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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 25. This is the beginning of the thread.
Posted by Peter S. on February 7, 2003, at 12:58:43
Here's a great site that lists all drugs in Development including the stages. I notice that applications have been submitted for duloxetine and gepirone- hope they'll be approved soon!
http://www.phrma.org/newmedicines/mentalillness/
Posted by johnj on February 7, 2003, at 13:33:26
In reply to New Drugs in Development, posted by Peter S. on February 7, 2003, at 12:58:43
Maybe I am not looking at the right place, but it seems that it is out of date as lexapro and effexor XR are not approved according to the chart. I wonder what phase things are in at this time?
Posted by Peter S. on February 7, 2003, at 14:14:04
In reply to Is there an updated list? » Peter S., posted by johnj on February 7, 2003, at 13:33:26
Yeah that's true. But some of them seem to be up to date- like it says that duloxetine has been submitted. It's confusing.
> Maybe I am not looking at the right place, but it seems that it is out of date as lexapro and effexor XR are not approved according to the chart. I wonder what phase things are in at this time?
Posted by River1924 on February 7, 2003, at 22:34:47
In reply to Re: Is there an updated list?, posted by Peter S. on February 7, 2003, at 14:14:04
If you look under the section titled notes, a lot of the approved drugs are being specifically tested for children. I believe the FDA has made that a new rule.
> Yeah that's true. But some of them seem to be up to date- like it says that duloxetine has been submitted. It's confusing.
>
>
> > Maybe I am not looking at the right place, but it seems that it is out of date as lexapro and effexor XR are not approved according to the chart. I wonder what phase things are in at this time?
>
>
Posted by SLS on February 8, 2003, at 11:40:10
In reply to Re: Is there an updated list?, posted by Peter S. on February 7, 2003, at 14:14:04
> Yeah that's true. But some of them seem to be up to date- like it says that duloxetine has been submitted. It's confusing.
>
>
> > Maybe I am not looking at the right place, but it seems that it is out of date as lexapro and effexor XR are not approved according to the chart. I wonder what phase things are in at this time?
>
>
Hi.I contacted Eli Lilly last week regarding the approval status of duloxetine (Cymbalta). The FDA granted Lilly an "approvable letter", which is one step away from full approval. It seems that the only thing left for the FDA to examine is the manufacturing facility. Sometimes the wording of the label (package insert) remains as the last obstacle. In any event, as of last week, duloxetine had not started production. Soon, hopefully. It is at the top of my list. In the interim, I don't know if I should just wait and give my poor brain a chance to catch its breath after these recent drug trials. Otherwise, I guess Lexapro would be my next choice; combined with desipramine at first, and perhaps switching from desipramine to Strattera.
I know it is tempting to feel smart by using our very limited understanding of the brain and what drugs do once they get inside it so as to predict the usefulness of any given drug. Obviously, some people show trends in their reactions to drugs within a class. However, one never knows. I recently witnessed someone whom was severely depressed with pronounced psychomotor retardation. Over the last two years of treatment, he failed to respond to Prozac, Zoloft, and Celexa. It's a good thing he wasn't educated enough to decline his doctor's recommendation to try Paxil next. He has attained full remission.
During a consultation with Patrick McGrath, MD at Columbia University, he told me quite simply that for every new drug that becomes available, a certain percentage of previously refractory cases of depression and bipolar disorder will respond and go on to lead healthy lives. To hear this has helped me to resist better occasional paroxysmal bouts of suicidal ideation.
I know at least one person who does better on Lexapro than he does on Celexa. I can't help but to have at least some hope that I'll get lucky with one of the new medications that have come out over the last 6 months.
After duloxetine and gepirone come to market, I am unaware of any other antidepressants close to obtaining FDA approval.
Is anyone aware of other antidepressants in phase III or close to being approved?
- Scott
Posted by Dave1 on February 8, 2003, at 15:34:22
In reply to Re: Is there an updated list?, posted by SLS on February 8, 2003, at 11:40:10
When they say that gepirone is a 5HT1A agonist. What does that mean?
Thanks,
Dave
Posted by jrbecker on February 8, 2003, at 16:07:07
In reply to Re: Is there an updated list? » SLS, posted by Dave1 on February 8, 2003, at 15:34:22
Gepirone plays a role of selectivity for both the 5HT1a pre- and post-synaptic receptors. Unlike Buspar, it has a much higher affinity for this receptor over the D2 receptor. Long-term studies have shown that gepirone has a differential action at presynaptic (agonist) and post-synaptic (partial agonist) 5-HT1A receptors.
It can be argued that the 5HT1a postsynaptic receptor's role in anxiety in depression is probably the most important of all the serotonin subreceptors. It is believed that the delayed onset of most SSRI's might be due to the period of time it takes for the desensitzation of the 5HT1a recpetors to occur. The receptor has a very distinct role in decreasing worry, aggression, and depression. It also helps increase vigilance as well as libido. Thus, it might have a very important role for atypical depressives. Columbia University in NYC is currently holding a trial of gepirone for just such a purpose. If you suffer from atypical depression and are interested in the trial, please call their Depression Evaluation Service at 212-543-5734. The renowned Columbia team of Stewart, McGrath, and Quitkin are all involved with this study. I know for a fact that they are closing down admittance into this study in the next month or so though.JB
Posted by noa on February 9, 2003, at 7:01:40
In reply to Re: Is there an updated list?, posted by SLS on February 8, 2003, at 11:40:10
Scott, I am glad you are holding on to your hope. I agree. There is still a lot that is not known about why one med works for one person and not another and why one med works and others don't.
BTW, What is duloxetine? Is it related to reboxetine and atamoxatine? What is gepirone?
Posted by noa on February 9, 2003, at 7:03:47
In reply to Re: Is there an updated list? » Dave1, posted by jrbecker on February 8, 2003, at 16:07:07
Does this mean that it is more highly selective than other serotonergic meds? Does it not blanket the other 5Ht receptors as much as other serotonergic meds? Meaning fewer side effects?
Posted by SLS on February 9, 2003, at 9:53:29
In reply to Re: another question on gepirone, posted by noa on February 9, 2003, at 7:03:47
Hi Noa.
In re: duloxetine (Cymbalta)
Duloxetine is a dual-action antidepressant being developed by Eli Lilly (makers of Prozac and Strattera). In this case "dual-action" refers to the ability of duloxetine to inhibit the uptake of both norepinephrine and serotonin. It is similar to Effexor in this regard. However, duloxetine is thought to be better balanced, inhibiting each to roughly the same extent. With Effexor, its action on serotonin is at least 10 times stronger than of norepinephrine. I don't recall the ratio for duloxetine, but I am pretty sure it is no greater than 3 times more potent at serotonin as norepinephrine. If the results of the investigations into the effectiveness of duloxetine can be trusted, it appears to be a particularly potent antidepressant. It demonstrates a robust ability to mitigate the somatic features (pain symptoms) of depression as well as those mental. The onset of antidepressant effect is reported to be quicker with duloxetine than the SSRIs (similar to Effexor), and at least one study found duloxetine significantly more effective than Paxil. An analysis of over 2000 subjects given Effexor demonstrates that, not only does it produce improvements in a larger number of people, but it also tends to bring people closer to full remission. I hope duloxetine does the same. It is hoped that it becomes available within the next few months. It is pending final FDA approval, having already been issued an "approvable letter."
In re: gepirone (Ariza)Gepirone is a serotonergic drug being developed by Organon. It is tentatively scheduled to be approved in 2004 as an extended-release preparation. Gepirone binds tightly to the serotonin receptor, 5-HT1a, without affecting dopamine D2 receptors. JRBecker explained this very well.
http://www.dr-bob.org/babble/20030208/msgs/140184.html
Gepirone is a full agonist of the 5-HT1a presynaptic autoreceptor. The stimulation of these receptors actually reduces the synthesis and release of serotonin, reducing neuronal activity. It also binds to postsynaptic 5-HT1a receptors, an action that tends to increase neuronal activity. Although bound to a receptor, it does not necessarily stimulate it. It is thus called a "partial agonist" at this site. Not only do 5-HT1a receptors exist on serotonergic neurons, they are also found on dopaminergic neurons. The stimulation of these receptors can increase the release of dopamine from these neurons.
* partial agonist: a drug with lower intrinsic activity than a full agonist, producing a lower maximum effect.
So, what is the net effect of gepirone on serotoninergic activity? I'm not sure. It appears to me that it might act as a sort of a synaptic stabilizer, moderating serotonergic tone to prevent hyperexcitability of neurons. There are several other sites along the neuron that 5-HT1a receptors are located. They appear on the axon (the "transmission cable") and the soma (cell body containing the nucleus and control machinery). I'm pretty sure that these receptors act as autoreceptors to regulate and decrease serotonergic activity. This is probably the mechanism by which it is reported by some that pindolol accelerates the antidepressant response to SSRIs (although not increasing the percentage of people who respond). Pindolol is probably acting as a temporary dampener of neuronal excitability until postsynaptic receptors are downregulated. That's my guess, anyway. I guess I should study this stuff more closely. I don't find myself with the energy nor motivation to research things so much anymore. I'd rather be married with children.
Oh well...
- Scott
Posted by ShelliR on February 9, 2003, at 12:28:24
In reply to Re: another question on gepirone » noa, posted by SLS on February 9, 2003, at 9:53:29
Hi Scott,
What has been your experience with effexor?
My last try was in the hospital. They pulled me off of oxycontin in one day and titrated me up to 150mg of effexor in two days. I kept blacking out everytime I got up; they blamed that on the detox from oxy (no one even helped me--like I deserved to black out and fall--bad drug addict person that I was). In reality, I'm sure my blackouts were from going up too fast, too high on effexor; I had never before blacked out from getting off an opiate, even in one day.
I'd like to see a study with effexor matched against Duloxetine, but I don't see the advantage to Wyeth-Ayerst Laboratories in participating.
Shelli
Posted by Dave1 on February 9, 2003, at 16:44:09
In reply to New Drugs in Development, posted by Peter S. on February 7, 2003, at 12:58:43
Some comments on some of the posts if I may. First, I've been on effexor for about 5 weeks and it hasn't work. I tried augmenting it with lithobid and thyroid hormone but that didn't work either.
Regarding pindolol, I've read alot about it and have been trying to get my docs to try it. I've read a few articles saying that it would make SSRI-non-resonders respond to the SSRI.
I'm still not sure I understand about gepirone. Would it be similiar to taking pindolol alone, not as an augmentor, or, does it work in a way totally different from any other antidepressants.
Thanks,
Dave
Posted by SLS on February 9, 2003, at 20:10:22
In reply to Re: another question on gepirone » SLS, posted by ShelliR on February 9, 2003, at 12:28:24
Hi Shelli.
> What has been your experience with effexor?
I have tried Effexor at least two times. Each time, I received some mild improvement from it, although it tends to plateau early. I found that I did better when adding a tricyclic (imipramine) to it. I can't say that it is written in stone, but I think there might be some overlap between Effexor responders and MAOI responders.
> My last try was in the hospital. They pulled me off of oxycontin in one day and titrated me up to 150mg of effexor in two days.
Oh, my. Johns Hopkins?
> I kept blacking out everytime I got up
Was it orthostatic hypotension? Did your heart race and you feel palpitations just before fainting? It was probably a synergistic effect of combining opiate withdrawal with Effexor-driven alterations in the autonomic nervous system to yield a sort of sympathetic overdrive (fight-or-flight). I had something similar happen to me when I was at the NIMH. They titrated me very quickly on clorgyline (experimental MAOI) after chronic exposure to a Remeron-type drug known as idazoxan. The idazoxan acted to prime the system to exaggerate the hypotensive effects of clorgyline. I was delirious for three days. In any event, I don't think you were treated with an appropriate prudence. <shaking head>
I don't know if I mentioned it in another thread, but I am out looking for a new doctor. I wish I had trusted my instincts earlier. The guy I had been seeing is far too conservative and lacks the creativity to treat a case like mine. He really misrepresented himself during my first appointment with him. He talked about using unspecified exotic drug combinations and said he would consult with his colleagues at NYU about my case. After two years, he did neither. What a f_cking waste of the time I have remaining to find a life worth living! I have an appointment with my old doctor in Princeton on Tuesday. It will be a sort of consultation in which I can get some of his recent thoughts regarding my treatment and to help me find doctor appropriate for treating TRD and who takes Medicare. He no longer participates with Medicare, and $170.00 for 15 minutes is cost prohibitive. Perhaps I'll have more luck if I just go through the phone book and cut out the individual names of all the listed psychiatrists practicing within a 20 mile radius. I could then place them all in a hat...
Have you considered Lexapro? What has been your experience with tricyclics? My next move might be to add Lexapro to my current combination of desipramine 300mg + Lamictal 200mg. You could add Lexapro to Strattera, especially if you should find Strattera at all helpful. I d/c'd Nardil two weeks ago. I'm still experiencing withdrawal effects. I would prefer to try duloxetine first, though. I don't know about gepirone. My doctor in Princeton was performing a clinical trial with it two years ago. It would be great if it were to be a robust antidepressant, but my first thought is that it might be more effective as an anxiolytic monotherapeutically or as an augmentor of antidepressants. I really don't know. I guess any drug yet untried becomes a ray of hope.
Take care.
- Scott
Posted by SLS on February 9, 2003, at 20:40:45
In reply to Re: Is there an updated list? » SLS, posted by Dave1 on February 8, 2003, at 15:34:22
Hi Dave.
Sorry I didn't see your post earlier.
First - what is a receptor?
A receptor is a site upon which specific chemicals (known as ligands) bind. The receptor usually functions to trigger biological events when it is stimulated. For instance, a serotonin receptor is a protein found on the surface of certain neurons. Serotonin (5-HT) is a neurotransmitter (ligand) that, when attached to its receptor, stimulates it and causes the receiving neuron to send a message.
A ligand can either stimulate a receptor or block that receptor from being stimulated by other ligands:
AGONIST: A ligand that attaches to and stimulates a receptor is an agonist of that receptor.
ANTAGONIST: A ligand that attaches to a receptor without stimulating it, thereby preventing stimulatory ligands to gain access to it is an antagonist of that receptor.
PARTIAL AGONIST: A ligand that attaches to and stimulates a receptor to a degree less than that of a full agonist.
There are often multiple receptor subtypes that bind the same neurotransmitter. 5-HT1a is a subtype of serotonin receptor. Not only does it bind natural serotonin, but also specific drugs. Often, a drug will bind to one subtype and not another. Gepirone binds to 5-HT1a receptors but not 5-HT2 receptors. With Serzone, the reverse is true.
I hope this was helpful.
- Scott
Posted by noa on February 9, 2003, at 22:17:48
In reply to Re: another question on gepirone » SLS, posted by ShelliR on February 9, 2003, at 12:28:24
I don't know anything about the effects of cutting off oxycontin cold turkey, but fwiw:
When I was at higher doses of effexor (which has been the most effective AD for me), I had similar black out experiences. Or shall I say that most of them were gray outs except the one time I fainted. That is why I no longer take such a high dose.
When I started, I started much much more slowly than what they had you start at.
Posted by noa on February 9, 2003, at 22:19:41
In reply to Re: another question on gepirone » noa, posted by SLS on February 9, 2003, at 9:53:29
Thanks, Scott. I think I followed what you wrote, but there sure is a lot more I need to learn about neurons and receptors! But I think I understood enough to get the gist. Thanks.
Posted by Stan on February 9, 2003, at 22:41:02
In reply to Re: another question on gepirone » ShelliR, posted by SLS on February 9, 2003, at 20:10:22
Scott wrote:
<<<<<<<<I don't know about gepirone. My doctor in Princeton was performing a clinical trial with it two years ago. It would be great if it were to be a robust antidepressant, but my first thought is that it might be more effective as an anxiolytic monotherapeutically or as an augmentor of antidepressants.<<<<<<<<<<<
i haven't read all of the messages in this thread or visited that site with the "new drugs in development" articles, but it's worth noting that gepirone is very closely related to buspirone (Buspar). i think the only main difference is that it has greater selectivity for the 5HT1 serotonin receptor whilst having less effect on dopamine receptors. it's been known for some time that buspirone binds to the D2 family of dopamine receptors, but it took a long time for researchers to figure out exactly what it accomplishes there, if anything. i think they finally discovered that it acts as both an agonist and an antagonist at those sites, in ways that i don't understand and thus can't describe. buspar was always marketed as a "serotonin drug" and the dopamine business was not talked about much until well after it was introduced.anyway, at the risk of sounding cynical, my guess would be that patients who have found buspirone to be lacking in effectiveness for treating their anxiety/depression might find that gepirone falls short as well. that's just an opinion, and i haven't done much reading about either medication in recent years -- i just remember gepirone being talked about back in the mid-90's...
Stan
Posted by jrbecker on February 10, 2003, at 0:10:41
In reply to Re: another question on gepirone, posted by Stan on February 9, 2003, at 22:41:02
Stan,
your cynicism is most likely shared by all of us in terms of gepirone being anyting more than a step above buspar. Fortunately, this is most likley not the case though. I myself participated in a gepirone trial a while back. It was most likely, however, that I got administered the placebo (I think we've all taken enough drugs to be cognizant of their effects).
While in the trial I did have the chance to talk in detail with the researchers in the study (Quitkin, Stewart, and McGrath). And in doing two separate trials for the drug already, they are fairly certain of its extreme effectiveness for the atypical features of depression. They believe it will most have more commonality with the SSRIs than with Buspar itself. McGrath even went so far to say that the mood effects might outmatch most SSRIs (I am reserving judgment of this statement until I try it myself though). However, it should be noted that the reason gepirone has had so much problems with the FDA is because of the results of its first trial which matched geprione against placebo and prozac. Gepirone performed very well, yet the prozac did not, thus it was somewhat of a failed trial. This is because in drug trials, the standard drug of comparison, which is prozac in this case, needs to perform well also, or the trial drug (gepirone) can't be deemed an effective AD. Unfortunately, prozac is not a great candidate in treating atypical depression to begin with so the study ran into some obvious methodological issues.
The current study is testing gepirone against paxil and placebo. And they hope to have similar success with this trial, but without the same methodoligical issues as the last one.
Time will only tell how gepirone will perform once on the market. Unfortunately, we'll have to wait about a year and a half to find that out.
JB
Posted by SLS on February 10, 2003, at 8:05:21
In reply to Re: another question on gepirone, posted by jrbecker on February 10, 2003, at 0:10:41
Hi.
If there is one thing that I've learned over the years about antidepressants is that "different is different". Quite a few people took it upon themselves to disuade people from trying Lexapro because, on paper, it was nothing more than a repackaged Celexa (s-citalopram + r-citalopram combination). After all, Lexapro is "nothing more" than a preparation of just one of the two components of Celexa (s-citalopram). How could the same molecule contained in Lexapro be any more effective in a given individual than it is when it is administered as a component of Celexa? I don't know. How could I? It just is.
Different is different. S-citalopram, in the absence of r-citalopram, is, de facto, operating in a very diffent environment, and might very well be yielding different alterations in the dynamics of the synapse or other sites within neurons.
I hope gepirone is better than buspirone at treating depression. I think hope is justified. After all, it is different.
- Scott
Posted by ShelliR on February 10, 2003, at 11:59:45
In reply to Re: another question on gepirone » ShelliR, posted by noa on February 9, 2003, at 22:17:48
> I don't know anything about the effects of cutting off oxycontin cold turkey, but fwiw:
>
> When I was at higher doses of effexor (which has been the most effective AD for me), I had similar black out experiences. Or shall I say that most of them were gray outs except the one time I fainted. That is why I no longer take such a high dose.
>
> When I started, I started much much more slowly than what they had you start at.Hi Noa,
They started me so quickly because I was so suicidal. If the doctor had even glanced at the PDR, he would have realized that effexor often causes hypostatic reactions. I read about it in the nurse's manual--that's all they had up there and it said to warn patients about this possibility. I have seen the ugliest side of psychiatrists this last year; they hate when you figure out something that they should have known. I've "greyed" out before, but this was the only time I've ever actually blacked out, over and over for very short times.
btw, Scott, it was a small unit in a Washington, D.C. hospital, not Johns Hopkins. It looked like a geriatric unit; mean age was about 80 because the director is a geriatric specialist. I think Hopkins is the only hospital I would try in my area and I probably wouldn't even try that, I am so down on hospitals and hospital pdocs.
I think there's a possiblity that effexor might have worked if I could have given it the time; but my pdoc (then) insisted that I give up opiates first. I can't afford to go through side effects because I can't afford not to work, or to work and keep disappointing people like I did last year. It's taken me too long to build up my business; plus both my pdoc and pain doc say that opiates will not prevent ADs from working.
At some point I may rethink effexor and try again, but I'm pretty much as scared of effexor as I am of opiates. My present doctor doesn't think he could get me high enough on effexor (because of my blackouts) for a therapuetic dose.
Shelli
Posted by iris2 on July 10, 2004, at 22:36:01
In reply to Re: another question on gepirone » noa, posted by SLS on February 9, 2003, at 9:53:29
> > In re: gepirone (Ariza)
>
> Gepirone is a serotonergic drug being developed by Organon. It is tentatively scheduled to be approved in 2004 as an extended-release preparation. Gepirone binds tightly to the serotonin receptor, 5-HT1a, without affecting dopamine D2 receptors. JRBecker explained this very well.
>
> http://www.dr-bob.org/babble/20030208/msgs/140184.html
>
> Gepirone is a full agonist of the 5-HT1a presynaptic autoreceptor. The stimulation of these receptors actually reduces the synthesis and release of serotonin, reducing neuronal activity. It also binds to postsynaptic 5-HT1a receptors, an action that tends to increase neuronal activity. Although bound to a receptor, it does not necessarily stimulate it. It is thus called a "partial agonist" at this site. Not only do 5-HT1a receptors exist on serotonergic neurons, they are also found on dopaminergic neurons. The stimulation of these receptors can increase the release of dopamine from these neurons.
>
> * partial agonist: a drug with lower intrinsic activity than a full agonist, producing a lower maximum effect.
>
> So, what is the net effect of gepirone on serotoninergic activity? I'm not sure. It appears to me that it might act as a sort of a synaptic stabilizer, moderating serotonergic tone to prevent hyperexcitability of neurons. There are several other sites along the neuron that 5-HT1a receptors are located. They appear on the axon (the "transmission cable") and the soma (cell body containing the nucleus and control machinery). I'm pretty sure that these receptors act as autoreceptors to regulate and decrease serotonergic activity. This is probably the mechanism by which it is reported by some that pindolol accelerates the antidepressant response to SSRIs (although not increasing the percentage of people who respond). Pindolol is probably acting as a temporary dampener of neuronal excitability until postsynaptic receptors are downregulated. That's my guess, anyway. I guess I should study this stuff more closely. I don't find myself with the energy nor motivation to research things so much anymore. I'd rather be married with children.
>
> Oh well...
>
>
> - Scott
>
>
>
> Scott,You made my day!
"I'd rather be married with children." Let's research that one for a while. It would most likely be more informative and might actually yield measurable results!
iris
>
Posted by SLS on July 10, 2004, at 23:38:43
In reply to Re: another question on gepirone, posted by iris2 on July 10, 2004, at 22:36:01
> > I don't find myself with the energy nor motivation to research things so much anymore. I'd rather be married with children.
> >
> > Oh well...
> >
> > - Scott
> You made my day!
>
> "I'd rather be married with children." Let's research that one for a while. It would most likely be more informative and might actually yield measurable results!
> iris
I'm glad that such an old post could still have so much impact.:-)
It's too bad that the drug I was researching at the time was rejected by the FDA this past month. It would have made a good tool to help treat depression and anxiety disorders. This kind of thing wouldn't be happening if Florida had used electronic balloting.
- Scott
Posted by KaraS on July 11, 2004, at 4:36:54
In reply to Re: another question on gepirone, posted by SLS on July 10, 2004, at 23:38:43
> > > I don't find myself with the energy nor motivation to research things so much anymore. I'd rather be married with children.
> > >
> > > Oh well...
> > >
> > > - Scott
>
>
> > You made my day!
> >
> > "I'd rather be married with children." Let's research that one for a while. It would most likely be more informative and might actually yield measurable results!
> > iris
>
>
> I'm glad that such an old post could still have so much impact.
>
> :-)
>
> It's too bad that the drug I was researching at the time was rejected by the FDA this past month. It would have made a good tool to help treat depression and anxiety disorders. This kind of thing wouldn't be happening if Florida had used electronic balloting.
>
>
> - Scott
>
>
Nor would it have happened if the Supreme Court weren't packed with right-wing political hacks!!
Posted by Dr. Bob on July 11, 2004, at 8:43:18
In reply to Re: another question on gepirone, posted by KaraS on July 11, 2004, at 4:36:54
Posted by dawnfawn on December 8, 2004, at 7:49:35
In reply to New Drugs in Development, posted by Peter S. on February 7, 2003, at 12:58:43
I'm confused was Gepirone approved? Is it still in testing? I would like to apply if it is in testing.
This is the end of the thread.
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