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Is Asenapine Any Good?

seep

Bluelighter
Joined
Nov 28, 2008
Messages
1,347
Does anyone have any subjective information on this new antipsychotic? It apparently has just been approved by the FDA. It is an antagonist at the following receptors:

5-HT1A
5-HT1B
5-HT2A
5-HT2B
5-HT2C
5-HT5A
5-HT6
5-HT7
α1-Adrenergic
α2A-Adrenergic
α2B-Adrenergic
α2C-Adrenergic
D1
D2
D3
D4
H1
H2

It has never been mentioned on bluelight. A close friend is being prescribed it tomorrow.

Thanks in advance.
 
It is yet another atypical antipsychotic with nothing all that interesting about it from what I've been able to gather.
 
"any good" from what perspective?

If we're talking recreational, which i'd assume since that's the topic of BL, i'd say definately not, as it's an antagonist at the fun places.

Antipsychotics and antidepressants are generally not interesting recreationally, and in fact block the effects of a lot of good stuff.
 
Sorry for the confusion. I didn't mean does it have any recreational value; simply, does it keep the voices, delusions, obsessions etc. at bay better than what are currently the popular options (aripiprazole, quetiapine, omeprazole olanzapine)? Does it keep functional schizophrenics and bipolars out of crisis units? Does it keep the sky, clouds, mountains and plains exactly where they need to be so that you can work, rest and breed without having everything spin out of control?

The attractive thing about this drug, from what I gather from the literature, is that it doesn't cause appreciable weight gain, unlike its competitors. Even aripiprazole at, say, 30 mg qam, will result in weight gain so this appears to be the niche asenapine is trying to carve into. The problem is that it presents a higher risk of EPS than aripiprazole and maybe even than olanzapine. Particularly of concern is akathesia.

If nobody that tunes in here has actually tried it, I'll post a follow up in a few weeks.

Late entry: Also, I've heard various explanations as to why atypicals lead to metabolic abnormalities; d2 antagonism has been implicated, as well as histamine affinity and augmentation of AMP-activated protein kinase activity. The last of these sounds more sensible to me but I'm still a little confused as to how much we know about the cause of metabolic changes during antipsychotic use. Has anyone looked into this and reasoned out a mechanism? Weight gain is one of the top 4 or 5 reasons people discontinue antipsychotics and sometimes drop out of treatment altogether. For females it's often the top reason.
 
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No need to wait a few weeks: this medicine is a dud. It's a sublingual pill and it is intended to be taken in the morning. According to the patient, the pill tastes like a pebble of magnesium sulfate. 45 minutes after administration she was passing out with a smile on her face.

Then the akathisia started. Now she's been trying to get to sleep for 2 hours but keeps jactitating every few seconds. This is EPS personified.

The search continues.
 
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