Abilify interactions?

[Kore]

Hey, I'm wondering about interactions between aripiprazole and other drugs, since not a lot is known about it. The best information I could find was actually http://en.wikipedia.org/wiki/Aripiprazole
I understand that it antagonises the 5-HT2A receptor. Does that mean it should negate the effects of the major psychedelics?

Also, I'm wondering if it would be safe to combine an MAOI with aripiprazole (specifically MAOI-A). I did a lot of searching and couldn't find anything on combining MAOIs with aripiprazole. Hopefully you neuropharmacological geniuses in ADD can answer my questions.

 

[monstanoodle]

Personally I wouldn't combine anything with MAOI's.. It' just far too dodgy.
And I'm sorry. but I have no idea as to other combinations between Aripiprazole.

It'd be best to avoid all rec. drugs for quite some time anyway to be honest.

 

[Kore]

I read elsewhere in BL that aripiprazole has the tendency to block everything... bit of a blanket statement, but I've found it to be the case. Like, I dropped two hits of quality acid and nothing happened.

I was wondering if MAOIs could temporarily undo the dampening effects of aripiprazole. Reversible MAOI type A drugs (i.e. harmine/harmaline/moclobemide) sound relatively safe to me, I just don't know how they get along with Abilify.

Having to completely avoid all "recreational" drugs would blow..

 

[monstanoodle]

Indeed it would, but also would having some seriously nasty interaction.

 

[mukaki]

I tok GBL with it and it wasn't really great. It just made me dysphoric. Benzos worked fine for me.

 

[Hammilton]

I'd worry about it enhancing the effects of opioids and sedatives, especially things like barbiturates. BZDs I wouldn't worry much.

An MAOI will do nothing to allow psychedelics or stimulants to work.

They prevent the monoamines from being broken down- but they don't remove the aripiprazole from the receptors to allow them to bind (or the psychedelic to bind)

 

[Kore]

Thanks for your input, Hammilton.

I guess I'll just scale down on the aripiprazole (under a p-doc's supervision). Too bad the half-life of this drug verges on eternity.

 

[nuke]

If you're taking antipsychotics for a mental disorder, it's probably not a wise decision to both discontinue antipsychotics and use psychedelic drugs.

 

[Hammilton]

wow, I can't believe I didn't mention that myself...

*bad hammilton, bad*

 

[Kore]

I know. But aripiprazole's giving me significant motor control trouble and lethargy, so I'll probably quit anyway. The costs outweigh the gains currently.

Maybe once I'm off it my reasons for trying psychedelics will have evaporated. One can hope.

 

[MurphyClox]

Known interactions:

...with Haloperidol
see: "Aripiprazole and haloperidol: a clinically relevant interaction with a dopamine antagonist and partial agonist."
Comment in: Ann Clin Psychiatry. 2008 Apr-Jun;20(2):113-4.
PubMed ID: 18568584
Burke Michael J; Lincoln Jana
Annals of clinical psychiatry : official journal of the American Academy of Clinical Psychiatrists (2006), 18(2), 129-30


Some years earlier was published:

"Aripiprazole: First of a new class of antipsychotics."
Luisi, Andrea F.
Formulary (2002), 37(11), 575-576, 579-582

Abstract

A review. Aripiprazole is an investigational atypical antipsychotic that received an approvable status from FDA in Sept. 2002 for the treatment of schizophrenia. The decision on approval could be made as early as the end of this year. Aripiprazole offers a unique mechanism of action as a dopamine system stabilizer. Aripiprazole has been effective in both short-term (4-6 wk) and long-term (26-52 wk) treatment trials. It appears to produce less hyperprolactinemia, wt. gain, and extrapyramidal symptoms than other antipsychotics. Aripiprazole is metabolized via the cytochrome P 450 system; however, no drug interactions are known at this time.

This statement was seconded in the same year here:

"Aripiprazole: profile on efficacy and safety."
Goodnick, Paul J.; Jerry, Jason M.
Expert Opinion on Pharmacotherapy (2002), 3(12), 1773-1781.

But please note that these article were released, when the drug was still new. They do not necessarily reflect the reality IMO.

Already more realistic sound this to me:

"Aripiprazole."
Winans, Elizabeth.
American Journal of Health-System Pharmacy (2003), 60(23), 2437-2445

quoting from the abstract:

Because aripiprazole is a substrate of both cytochrome P-450 isoenzymes 3A4 and 2D6, there is a potential for other drugs to affect its metabolism. The recommended starting dosage is 10 or 15 mg daily, preferably administered with meals.

There seems to be no interaction with lithium and valproate (Pharmacology (2005), 45(1), 89-93).

Ok, and finally a short abstract that calls for caution when taking compounds that are metabolized via the same enzymes like Aripiprazole:

"Effects of comedication on the serum levels of aripiprazole: evidence from a routine therapeutic drug monitoring service."
Castberg, I.; Spigset, O
Pharmacopsychiatry (2007), 40(3), 107-110

Abstract

Introduction: The objective of the study was to compare the serum concns. of the atypical antipsychotic aripiprazole in monotherapy with the concns. found during concomitant therapy with other drugs. Methods: Samples analyzed for aripiprazole by a liq. chromatog.-mass spectrometry method in a routine therapeutic drug monitoring setting were collected consecutively. Results: Samples from 81 patients were included in the study. Comedication with the CYP3A4 inducer carbamazepine lowered the dose-adjusted aripiprazole concn. by 88%. Comedication with CYP2D6 inhibitors gave a mean concn. 44% higher than in the monotherapy group. Subjects comedicated with valproate had lower aripiprazole concns., while subjects comedicated with lamotrigine, citalopram/escitalopram and lithium had higher concns. than the subjects in the monotherapy group. Conclusion: Although the study is small and the results should be interpreted very cautiously, it indicates that comedication with drugs inhibiting or inducing CYP2D6 or CYP3A4 affects the serum concns. of aripiprazole. The other findings should be considered as preliminary and have to be replicated in a larger setting before firm conclusions can be drawn.

Peace! Murphy

 

[Scarletta]

From experience I know it interacts with Adderall (amphetamine). My dr. prescribes me 5 mg Abilify for refractory depression and the Adderall for adult ADD. When taking them at the same time I can definitely tell the Adderall is blocked, and this is only with 5 mg of Abilify! And no matter how much Adderall I take. It sucks. Plus the Abilify half-life is something like 3 days so it inteferes for a long time!

The Abilify DOES help even out my moods and make me less anxious however. I just don't know why my doc has me on both of them since it seems counterproductive.

I'd think Abilify would work this way on any type of stimulant drug. Read here:

http://www.ncbi.nlm.nih.gov/pubmed/15988473?dopt=Abstract&holding=npg
Aripiprazole attenuates the discriminative-stimulus and subject-rated effects of D-amphetamine in humans.

 

[Sturnam]

This isn't an interaction, but something that seems to be rather important, I would say.

cocaine-dependent
participants were maintained on both placebo and aripiprazole
(15 mg/day) capsules for 17 days before the onset of
cocaine self-administration sessions...Preliminary
data show that aripiprazole maintenance robustly
increased cocaine (12, 25 mg) self-administration compared
to placebo maintenance. Aripiprazole did not appear to alter
cocaine intoxication, although it increased baseline rates of
anxiety

also with that,

a recent
clinical trial for amphetamine dependence was terminated
early because the aripiprazole group showed greater
amphetamine use than those receiving placebo (Tiihonen
et al. 2007), which appears consistent with the human
laboratory findings with cocaine.

ALL D1 and D2 antagonists seem to have this effect, so if you go on to another antipsychotic (assuming its a D1 or D2 antagonist) it would seem very wise to avoid any psychostimulant.

edit: Just read the above post. It seems like for amphetamine USE that abilify blunts the effects, but for amphetamine ABUSE it increases want for the drug. the study where abilify decreased effects was 0-20mg abilify with 15mg d-amphetamine orally. I'm guessing with the abuse study they gave them access to more amphetamine and by the IV route.

 

[Scarletta]

I'm betting it goes both ways. The Abilify reduces the subjective euphoric (and other effects) of stimulants and therefore makes it not as much fun to do anymore, if you've only got a limited amount of stimulants. If you have a lot you'll just keep doing more and more of the stimulant in an attempt to "override" the Abilify nullification. At which point that happens, I don't know. Can't find any studies to that effect.

 

[Sturnam]

hmmmm, that's what I thought too. But instead, they came to this conclusion.

Note that it does not appear that either aripiprazole or ecopipam increased cocaine self-administration by antagonizing the reinforcing effects of cocaine because cocaine “high” was not blunted by either ecopipam or aripiprazole maintenance compared to placebo. That is, if these medications increased cocaine self-administration in an attempt to overcome a blockade of reinforcement, one would expect to see a parallel decrease in ratings of cocaine intoxication. Rather, the fact that the acute effects of ecopipam and
aripiprazole in combination with psychostimulants were in an opposite direction as when these medications were given repeatedly suggests that maintenance on dopamine antagonists or partial agonists may enhance the reinforcing effects of psychostimulants.

I think that the D1 and D2 receptors are just strange. Acute pretreatment of an antagonists decreased self-administration, but chronic exposure increased it.

 

[Hammilton]

Huh... that's interesting. There are many other DA receptors, perhaps it is that when D1/2 is/are blocked the available receptors produce more euphoria?

Or life on DA antagonists is so terrible that any reprieve will be sought?

 

[Sturnam]

Huh... that's interesting. There are many other DA receptors, perhaps it is that when D1/2 is/are blocked the available receptors produce more euphoria?

Hmmm, one of the places D3 receptors are most widely distributed is the nucleus accumbens (NA). Now, I don't know how the NA fits into the role of euphoria, but I know that its definitely plays a strong role in addiction. I suppose its possible that by antagonizing D1 and D2 it forces the psychostimulant to bind to D3 in higher concentrations. It would be interesting to see if there's any study that has the binding affinity of amphetamine or cocaine for D3 receptors. If this theory is true, the D3 binding affinity should be much lower than that of either D1 or D2.

Or life on DA antagonists is so terrible that any reprieve will be sought?

lol. then they'll have to sell us another drug for our melancholy. prescriptions of cocaine for everyone!