# Vilazodone



## crayzyMed (Nov 2, 2006)

Vilazodone (EMD-68,843, SB-659,746-A) is an antidepressant and anxiolytic currently under development by Clinical Data for the treatment of major depressive disorder.[1] It acts as a serotonin transporter blocker (IC50 = 0.5 nM) and 5-HT1A receptor partial agonist (IC50 = 0.2 nM; IA = ~60-70%).[2][3] As of 2009, vilazodone has completed two phase III clinical trials with positive results. An NDA is currently pending confirmation by the FDA and vilazodone is likely to be expected on the market sometime in 2010 if it is approved.[4]

http://en.wikipedia.org/wiki/Vilazodone

NEW YORK (Reuters Health) - Vilazodone, the first of a new class of antidepressants known as indolalkylamines, has been shown in a phase III trial to be effective and well tolerated for the treatment of major depressive disorder, with a rapid onset of effect.

The researchers explain in the March issue of the Journal of Clinical Psychiatry that vilazodone "combines properties of a selective serotonin reuptake inhibitor with 5-hydroxytryptamine-1A partial agonist activity." They add that in addition to offering a rapid antidepressant effect, this agent likely has "a lower risk of sexual dysfunction" than currently available therapies.

Dr. Karl Rickels at the University of Pennsylvania in Philadelphia and colleagues report on their intention-to-treat analysis of a randomized trial in which 410 adults with major depressive disorder received either vilazodone or placebo for 8 weeks. Vilazodone was titrated from 10 mg to 40 mg once a day over the course of two weeks.

Compared to the placebo group, after 8 weeks the vilazodone group had greater mean improvements from baseline on the Montgomery-Asberg Depression Rating Scale (MADRS; p = 0.001) and the 17-item Hamilton Rating Scale for Depression (HAM-D-17; p = 0.022).

In fact, the researchers note, the treatment group was already demonstrating significant improvements on both scales after just one week.

The vilazodone-treated subjects also had significantly higher response rates on the MADRS (p = 0.007), the HAM-D-17 (p = 0.011), and the Clinical Global Impressions-Improvement scale (p = 0.001).

Most treatment-related side effects were mild or moderate, according to the article. Five patients in each group experienced a major adverse event.

"Vilazodone is effective for the treatment of major depressive disorder in adults, with symptom relief starting at 1 week, and is well tolerated at a dose of 40 mg/day," the investigator conclude.

Reference:
J Clin Psychiatry 2009;70:326-333.
http://www.thedoctorschannel.com/video/1782.html?specialty=9


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## IllusionalFate (Sep 10, 2008)

So, yet another SSRI may be out on the market sometime this year if approved by the FDA. Except in addition to being a SERT inhibitor, vilazodone is also a partial agonist at 5-HT1A and has been shown to increase extracellular 5-HT levels to a higher degree than existing SSRIs.

EMD 68843 = Vilazodone


> In behavioral studies, EMD 68843 produced antidepressant-like effects in the forced swimming test in both rats and mice *but only within a narrow dosage range.*





> At higher doses, however, weak efficacy of EMD 68843 at postsynaptic 5-HT1A receptors may inhibit the expression of rodent antidepressant-like behaviors


It appears that at low doses, vilazodone binds preferentially to presynaptic autoreceptors, which increases 5-HT release by decreasing autoreceptor activity (since vilazodone is only a partial agonist in contrast to 5-HT being a full agonist). See below:


> Previous studies have shown that combining SSRIs with 5-HT1A receptor antagonists, such as WAY 100635, augment extracellular levels of 5-HT in the cortex to a range above levels achieved by SSRIs given alone but less than fenfluramine (Artigas et al., 1996). _*The blockade of 5-HT1A*_ *receptors limits the ability of endogenous 5-HT to interact with autoreceptors that decrease cell firing and synthesis of 5-HT and, consequently, enhances extracellular 5-HT levels in terminal regions *(Artigas et al., 1996; Hjorth et al., 2000).





> ...additional pharmacological mechanisms may contribute to augmenting extracellular 5-HT levels in terminal regions when 5-HT1A receptor partial agonists are combined with SSRIs. One possible mechanism may be that partial agonists rapidly desensitize 5-HT1A autoreceptors, thereby inhibiting their functional activity and reducing their ability to inhibit 5-HT transmission (Romero et al., 1996). Other possible mechanisms could involve postsynaptic 5-HT1A receptors in terminal regions that participate in an inhibitory feedback loop to negatively regulate 5-HT transmission (Bosker et al., 1997; Casanovas et al., 1999) or direct effects on 5-HT release.


However, higher doses most likely decrease 5-HT1A postsynaptic receptor activation, as the selectivity to the autoreceptors is lost and vilazodone also binds to postsynaptic receptors which allows less sites for the endogenous full agonist (5-HT) to bind to:


> ...doses of EMD 68843 higher than 1 mg/kg were ineffective in both the mouse and the rat FST.





> ...although the 5-HT1A receptor partial agonist component of EMD 68843 may enhance extracellular 5-HT levels, *at high doses it could also restrain expression of antidepressant-like behaviors in the FST*, which predict clinical activity.





> Whether the 5-HT1A receptor partial agonist component of EMD 68843 would impede or facilitate antidepressant responses when tested clinically is unknown.


Makes sense. The optimum dose for vilazodone would be an amount that would most potently selectively bind to presynaptic autoreceptors, while also allowing serotonin access to the postsynaptic receptors. This SSRI should have a quicker onset of action and dose-dependently increase firing rate of serotonergic neurons leading to increased serotonergic neurotransmission compared to the SSRIs currently available. Sounds promising!
[[Link to study...]]


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## crayzyMed (Nov 2, 2006)

I was first!:spank

Very informative thread tough, better then mine:yes.


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## IllusionalFate (Sep 10, 2008)

You beat me to it! Heh.

Mods, can you merge my thread into this one? Here's the link:
http://www.socialanxietysupport.com/forum/f30/vilazodone-82779/


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## crayzyMed (Nov 2, 2006)

IllusionalFate said:


> You beat me to it! Heh.
> 
> Mods, can you merge my thread into this one? Here's the link:
> http://www.socialanxietysupport.com/forum/f30/vilazodone-82779/


I was actually going to ask to merge my thread into yours as your post is more informative and better as openingspost:b.


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## Ehsan (Mar 21, 2009)

i'm awaiting for CRF antagonists like antalarmin.


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## jim_morrison (Aug 17, 2008)

Yeah I've read about Vilazodone, the strange thing is that it's said to have no sexual side effects, in contrast to most SSRI's, Perhaps through some facilitation of dopamine release caused by 5HT1A agonism.


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## jim_morrison (Aug 17, 2008)

IllusionalFate said:


> Mods, can you merge my thread into this one? Here's the link:
> http://www.socialanxietysupport.com/forum/f30/vilazodone-82779/


You got it.


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## Ash09 (Apr 27, 2009)

Sounds like SSRI + Buspirone to me. 5HT1A agonism may be useful but serotonin re-uptake is crap.


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## burner00 (Oct 11, 2009)

Or more like another Trazadone minus the strong hypnotic properties


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## crayzyMed (Nov 2, 2006)

jim_morrison said:


> Yeah I've read about Vilazodone, the strange thing is that it's said to have no sexual side effects, in contrast to most SSRI's, Perhaps through some facilitation of dopamine release caused by 5HT1A agonism.


No, in fact it only agonizes the autoreceptors wich results in those receptors downregulating, and at the same time it takes the place of serotonin on those receptors (its a partional agonist, while serotonin is a full agonist) wich will result in alot less agonism of autoreceptors by serotonin and at the same time a faster downregulation of them.


> Neurochemical evaluation of the novel 5-HT1A receptor partial agonist/serotonin reuptake inhibitor, vilazodone
> by
> Hughes ZA, Starr KR, Langmead CJ, Hill M,
> Bartoszyk GD, Hagan JJ, Middlemiss DN, Dawson LA.
> ...


Anyway its good to see some antidepressants show up without those sexual side effects (agomelatine another example).


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## korey (Apr 25, 2006)

burner00 said:


> Or more like another Trazadone minus the strong hypnotic properties


That's what I was thinking.


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## crayzyMed (Nov 2, 2006)

Thank you for clarifying, this med has gotten my intrest as it appears that the 5HT1A autoreceptors explain why many ppl do not respond to antidepressant treatment, atleast according to this article:



> Why Some Brains Are More Vulnerable To Stress And Resistant To Antidepressants
> 
> A new study provides insight into the molecular characteristics that make a brain susceptible to anxiety and depression and less likely to respond to treatment with antidepressant medication. The research, published by Cell Press in the January 14th issue of the journal Neuron, may lead to more effective strategies for treating depression, a major health concern throughout the world.
> 
> ...


It appears that the presynaptic receptors explain why SSRI's suck.


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## crayzyMed (Nov 2, 2006)

rocknroll714 said:


> Don't forget 5-HT2C and 5-HT7!


Yes, your correct.


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## soto (Oct 19, 2009)

yeah I've been keenly following the development of Vilazodone over the past 12 months also, however there are a couple of points I think are worth mentioning:

1) Vilazadone was originally under development by the big Pharma heavy-hitters GSK and Merck, and was subsequently dropped after phase II trials involving more than 1000 patients failed to demonstrate efficacy in MDD.

2) The small Rx firm Clinical Data took over development of Vilazodone, with the rationale that they could identify pharmacogenetic 'markers' that could predict it's efficacy. Basically, if you have the right polymorphism of a certain gene you respond alot better to this drug - I think this is the case for about 30% of the population.

It smells a bit fishy to me, the fact that a company the size of GSK would abandon drug development on something that is now being heralded as the next breakthrough in antidepressant therapy by a relatively unknown firm, but then again stranger things have happened in clinical research - investigational drugs with great potential are abandoned all the time due to badly designed research protocols or unnaceptable adverse events (to name a few).

If Vilazodone is succesful then I'm hoping it will also work for OCD, and put an end to the sexual side effects that every single SSRI produce (despite the marketing spin).

I've heard that a NDA is currently being processed, does anyone know when it is likely to hit the market, and for how much $?


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## IllusionalFate (Sep 10, 2008)

Perhaps the big pharma companies didn't get their doses right. If this medication is dosed too high, the 5-HT1A partial agonism will "spread" to the postsynaptic receptors, decreasing overall 5-HT neurotransmission.


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## BearFan (Mar 22, 2008)

From what I've read, it has had good efficacy in both HAM-D and tolerability profile. If it truly has less sexual dysfunction, it would be a welcome compound.


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## Vilazodone (Mar 22, 2010)

*Lu AA21004 vs Vilazodone, your opinions whether 21004 is worth waiting for?*

FIRST, SOME GATHERED INFO ABOUT 21004 (excuse messiness but it's pasted from pdf from Lundbeck site):

"The in vitro profile of Lu AA21004, a novel multitarget drug for the treatment of mood disorders. [Huailing Zhong, Ph.D. , Tine B. Stensbøl, Ph.D. , Kristen Frederiksen, Ph.D. , Benny Bang-Andersen, Ph.D. 1 2 NR4117 Lundbeck Research USA Inc., Paramus, NJ 07652, USA and H.Lundbeck A/S, DK-2500, Copenhagen Valby, Denmark]

Abstract: Objective: To characterize the in vitro pharmacological properties of Lu AA21004. 3 Methods: Affinity for human 5-HT receptors was measured by displacement of [ H]BRL 3A 43694 binding. The functional response at human 5-HT receptors was measured as 3A changes in serotonin (5-HT) induced currents in HEK293 cells. Affinity for human 5-HT 1A receptors was evaluated by displacement of [3H]8-OHDPAT binding at cloned receptors and native receptors in human post-mortem cortical brain tissue. The functional intrinsic activity (IA) was assessed by [35S]GTPgammaS binding using cloned human 5-HT 1A 
receptors. Affinity for cloned human 5-HT transporters was determined by displacement of [3H]escitalopram, and functional activity was measured in a [3H]5-HT uptake assay using cloned human 5-HT transporters. IC values were corrected by the Cheng- Prusoff method 50 to derive corrected IC (cIC ). 50 50 Results: Lu AA21004 showed high affinity binding for the cloned human 5-HT receptor 3A (K=4.5 nM), and displayed functional antagonism using human 5-HT receptor expressed i 3A in HEK293 cells (IC =10 nM). Lu AA21004 displayed moderate to high affinity binding for 50 
the cloned human (K=15 nM) and the native 5-HT receptor (K=40 nM). In functional i 1A i [35S]GTPgammaS binding assays, Lu AA21004 demonstrated agonism (IA=96%) for the cloned 5-HT receptor. Lu AA21004 showed high affinity binding for the cloned human 5-HT 1A 
transporter (K=1.6 nM), and binding to the transporter resulted in inhibition of 5-HT uptake i (cIC =5.4 nM). At 1 microM, Lu AA21004showed no significant activity when tested against 50 70 other receptors, enzymes, ion channels, or transporters. Conclusions: Lu AA21004 is a high affinity 5-HT receptor antagonist, a 5-HT receptor 3 1A agonist, and a high affinity 5-HT transport inhibitor. This in vitro profile translates into 
enhanced levels of 5-HT as well as other neurotransmitters (ie, 
noradrenaline, dopamine, acetylcholine) in vivo (1,2), and may result in a unique antidepressant profile.

Lu AA21004 blocks 5-HT uptake. 21004 Binds human 5-HT transporter at 
concentration profile similar to that of Sertraline At 1 μM, Lu AA21004 displayed no relevant pharmacological affinity (% inhibition <50% 
at 1000 nM) when tested against 63 different receptors, enzymes, ion channels, and transporters (Cerep High-Throughput Profile screen). 
For the following human receptors, only modest binding affinities were 
found (K >180 i nM) for Lu AA21004: histamine H , melanocortin ML , adrenergic ß , serotonin 5-HT , 2 1 2 2C 
5-HT , and 5-HT .

CONCLUSIONS 
Lu AA21004 is a potent 5-HT receptor antagonist in vitro. 3 Lu AA21004 is an agonist at 5-HT receptors and an inhibitor of 1A 5-HT reuptake in vitro. The pharmacological profile of Lu AA21004 is unique in that it combines antagonism and agonism at relevant serotonin receptors as well as inhibition of 5-HT reuptake. This serves as the underlying mechanism by which treatment with Lu AA21004 in vivo leads to significant increases in acetylcholine, NE, DA, and 5-HT levels in brain regions associated with mood regulation.

REFERENCES 
1 Moore NA, Bang-Andersen B, Brennum LT, Frederiksen K, Hogg S, Mørk 
A, Stensbøl 
TB, Zhong H, Sanchez C, Smith DG. Lu AA21004: A novel potential 
treatment for 
mood disorders. Eur Neuropsychopharmacol 2008:18 (Suppl 4): S321. 
2 Dremencov E, Weizmann Y, Kinor N, Gispan-Herman I, Yadid G. 
Modulation of 
dopamine transmission by 5-HT and 5-HT receptors: a role in the 
antidepressant 2C 3 
response. Curr Drug Targets 2006; 7:165-175.

----------------------------------------------------------- 
"About Lu AA21004
Lu AA21004 is a 5-HT3, 5-HT7 and 5-HT1B receptor antagonist, 5 HT1A receptor agonist and 5-HT transporter inhibitor. A number of investigations in vivo have demonstrated that Lu AA21004 increases extracellular monoamine (5-HT, noradrenaline and dopamine) and acetylcholine levels in specific areas of the brain. All of these activities are considered to be of clinical relevance and involved in the mechanism of action of Lu AA21004.
Lu AA21004 has demonstrated a low drug-drug interaction potential. It is extensively metabolized in the liver and the absorption of Lu AA21004 is independent of food intake.
About Lu AA24530
In pre-clinical studies, Lu AA24530 has demonstrated activities as a multi-modal enhancer with reuptake inhibition at monoamine transporters, and antagonist activity at 5-HT3 and 5-HT2c receptors. In vivo rat studies have demonstrated that treatment with Lu AA24530 leads to increases in acetylcholine, noradrenaline, dopamine and 5-HT levels in brain regions that play a key role in the regulation of mood."
SOURCE: http://www.drugs.com/news/lundbeck-...nical-trials-lu-aa21004-lu-aa24530-22982.html

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So far my analysis is sparse as I'd rather hear other ppl's opinion:

So it appears that like Vilazodone, LU 21004 also has SRI as probably the MAJOR (crucial) part of it's MOA (except for some fancy 5-HT 3 antagonism as well which probably makes an overal difference in the way the med feels.)

I personally found myself baffled by this particular statement:
"Lu AA21004 is a 5-HT3, 5-HT7 and 5-HT1B receptor antagonist, 5 HT1A receptor agonist and 5-HT transporter inhibitor"

>>So it has activity at 5-HT7 & 1B as well?? Why is this the ONLY place I'm reading this?

To be honest I can't yet see any MechOfAction advantages of 21004 over that of Vilazodone. Well I'd rather have you guys give your opinions. Given what has already been deduced on this forum as Vilazodone's MOA. Now compare it to 21004.. These are likely the best drugs in the Phase III pipeline and have comparable MOA. That is why I'm curious to your opinions. Sorry about the jumbled writing, it was written in haste.


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## Vilazodone (Mar 22, 2010)

Phase III options (ie the only drugs likely to be available next 2-5 years, except for the occasional Easter egg popping out of Russia/etc). Yes this probably isn't all inclusive but just using it as a reference to get to my point:

Top candidates:
Agomelatine: Currently available EU. (User-Description: mild benefits with very low side effect profile.)
Vilazodone: 5-HT1A partial agonist, serotonin reuptake inhibitor (my GUESS is it will likely be as good as 21004, without the tedious wait) 
Lu AA21004: 5-HT3 antagonist, 5-HT1A partial agonist (My guess is that this one is likely to have a relatively low side effect profile, but mild on the benefits) - depending on how much its MOA is dependant on being an SRI.) 

Some of (well actually MOST of - sadly) the others (and my own guesswork, feel free to give yours as well):

SEP-227162: DA/NE/5-HT reuptake inhibitor (DRI is the only part that mildly interests me about this drug. Who knows it could be interesting depending on side effect profiles , etc)

LY2216684: Norepinephrine reuptake inhibitor (I'm telling you I seriously doubt how this will be an improvement over a drug like Agomelatine.)

Feel free to list other Phase III drugs as comparison to Vilazodone (the next drug likely to become available to us).


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## Vilazodone (Mar 22, 2010)

Ok... SEP-227162 fails to excite even after visiting the Sepracor website, it's likely just another med that won't ever reach fruition.

The guy running http://www.neurotransmitter.net/newdrugs.html seems to need some professional help keeping his list of drugs current. Used to be the best 1page list on the net (besides an annually published pdf list).

Amazing what havoc an economic depression can have on the pharmaceutical pipeline. More rejections from EMEA/CHiMP as well as FDA.

I seriously don't mind partial-solution drugs, certainly beats the hell out of NOTHING!!!! :stu

So as far as interesting Phase III neuro-drugs this is all I see in the near future:
Almorexant
Vilazodone
LU 21004

We'll be lucky if only one passes the way 'progress' and 'change' have been going..


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## Ash09 (Apr 27, 2009)

I can't say any upcoming monoaminergic drug interests me, the drugs based on novel approaches currently in phase II trials might actually advance psychiatric treatment, if they ever make it.


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## jim_morrison (Aug 17, 2008)

Yeah SNDRI's will probly be pretty good, IMO they'll possibly be reminiscent of parnate with less medical restrictions and no dietry restrictions. And no orthostatic hypotension obviously.


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## Vilazodone (Mar 22, 2010)

Thanks all for the well-thought analysis. I have to agree that I'm not terribly excited over the phase 3 pipeline. It's actually somewhat of a downer. 

Nothing seems to be going right. Makes one want to give up entirely the idea that pharma can be an option... yea maybe in 300 years, but by then it won't matter much for any of us will it.

Btw, on a more positive note, Agomelatine is a decent drug. Not necessarily friggin strong but the side effect profile is for the most part CLEAN.

Almorexant is likely to be useful for those w/ insomnia issues aggravating their mental condition, except they won't disclose what the recently discovered 'safety observations' were. I know eplivanserin had issues w/ aggravating diverticulosis but that med has a completely different MOA than Almorexant.

Please excuse my poor grammar, I just can't get myself to care about junk like that


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## Vilazodone (Mar 22, 2010)

*NDA filed... yippy-do-da*

http://behavioralhealthcentral.com/...e-treatment-of-major-depressive-disorder.html

http://www.streetinsider.com/Press+...ent+of+Major+Depressive+Disorder/5461918.html

http://www.empr.com/nda-submitted-for-vilazodone-for-major-depressive-disorder-mdd/article/166325/

Vilazodone NDA submitted, now the next stage is more waiting...

Hope this med 'cures' someone here, that would be nice too see


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## Vilazodone (Mar 22, 2010)

http://investor.clda.com/releasedetail.cfm?ReleaseID=453924

the official release

maybe those who cannot tolerate other SRI's will be able to use Vilazodone.. that alone should merit it's approval I would think


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## CopadoMexicano (Aug 21, 2004)

Just because we have a new drug doesnt mean its better.


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## Vilazodone (Mar 22, 2010)

NOT necessarily 'better' but less side effects.. I'd take even HALF the benefit of sertraline (but w/out the side effects) as an improvement

I have my fingers crossed on this one. I've tried numerous polypharms and meds, so far only ONE weak but side effect free antidepressant is at my disposal. Even though it is weak it is STILL so much better than nothing. If I can add another weak antidepressant onto it may just be enough to achieve a suitable response. That is all I'm hoping for, not sure about you guys but I don't expect a magic bullet cure to happen during my lifetime.. The only magic bullet likely for me will be an actual bullet.. 

Crumby meds with some benefit still much better than nothing.


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## jim_morrison (Aug 17, 2008)

Vilazodone said:


> NOT necessarily 'better' but less side effects.. I'd take even HALF the benefit of sertraline (but w/out the side effects) as an improvement


I guess thats all relative to the individual as I find effexor better than SSRI's without the side effects.


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## IllusionalFate (Sep 10, 2008)

Whenever this appears on the market, be prepared to pay big bucks for it.



jim_morrison said:


> Yeah SNDRI's will probly be pretty good, IMO they'll possibly be reminiscent of parnate with less medical restrictions and no dietry restrictions. And no orthostatic hypotension obviously.


I don't like the constant blockade of NET, so a SNDRI which is roughly equal in SERT and DAT affinity but with lower NET affinity would be much more preferable. I'd take clonidine at night if the NET affinity is higher than DAT, which will obviously be the case.


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## jim_morrison (Aug 17, 2008)

IllusionalFate said:


> I don't like the constant blockade of NET, so a SNDRI which is roughly equal in SERT and DAT affinity but with lower NET affinity would be much more preferable. I'd take clonidine at night if the NET affinity is higher than DAT, which will obviously be the case.


It's a shame that sertraline has such potent SERT blockade, if it's SERT blockade was weaker, or atleast only as potent as it's DAT blockade it would be a pretty decent selective serotonin-dopamine reuptake inhibitor.


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## Vilazodone (Mar 22, 2010)

Anyone have access to Benthamdirect.org?

I am trying to obtain...


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## BearFan (Mar 22, 2008)

So what company is marketing this Vilazodone? I'm not surprised a big pharma passed it up, because they were probably trying to re-tweak their old existing compounds to make more money. Big Pharma sux and isn't innovative anymore. Like a previous poster stated, if Vilazodone, works nearly as good as a typical SSRI without the weight gain, jitterness and sexual dysfunction, the fact that it lacks those side effects would improve the person's quality of life and thus reducing the depression. Who is going to be happy if there fat, jittery and can't get a boner on an SSRI/SNRI?


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## BearFan (Mar 22, 2008)

How long do NDAs typically take from the FDA to the Pharmacy after passing clinical trials? If Vilazodone has near or better efficacy than common SSRIs, the nice thing would be that dosage increases may bump up efficacy without adverse tolerability. I really hope this medicine is helpful, and becomes first-line. The only ADs that don't have a substantial adverse sexual dysfunction profile are Remeron and Wellbutrin and many cannot tolerate these.


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## Noca (Jun 24, 2005)

Does it affect appetite?


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## odspot (Sep 1, 2009)

rocknroll714 said:


> 5-HT3 blockade is NOT a welcome addition to its pharmacological profile, as 5-HT3 receptors play a major role in facilitating dopamine release in the mesolimbic reward pathway. While 5-HT3 antagonism is anxiolytic and antiemetic, this substance is bound to induce worse emotional blunting even than the SSRIs.


Would that apply to something like Memantine (a 5HT3 antagonist)? or is antagonism different to blockade?


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## crayzyMed (Nov 2, 2006)

odspot said:


> Would that apply to something like Memantine (a 5HT3 antagonist)? or is antagonism different to blockade?


Well in some cases memantine induces dysphoria, in others euphoria but for most its mild and doesnt cause much mood changes, its been said to potentiate amphetamine where 5HT3 also mediates dopamine release from, so the effect should be mild. Why some ppl get depressed from memantine i have no idea. I think NMDA antagonism itself can be dysphoric.


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## Arisa1536 (Dec 8, 2009)

So its not available for at least 2 years? 
that kind of sucks, have there been any tests done to determine the withdrawal success rate? or are they similar to SSRI/SNRI withdrawals? if so then i would not wanna go there :afr

All AD's can increase and decrease appetite and/or libido so i expect the results will vary from person to person


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## jim_morrison (Aug 17, 2008)

Arisa1536 said:


> So its not available for at least 2 years?


It's been available in the US since January, not sure about other countries.


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## billyho (Apr 12, 2010)

jim_morrison said:


> It's been available in the US since January, not sure about other countries.


Can someone tell me where it is available in the US? I don't know if my doc knows about it, nor if my pharmacy knows about it. thought it got bought by another company which was delaying the release?? was i just misinformed?


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## Arisa1536 (Dec 8, 2009)

jim_morrison said:


> It's been available in the US since January, not sure about other countries.


So you dont know about australia/new zealand?


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## jim_morrison (Aug 17, 2008)

Arisa1536 said:


> So you dont know about australia/new zealand?


I assume we'll get it late, if at all (as usual :mum).


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## martyboi (Sep 18, 2009)

I live in the US and I asked my doctor about this stuff just a week ago and he'd never heard of it........??


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## n95 (Jul 17, 2010)

*forget about meds*

People, forget about new meds, the cure for all anxiety based disorders is right here at our disposal, and it basically is nuking the **** out of amygdala with gamma rays until the darn thing shrivels.

Sure, it seems unorthodox approach enough to wonder if ever conventional medicine will accept such a radical form of psycho-surgery (again), but hey, just wait until Mexicans get their hands on one of them gamma ray cannons, and we'll have gamma ray clinics popping out like mushrooms along the Arizona border


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## n95 (Jul 17, 2010)

n95 said:


> People, forget about new meds, the cure for all anxiety based disorders is right here at our disposal, and it basically is nuking the **** out of amygdala with gamma rays until the darn thing shrivels.
> 
> Sure, it seems unorthodox approach enough to wonder if ever conventional medicine will accept such a radical form of psycho-surgery (again), but hey, just wait until Mexicans get their hands on one of them gamma ray cannons, and we'll have gamma ray clinics popping out like mushrooms along the Arizona border


and here's the link

http://news.sciencemag.org/sciencenow/2010/12/fearless-woman-lacks-key-part-of.html


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## crayzyMed (Nov 2, 2006)

The cure all for social anxiety is listening to crayzymed.


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## n95 (Jul 17, 2010)

crayzyMed said:


> The cure all for social anxiety is listening to crayzymed.


LOL Not quite the cure but remedy for sure


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## BearFan (Mar 22, 2008)

The above poster is incorrect; Viibryd/Vilazodone hasn't been available since January, it was FDA Approved then. It's due to be released Q2 (Spring) 2011, but for isn't on Pharmacies shelves yet.


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## Vilazodone (Mar 22, 2010)

What BearFan says is true, plus Viibryd may take ever longer until it arrives at pharmacies, these things take time I suppose.

"
People, forget about new meds, the cure for all anxiety based disorders is right here at our disposal, and it basically is nuking the **** out of amygdala with gamma rays until the darn thing shrivels. 
"

n95, That is one hilarious quote, thanks for the laughs =-D


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## criesovernothin (May 17, 2011)

Very informative thread! I am a newbie and, after reading the posts on this forum, feel I am standing on the shoulders of giants! You all have a lot of good smarts about the pharmacology/neurology love story going on in our buckets! Now, Monday the 23rd of May (next Monday) I am going to see a MD regarding Vilazodone. I don't have much experience in script cocktails, but I can tell you this... The best I've ever felt is during a time in the late '90's when I was taking Phentermine (diet pill) and Prozac...it was for a short time (before fen-phen lawsuits) and long ago. But since I can't have that "sense of euphoria" without diving off totally naked into the pill bottle, AND after years of 40 mg of Prozac daily (which only controlled the anger/anxiety), 20+ pounds of weight gained, lack of motivation to do anything but sleep----I've GOT to try this medication. I will report back with findings....although I feel somewhat a treatment virgin in comparison to others here-perhaps my experience will benefit someone as yours' have enlightened me. Signed Criesovernothin, but HOPEFUL!~


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## criesovernothin (May 17, 2011)

going to MD on the 23rd of this month to request this medication...will post results soon thereafter.


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## BearFan (Mar 22, 2008)

I don't believe its available until late June, does the Doctor have sample? I went to the pdoc a week and 1/2 ago and didn't have any samples, rep meetings or it wasn't in the pharmacies.


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## TyrosineKinase (Jan 20, 2010)

I'm not sure if this is old news or not, but I just read a news article stating that Lu AA21004 *did not* produce significantly reduced depression in the U.S. while it *did* produce a significant reduction of depression in Europe.

I can't link the article because it requires registration but it's from Medscape. They referenced things such as placebo response growing over the last 30 years and the fact that people are heavier in the U.S. and thus a higher dosage is needed to test it's effects.

But doesn't it make some people kind of disheartened to hear that all of these anti-depressant drugs pretty much are just little bit better than placebo. Besides the fear of addiction, is there anything chemically or biologically stopping us from designing a drug that works so much more noticeably for depression as Benzos do for social anxiety and adderall does for depression and anxiety?


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## michael10364 (Feb 4, 2011)

so are there any other interesting antidepressants coming to the market any time soon besides viibryd?


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## crayzyMed (Nov 2, 2006)

michael10364 said:


> so are there any other interesting antidepressants coming to the market any time soon besides viibryd?


Not really:roll


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## n95 (Jul 17, 2010)

n95 said:


> People, forget about new meds, the cure for all anxiety based disorders is right here at our disposal, and it basically is nuking the **** out of amygdala with gamma rays until the darn thing shrivels.
> 
> Sure, it seems unorthodox approach enough to wonder if ever conventional medicine will accept such a radical form of psycho-surgery (again), but hey, just wait until Mexicans get their hands on one of them gamma ray cannons, and we'll have gamma ray clinics popping out like mushrooms along the Arizona border


and now I don't even need Mexicans any more


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