneously considered dead by the bot, you can report them with this tool.
  • If you found an error with any archives or the URLs themselves, you can fix them with this tool.

If you are unable to use these tools, you may set |needhelp=<your help request> on this template to request help from an experienced user. Please include details about your problem, to help other editors.

Cheers.—InternetArchiveBot (Report bug) 20:48, 17 October 2016 (UTC)


According to recent research, the endogenous cannabinoid anandamide is a substrate for the CYP2D6 enzyme. Therefore, is aripiprazole a potential endocannabinoid enhancer or selective FAAH inhibitor? Tkadm30 (talk) 13:18, 23 March 2017 (UTC)

This page is not a forum for general discussion. You can ask your question at WP:Reference desk. Jytdog (talk) 15:22, 23 March 2017 (UTC)
I think this information is missing from the page and needs clarification. Tkadm30 (talk) 09:26, 26 March 2017 (UTC)
That source is what we call a "primary source" - we base Wikipedia content about health on what we call "secondary sources" --- see WP:MEDDEF. Jytdog (talk) 15:08, 26 March 2017 (UTC)