Abilify (aripiprazole) is approved by the FDA for augmentation to antidepressant agents that have failed patients.

It is also the only atypical antipsychotic indicated. It is peerless in the fact that has dopaminergic partial agonism, but what are its primary serotonergic mechanisms? Antagonism at the 5-HT2A receptor (Ki = 8.7 nM), and partial agonism at the 5-HT1A receptor (Ki= 5.6 nM), 5-HT7 receptor (Ki = 10 nM), 5-HT2C receptor (Ki = 22.4 nM) Latuda is indicated for bipolar depression, however. What serotonergic actions does lurasidone have? Antagonism at the 5-HT2A receptor (Ki = 2.0 nM), 5-HT7 receptor (Ki = 0.5 nM), 5HT2C receptor (Ki = 415 nM) and partial agonism at the 5-HT1A receptor (Ki = 6.8 nM). According to Wikipedia (disclaimer, I wrote this myself): Aripiprazole's primary serotonergic effect is at the 5-HT2B receptor where it functions as an antagonist with a Ki of 0.36 nM. Trazodone antagonizes the 5-HT2B (Ki = 78.4 nM) stronger than any serotonergic receptor except for 5-HT2A (Ki = 8.7 nM). Also, there are six 5-HT receptors that trazodone and aripiprazole both effect, but their strength varies in order. Aripiprazole's order of strength is as follows: 5-HT2B receptor, 5-HT1A receptor, 5-HT7 receptor, 5-HT2A receptor, 5-HT2C receptor, 5-HT1D receptor. Trazodone's order of strength is as follows: 5-HT2A receptor, 5-HT2B receptor, 5-HT1D receptor, 5-HT1A receptor, 5-HT2C receptor, 5-HT7 receptor. Trazodone has strong similarities to the atypical antipsychotic, aripiprazole, and both psychiatric medications produce the mCPP metabolite. With Abilify and Latuda, the mutual serotonergic receptors are as follows: 5-HT2A, 5-HT7, 5HT2C, and 5-HT1A. Abilify is unique because it has partial agonism properties paralleled to the other atypical antipsychotics. Also, you cant discount the fact that trazodone possess 5-HT2A/2C antagonism. 5-HT2A/2C antagonists could mediate antidepressant effects by raising the levels of dopamine and norepinephrine in the prefrontal cortex. 5-HT2A/2C antagonism augmentation to SSRI/SNRI action may potentiate the antidepressant effects in depressed patients. Atypical antipsychotics, which have 5-HT2A antagonist effects as prominent properties, are proven to potentiate the actions of SSRIs/SNRIs (see Abilify) in certain depressed patients, especially those who are diagnosed with treatment resistant depression. There are several agents with 5-HT2C antagonist actions that are approved as antidepressants. Serotonin is indicated as the primary factor for depression, and I believe that Abilifys strong antidepressant effects are exerted by its serotonergic action which could also be mediated via trazodone. SERT inhibitors, such as SSRIs and SNRIs, raise every serotonin receptors all at once and simultaneously cause antidepressant actions by stimulating the 5-HT1A receptors, but they cause

side effects in patients by stimulating 5-HT2A and 5-HT2C receptors. However, with trazodone, when its SERT inhibition is combined with its 5-HT2A/2C inhibition it leads to antidepressant actions without sexual dysfunction, anxiety, or insomnia associated with stimulation of the 5HT2A and 5-HT2C receptors. Simultaneous obstruction of 5-HT2A and 5-HT2C receptors with the SARI (serotonin antagonist and reuptake inhibitor) trazodone, when SSRIs/SNRIs are administered can also theoretically treat the insomnia and anxiety associated with the depression initiated by SERT inhibition. There is enhanced tolerability of SSRIs/SNRIs by concurrently blocking 5-HT2A/5-HT2C receptors, and this may account for why low dose trazodone is one of the most frequently prescribed concomitant agents with an SSRI/SNRI. My hypothesis is that Oleptro XR may perhaps function as a form of Abilify for patients that have problems with the side effects that arise from its atypical antipsychotic mechanism of action such as akathisia, extrapyramidal side effects and orthostasis. Of note, trazodone and aripiprazole both produce the metabolite mCPP and are both processed via CYP2D6. My choice formula of trazodone is the extended-release version, Oleptro XR, should have a low prevalence of sedation due to its time-release mechanism. This stratagem may deliver the preeminent opportunity for raising the dose of trazodone adequately to become an antidepressant while retaining acceptable reliability in terms of low perverseness of daytime sedation linked to trazodone IR. Oleptro XR should deliver satisfactory and perpetual blood levels of trazodone for antidepressant actions, yet be notionally no more anesthetizing than a lower dosage of trazodone IR. The continual blood levels generated by Oleptro XR, since it is in a time-release mediation, is idyllic for triggering tolerance to the side effect of torpor. Oleptro XR according to the PI sheet, has a low frequency of anxiety, insomnia, and sexual dysfunction; it can create another alternative for depressed patients prescribed SSRIs/SNRIs whom are unable to sustain those medications due to those side effects. Oleptro XR necessities a diminutive dosage of 150mg. administered for a patient to obtain the preferred pharmacological effects. The maximum dosage is 375mg. Oleptro XR is only available in 150mg. and 300mg. bisectable tablets, e.g. to obtain the 375mg. maximum dosage (400mg. is the maximum dosage of IR, 600mg. IR for inpatients), youd need #75 150mg. tablets. I suggest a target dosage of at least 225mg. to ensure youre getting the predominant antidepressant effects, but you should always dose rendering to your response. I have confidence that Oleptro XR is substantially unappreciated. Trazodone has indispensable implications, but its robust antidepressant properties have been underutilized due to TID dosing requirement of the IR form and its sedating daytime side effects both of these negatives are unconcerned with Oleptro XR, which fundamentally offers us an innovative drug with this inimitable release mechanism. It is not merely a patent-extender; rather, it is a fresh panamera for patients to procure compulsory amelioration.