Retigabine (Trobalt, Potiga) — General Discussion

It isnt a law stopping me its the fact that there are none of these tables available to get. The medication was approved last year but the supplier of this medication ( gsk ) have not decided on a date when it will be made available here, so thats the reason why i cannot get any, as per below..


TGA registers Trobalt
GlaxoSmithKline has announced the TGA registration of Trobalt (retigabine). The product is not currently commercially available in Australia, with GSK saying it will work with its partner company Valeant to provide certainty as to how Trobalt may be supplied to patients. Trobalt is used for the treatment of epilepsy.
The above snippet is the first part of an article sent to subscribers in Pharmacy Daily's issue from 29 Oct 13

That is really freaky, I hope you get your stuff soon, either by local or international suppliers.
 
That is really freaky, I hope you get your stuff soon, either by local or international suppliers.

hopefully gsk will release it soon enough, why it takes nearly a year up to now to get it on the market is beyond me, its not like this is the first country they have marketed it in is it, just dont understand what the hold up is, so it is very frustrating to have the ability to get it but none available.
 
It is not offtopic as many here are talking about a solution that will cure them. I am expanding upon the concept. I am saying that our potassium channels are in at least a portion of it permanently damaged and that we are generations away from something that will fix it. For now we can probably remove the tinnitus with various pills but not remove the defect that causes it. The whole point is that there is no trade-off. The concept that life is balanced is a lie. If our evolution was any better we would have intelligence and valuable properties which we lack. The thing is that we are not evolving ourselves we are only evolving a specific fraction of the tools in our daily usage.
I hear what you are saying. More discussion on Kv potassium channels. Look to wiki that benryu said he is starting.
 
Ok. I have two boxes of Trobalt. 21x50mg and 84x100mg. From now (15.00 Paris time) i decided to join experimental group.

first week 3x50mg, the second one 100mg. I dont know yet, if i increase dosage to 150 or 200mg.

I take per day:
A vit 6000iu, E vit 400iu, C vit 1000mg, Zinc citrate 25mg, 3x500magnesium lactate, 3x600mg NAC, 1x20mg Lutein and 2x betahistine 24 mg
1x5mg melatonin - before sleep
and for now Trobalt.

I will report every changes of T or adverse effect of course.

Short about my T:
Acoustic trauma 6.7. 2012 at 10.30am

multitonal tinnitus in both ears, and white noise type hissing
worsened hearing (with many notches)

How did you manage to obtain the meds johno, through a Dr or some other source ?
 
I find some of the "people never heal" from anything talk on here simply pessimistic, but I think taken to an extreme, it's pessimistic and unrealistic.

A great example is people who have severe strokes that destroy their ability to communicate verbally, and then are able to re-learn that using different parts of their brain, even late in life. If plasticity and rewiring wasn't a thing, that simply wouldn't be possible.

A less tangential example is a good number of people I've communicated with over the years who developed what seemed like intractable tinnitus as a result of withdrawal from benzodiazepines, and then recovered from it completely. I've spoken to at least a half dozen people who had that symptom for 2-3 years following benzo withdrawal, and woke up one day and it was gone. (Yes, I have also communicated with people who developed this problem in that way and never had it resolve, but they're actually in the minority, in the demographic of people who did not have tinnitus prior to benzo withdrawal).

As far as tissue/muscle injuries go; I was knocked off my bike by a truck two and a half years ago, and couldn't hold weight on my right leg for months afterwards. Yes, I still have scars, and that knee will never be exactly the same as it was during the accident, but at this point I routinely go on 5-6 mile hikes into the mountains.
 
I find some of the "people never heal" from anything talk on here simply pessimistic, but I think taken to an extreme, it's pessimistic and unrealistic.

A great example is people who have severe strokes that destroy their ability to communicate verbally, and then are able to re-learn that using different parts of their brain, even late in life. If plasticity and rewiring wasn't a thing, that simply wouldn't be possible.

A less tangential example is a good number of people I've communicated with over the years who developed what seemed like intractable tinnitus as a result of withdrawal from benzodiazepines, and then recovered from it completely. I've spoken to at least a half dozen people who had that symptom for 2-3 years following benzo withdrawal, and woke up one day and it was gone. (Yes, I have also communicated with people who developed this problem in that way and never had it resolve, but they're actually in the minority, in the demographic of people who did not have tinnitus prior to benzo withdrawal).

As far as tissue/muscle injuries go; I was knocked off my bike by a truck two and a half years ago, and couldn't hold weight on my right leg for months afterwards. Yes, I still have scars, and that knee will never be exactly the same as it was during the accident, but at this point I routinely go on 5-6 mile hikes into the mountains.

I do not think that it is pessimistic, on the contrary, we tend to focus on positive stuff. The amount of sad and expectedly bad prognosis stories getting rememebered and focused on by society and individuals in general are small although they are dominant. From all the people who have chronic tinnitus or any other chronic illness most of what I have found out is that they are taking something to numb their experiance. Your example is of a tinnitus from benzodiazepine withdrawal is a very tiny part of the community, most of which is made up of people who got tinnitus from acoustic damage and not just chemical disbalance (side of a drug).

You also seem to not differentiate between regaining some function and regeneration. I do not think that a realistic view of potassium channel changers as treatment and not a cure is pessimistic. Cure is supposed to fix you are remove something permanently. Pharmaceutical industry is generally not in the business of curing anything, but of management of diseases.

Finally trough Dr, but he is friend of my good friend (woman, but not girlfriend) :)

he is a woman?
 
OK...no doubt I will catch some flak for this, but I am having enough trouble keeping track in this thread without diatribes about the capacity of the body to heal or not to heal. All I need is evidence of my own history to emphatically answer that question for myself (Ummm, just look at the zillions of people who got sick then went on to live normal lives for another 50 years...though yes, if you get your leg blown off in Iraq it's not going to regenerate)...It's a non-issue for this thread and may I politely suggest it's an example of one that could be in a new thread.
Valid subject, wrong place.
Let's try hard to keep this focused on Retigabine, and now inevitably, on "K-channels" and the mechanisms of how these sister drugs (including AUT00063 of course) are potentially working on Tinnitus (hell even Glutamate functioning is integrally intertwined so that too is another add-on/add-in!). Personally, I find the explanation of these mechanisms absolutely imperative to my decision as to whether to take the drug or not, so it's not just mind games and intellectual interest, etc.

@attheedgeofscience ...(now way back, a day or so ago in this thread!) Yes I agree with you that waiting a few more days or weeks to see what the Autifony Phase II requirements are is not too big a deal. As you say, we won't know until they say, and if they don't dilly dally, what's a few more weeks in over a half century of my tinnitus! However, I stick to my sense that I'm not a likely candidate and the competition will be fierce. They will have boatloads of guinea-pigs falling off the decks once word gets out.

Another point...even though Retigabine is a blunt instrument (shotgun) and is not laser guided to Kv3, it still seems to be having an effect on our two main guinea pigs so far...Matt and Christian. Of course, the more folks we have trying it the better, especially "long term T'ers" to see how it deals with an 'entrenched' brain functioning pattern.

Also the next big question is what happens when they taper or stop. Now THAT is going to be very intriguing!

Lastly, as an aside..."side effects" are no small matter in my view, no matter how crappy a lot of other meds look...messing with eyes is a flag worth paying attention to, even if it's a supposedly 'down the road' with longer term use thing. There are always exceptions...Again I have personal experience with that! You never really know as there are lots of people out there that have had "unexpected" reactions to meds and become a statistic. Not trying to scare anyone off, but just trying to emphasize caution and careful tapering, up or down...and patience if trialing this stuff.

Best...Zimichael
 
http://qjmed.oxfordjournals.org/content/93/12/787.full
I do not share the rosy view that any medicine will fix our hearing nerves, as this is a illness that in most cases is something you die with it only seems logical that a non-permenent solution that you also seem to need to take until you die is the only thing that will fix it.

I don't think blanket statements like this are true. It really depends on the details and specifics. In particular, it may depend on whether the underlying mechanism which causes the Kv channel down regulation is reversible or not. It might be the case that there is no real 'damage', but that the down regulation is simply a plasticity response by the brain to a new state (lack of input from certain hair cells), in which case it might be possible to use similar plasticity mechanisms to revert it to the original state.

In any case, given the lack of details of the mechanism of action for the cause of the problem, we can't really say whether it is permanently reversible or not.

You also seem to not differentiate between regaining some function and regeneration. I do not think that a realistic view of potassium channel changers as treatment and not a cure is pessimistic. Cure is supposed to fix you are remove something permanently.

Again, this depends on the detailed neurobiology of the brain's response to potassium channel changers. There simply isn't enough data now to know one way or the other.

Pharmaceutical industry is generally not in the business of curing anything, but of management of diseases.

Antibiotics and vaccinations are just a few counterexamples to that statement that come to mind.
 
I don't think blanket statements like this are true. It really depends on the details and specifics. In particular, it may depend on whether the underlying mechanism which causes the Kv channel down regulation is reversible or not. It might be the case that there is no real 'damage', but that the down regulation is simply a plasticity response by the brain to a new state (lack of input from certain hair cells), in which case it might be possible to use similar plasticity mechanisms to revert it to the original state.

In any case, given the lack of details of the mechanism of action for the cause of the problem, we can't really say whether it is permanently reversible or not.

Again, this depends on the detailed neurobiology of the brain's response to potassium channel changers. There simply isn't enough data now to know one way or the other.

Antibiotics and vaccinations are just a few counterexamples to that statement that come to mind.

The burden of proof rests upon those who claim that it is reversible and will stay that way. There is no convincing reason to assume that it will behave differently than other neurological-illness management drugs.
 
Geeez...@Hengist just give peace a chance. We're not talking the Middle East here.

Patience my man, patience...Let's just wait and see, it's going to all come out in the wash in due course.

Zim.
 
How about this little idea - instead of fiddling with the Kv channels to control the firing of the cell, find a way to DESTROY the haywire cell completely. Fight it like a cancer - chemo kills the cancer cell, it doesn't try to repair its dna,etc. back to normal.

If that can be done selectively enough - to only destroy the cells with improperly functioning Kv channels (or other deviations that cause it to fire abnormally), then the rest of hearing can be preserved.

Of course, this is assuming that no output from a cell is better than aberrant output...i.e. that lack of output will not cause some further plasticity/adaptation/up-down regulation of other neurons further upstream.
 
How about this little idea - instead of fiddling with the Kv channels to control the firing of the cell, find a way to DESTROY the haywire cell completely. Fight it like a cancer - chemo kills the cancer cell, it doesn't try to repair its dna,etc. back to normal.

If that can be done selectively enough - to only destroy the cells with improperly functioning Kv channels (or other deviations that cause it to fire abnormally), then the rest of hearing can be preserved.

Of course, this is assuming that no output from a cell is better than aberrant output...i.e. that lack of output will not cause some further plasticity/adaptation/up-down regulation of other neurons further upstream.

That would be an awesome method, could probably solve numerous neurological issues, however I think that requires nanotechnology guiding those terminator cells. However it would lead to hearing loss probably equivalent to the loudness of tinnitus.
 
How about this little idea - instead of fiddling with the Kv channels to control the firing of the cell, find a way to DESTROY the haywire cell completely. Fight it like a cancer - chemo kills the cancer cell, it doesn't try to repair its dna,etc. back to normal.

If that can be done selectively enough - to only destroy the cells with improperly functioning Kv channels (or other deviations that cause it to fire abnormally), then the rest of hearing can be preserved.

Of course, this is assuming that no output from a cell is better than aberrant output...i.e. that lack of output will not cause some further plasticity/adaptation/up-down regulation of other neurons further upstream.

But if you REPAIR damaged cell metabolism instead destroying it, maybe you will repair its function and improve hearing. Of course, not at - before acoustic trauma level, because missing stereocilia. This looks like better option :)
 
How about this little idea - instead of fiddling with the Kv channels to control the firing of the cell, find a way to DESTROY the haywire cell completely. Fight it like a cancer - chemo kills the cancer cell, it doesn't try to repair its dna,etc. back to normal.

This is exactly what HIFU ablation is. There is a clinic in switzerland gearing up to do this for tinnitus. They will use fMRI to pinpoint the hyperactivity down to a 0.5mm spot, and then use ultrasound ablation to drill a tiny hole in your brain. It will cost about $40,000, and of course at this point the longitudinal risks are unknown.

But if you REPAIR damaged cell metabolism instead destroying it, maybe you will repair its function and improve hearing. Of course, not at - before acoustic trauma level, because missing stereocilia. This looks like better option :)

There is a trial being done in humans now, using a synthetic virus that codes for the protein that causes cilia to grow in the first place. So, they peel back your ear drum, inject the virus, and then it generates the protein which should in turn cause your body to grow new hair cells. The trial being done now is using people who are profoundly deaf to start with, because the biggest risk seems to be that this could have some deleterious effect to whatever hearing you have prior to the procedure.

Both of these things are probably at least 5-10 years away from the point where a normal person could feel good about attempting them, in my opinion -- but it's pretty fascinating to me that it's even possible at all; 20 years ago it was pure science fiction.
 
That would be an awesome method, could probably solve numerous neurological issues, however I think that requires nanotechnology guiding those terminator cells.

Nanotechnology is the most obvious (but perhaps hard to implement right now) method - you just have nanobots attach to synapses and measure firing rates, and destroy the cells firing abnormally. But there are many others conceivable methods - for example some molecular compound or protein that is sensitive to the frequency of neurotransmitter release, and is activated by a specific frequency and other biological markers that only exist near the area of target cells (such as the spiral ganglion).

However it would lead to hearing loss probably equivalent to the loudness of tinnitus.

If you only destroy the cell that is misfiring, I don't see why it would lead to hearing loss - e.g. if the spiral ganglion neuron that is misfiring has as its input hair cells at the 10khz frequency, and damage to those hair cells is what caused the misfiring in the first place, then hearing at 10khz is lost anyway already. The problem is the irregularly firing spiral ganglion neuron associated with 10khz that is causing a phantom sound at 10khz, through its firing. Destroying it would quiet it down, but again, provided that something further upstream will not react to this quieting down.
 
THANK YOU BEDOUIN! I really appreciate that.
If you inquire at your local chemist's/doctor could you also ask if that is the price a non-national would also pay and if not, then what is. Merci.

p.s. dont forget to tag my name so I will see your post :)
No problem. I'm not mobile at the moment but as soon as I am I will be sure to track it down and tag you in the response.
 
Wow, I have been in this thread for a few days and it's like war here. *__*

I am really busy at the moment but I have seen so much misinformation around that it will be useful if I clear a few things out.

You guys seem to trip on the area I did not explain much because of its complexity (glutamate action and link).
I also saw some crazy theories about T. being permanent and irrevocable state. W T F people lol

I clear this area for once in the most simple way I can.

We all agree to that:

Noise trauma ==> Hair Cell death ==> glutamate release ==> Kv3.1 channel "lock"==> abnormal spontaneous firing ==> T.

So what happened beteween glutamate release and the Kv channel abnomality, and why it's reversible.

We all know that this bitch of glutamate is excitotoxic:
http://en.lmgtfy.com/?q=glutamate excitotoxicity
(CTRL+F, glutamate)

When the glutamate is released it forces the postsynaptic bouton to swell and burst.

(the pink thing is not a testicle)
1.jpg


"But but this Ca2+ is not glutamate, I don't understand, we will all die of T. !!"

Calm down son, increased extracellular glutamate levels leads to the activation of Ca2+ permeable NMDA receptors on myelin sheaths and oligodendrocytes, leaving oligodendrocytes susceptible to Ca2+ influxes and subsequent excitotoxicity.


(Boom )
2.jpg


"OMG OMG the postsynaptic bouton has exploded, my body is broken, we will all die of T. or maybe diarrhea!!"

No worries contrary to what was said above in the thread, we are the most complex mammal on earth because of our brain, and we are fully equiped to regenerate every fucking cell of our body, it's just not activated. Otherwise we would be Wolverines.

Which is not ok for me because I don't have a hairy chest...
3.jpg


Quite luckily the postsynaptic bouton is a little wolverine!!!

4.jpg


Step 1 it's normal, you just receive the acoustic trauma
Step 2 it fucking explode as mentionned above
Step 3 after 1 day it's reforming and the afferent dendrite has begun to grow upwards and some filopodia already reach the IHC. Wolvyyy powwaaa....Cochlear action potential begins to recover.
Step 4 the synaptic pattern is back on track and normal, well almost normal.

To rebuild any part of your body, exactly like for Ikea your body needs guidelines. And the plan of your body is in your genes.
5.jpg


However when the body reads the gene code to rebuild a part, it can be affected by external factors.
And this is here the glutamate comes into action to messs things up.

The over-expression of NMDA glutamate receptors change the structure of the dendrite, and synapse, because it wants to adapt to its new environement. We casually call that plasticity.

When the glutamate is gone (end of hair cell death), the dentrite and synapse stay locked in this particular way.

AM-101 try to avoid glutamate to provoke this "state" we casually call Tinnitus :)


"OMG OMG, so you see we have mutant dentrite creating never ending broken synapse, we will all die of T."

Calm down agaiiin!!! Morphogenesis and plasticity will save the day. This is the most flexible, evolutive, adaptive part of the body. Those fucking dentrites will readapt if we induce them in a new state and let plasticity consolidate it.

Unlike most neuro diseases, the error is not in your gene, your body knows what's the normal state.

So "in many cases, spine morphogenesis, plasticity, and maintenance also depend on synaptic activity", if you change this synaptic activity, give it enough time, and if it makes sense considering the initial physiological structure, then it will consolidate back again.

(More info on the phenomenon, http://onlinelibrary.wiley.com/stor...38&s=ac1eb57600a4c22d4ab92eb463198f60a6bc3bea)

Conclusion, your brain is a little wolvy and knows what should be a normal state of connections (Kv & shit), it's just lock in a way becauce glutamate came to interfere with the natural reconstruction. If you force manually the right kv channel to work and let them consolidate, your brain will be like, "oh fuck this is the way, let's consolidate, yay".

End fo T.

(PS LoL: to the idiots who will think, if we destroy again the postsynaptic bouton without the glutmate it should be fine. NO NO NO it's a dumb idea you may kill the connection and there is high chance of no regeneration at all, meaning, hearing loss).

Peace :)
 
@bedouin I do not appreciate my arguments being called rantings, I am all for these drugs and development but there seems to be lacking evidence showing that there is a permanent solution. I am mildly critical of what seems like overt optimism about this issue.

@benryu I appreciate your detailed explanation but has this been demonstrated and proven as fact on humans in practice or is it a theory? And btw did you just call members of this forum, and it seems you are talking about @cdog idiots for theorycrafting about their illness and possible solutions?!

I have seen many papers proving and even microscopically showing one effect of a certain drug and than when I took it, it had the exact opposite effect ruining my health.
 
Fun reply with graphics, but I'm still not sure it answered the question it posed :

Noise trauma ==> Hair Cell death ==> glutamate release ==> Kv3.1 channel "lock"==> abnormal spontaneous firing ==> T.

So what the fuck happen beteween glutamate release and the Kv channel abnomality, and why it's fucking reversible.

So the question is : what's the link between glutamate release and Kv channel abnormality?

...

The over-expression of NMDA glutamate receptors change the structure of the dendrite, and synapse, because it wants to adapt to its new environement. We casually call that plasticity.

...

When the glutamate is gone (end of hair cell death), the dentrite and synapse stay locked in this particular way.
...

Conclusion, your brain is a little wolvy and knows what should be a normal state of connections (Kv & shit), it's just lock in a way becauce glutamate came to interfere with the natural reconstruction.

So what I'm getting from above is : glutamate excitotoxicity -> destruction and regrowth of synaptic bouton -> during regrowth the overabundance of glutamate causes some structural changes in the regrowing dendrite -> ??? -> Kv channel is screwed up (down regulated).

So, what's the ???
 
Wow, I have been in this thread for a few days and it's like war here. *__*

I am really busy at the moment but I have seen so much misinformation around that it will be useful if I clear a few things out.

You guys seem to trip on the area I did not explain much because of its complexity (glutamate action and link).
I also saw some crazy theories about T. being permanent and irrevocable state. W T F people lol

I clear this area for once in the most simple way I can.

We all agree to that:

Noise trauma ==> Hair Cell death ==> glutamate release ==> Kv3.1 channel "lock"==> abnormal spontaneous firing ==> T.

So what the fuck happen beteween glutamate release and the Kv channel abnomality, and why it's fucking reversible.

We all know that this bitch of glutamate is excitotoxic:
http://en.lmgtfy.com/?q=glutamate excitotoxicity
(CTRL+F, glutamate)

When the glutamate is released it forces the postsynaptic bouton to swell and burst.

(the pink thing is not a testicle)
View attachment 2703

"But but this Ca2+ is not glutamate, I don't understand, we will all die of T. !!"

Calm down son, increased extracellular glutamate levels leads to the activation of Ca2+ permeable NMDA receptors on myelin sheaths and oligodendrocytes, leaving oligodendrocytes susceptible to Ca2+ influxes and subsequent excitotoxicity.


(Boom )
View attachment 2704

"OMG OMG the postsynaptic bouton has exploded, my body is broken, we will all die of T. or maybe diarrhea!!"

No worries contrary to what was said above in the thread, we are the most complex mammal on earth because of our brain, and we are fully equiped to regenerate every fucking cell of our body, it's just not activated. Otherwise we would be Wolverines.

Which is not ok for me because I don't have a hairy chest...
View attachment 2705

Quite luckily the postsynaptic bouton is a little wolverine!!!

View attachment 2706

Step 1 it's normal, you just receive the acoustic trauma
Step 2 it fucking explode as mentionned above
Step 3 after 1 day it's reforming and the afferent dendrite has begun to grow upwards and some filopodia already reach the IHC. Wolvyyy powwaaa....Cochlear action potential begins to recover.
Step 4 the synaptic pattern is back on track and normal, well almost normal.

To rebuild any part of your body, exactly like for Ikea your body needs guidelines. And the plan of your body is in your genes.
View attachment 2707

However when the body reads the gene code to rebuild a part, it can be affected by external factors.
And this is here the glutamate comes into action to messs things up.

The over-expression of NMDA glutamate receptors change the structure of the dendrite, and synapse, because it wants to adapt to its new environement. We casually call that plasticity.

When the glutamate is gone (end of hair cell death), the dentrite and synapse stay locked in this particular way.

AM-101 try to avoid glutamate to provoke this "state" we casually call Tinnitus :)


"OMG OMG, so you see we have mutant dentrite creating never ending broken synapse, we will all die of T."

Calm down agaiiin!!! Morphogenesis and plasticity will save the day. This is the most flexible, evolutive, adaptive part of the body. Those fucking dentrites will readapt if we induce them in a new state and let plasticity consolidate it.

Unlike most neuro diseases, the error is not in your gene, your body knows what's the normal state.

So "in many cases, spine morphogenesis, plasticity, and maintenance also depend on synaptic activity", if you change this synaptic activity, give it enough time, and if it makes sense considering the initial physiological structure, then it will consolidate back again.

(More info on the phenomenon, http://onlinelibrary.wiley.com/stor...38&s=ac1eb57600a4c22d4ab92eb463198f60a6bc3bea)

Conclusion, your brain is a little wolvy and knows what should be a normal state of connections (Kv & shit), it's just lock in a way becauce glutamate came to interfere with the natural reconstruction. If you force manually the right kv channel to work and let them consolidate, your brain will be like, "oh fuck this is the way, let's consolidate, yay".

End fo T.

(PS LoL: to the idiots who will think, if we destroy again the postsynaptic bouton without the glutmate it should be fine. NO NO NO it's a dumb idea you may kill the connection and there is high chance of no regeneration at all, meaning, hearing loss).

Peace :)
Goddd i loveee you being on here ;)
 
I take per day:
A vit 6000iu, E vit 400iu, C vit 1000mg, Zinc citrate 25mg, 3x500magnesium lactate, 3x600mg NAC, 1x20mg Lutein and 2x betahistine 24 mg
1x5mg melatonin - before sleep
and for now Trobalt.

@Johno We're all excited for you! But I probably wouldn't include all those supplements. It might be useful to get a pure reading with just the Trobalt.

Maybe @benryu has an opinion on this?
 
OMG @benryu I just about peed in my pants reading your latest visual/verbal extravaganza...Almost makes it worth having T just to be so educationally entertained!
Now how to edit it so my doc can see the wizdum within and not be blinded by the hilarious light.

SO GREAT to have you aboard!

(n) Zimichael
 
@Johno We're all excited for you! But I probably wouldn't include all those supplements. It might be useful to get a pure reading with just the Trobalt.

Maybe @benryu has an opinion on this?

All of those stuff I take for very long time and it didnt help me with T (maybe a little bit, but not significantly). NAC and vitamines for prevention, melatonin for better sleeping. My T is very stable. Only supplement what is new is Trobalt and Lutein to help prevent retina changes. Dont afraid, if my T improves, it will be definitely due to Trobalt. ;):p
 
unsurprisingly, my insurance has balked at covering Potiga for off-label use. I'm waiting to see if the prescribing doctor's office is able to get that worked out with them, or not -- if not, then it's going to cost me ~$250 for the initial 100x50mg, which means just ramping up to a significant dose and backing off a month or two later could be close to a thousand dollars.
 

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