Retigabine (Trobalt, Potiga) — General Discussion

#1,952
raymundo2245 said:
I read on one of these threads that meclizine helped a guy get rid of T, so today im gonna try it, i hop3 it at least lowers the sound, i can live with it if the sound lowers just a little.....im gonna try several meds and i will report back......
Click to expand...
Raymundo. My thoughts go out to you my friend but I think we are getting away from the subject of the thread.
Please direct this to the meclezine thread.
 
#1,953
Juan Carlos said:
Hi! first of all is not boring at all. Thanks for your thoughts.
IMHO, the 'side effects' of Trobalt doest have much to do with its effect on T, As people that had T for years probably tried tranquilizers and muscle relaxants or any other kind of med and didn't feel so much effect as Trobalt is doing. I think that the cause is not so important as some people thing as the effect seems to be the same: hiperexcitability of some parts of the auditory system, going from cochlea to the auditory cortex. Once the cause is gone, there might be no difference between one that had it for stress or another for infection or neck trauma. Maybe acoustic trauma could be diferent case because it affects to haircells, i can't guess so. The fact that many people with lots of acoustic traumas in life have zero tinnitus makes me think that there is no diference for them also despite they could be a bit more deaf.
People that go to concerts experience tinnitus for some hours after it, and then after hours or days is gone (their K channels are working fine), so i dont think that acoustic trauma makes irrevertisible tinnitus (maybe just irreversible partial deafness)
The big question is why on Zirmichael caused absolute zero effect on T, maybe is just a matter of amount and time on drug and for your case the risk/benefit on Trobalt is not worthing so must wait for Autifony or other K modulator with less side effects. Or maybe it caused some effect but you were not able to see it because your T is too high? I guess will have the answer when Aut63 comes out to the pharmacyes
Click to expand...

Juan Carlos...Well, we all have that "wonder" about how so many people can get blasted by discos and concerts, etc. and think it's "cool" to come out of it with T ringing in their heads...and it just goes away. Then there are the few where it does not, and they end up on places like this TT forum. And then 80% or whatever of those "adapt". And so on...It's the "non adapters" or the "repeat offenders" (with T being the "offender"!) that do things like trying Retigabine.

However, within this T population, I feel quite strongly that "acoustic trauma" induced T, and probably "ototoxic" induced T (where actual hair cell or audile nerve damage seemingly takes place), are different from the fairly wide array of possibilities for T c/o circulatory issues, TMJ, spinal nerve issues, etc. These latter are much more likely to give what I will call "variable" tinnitus. It just makes sense that that would be so. Also, there are plenty of reports of T being reduced or cured after some kind of physical remediation of those issues (craniosacral therapy, spinal adjustment or block, surgery, etc.). Whereas "hard core" sound trauma T seems to not be affected as easily.
This is where the Kv drugs I think will have their heyday. They seemingly go in and deal with the "trauma" aspect of the T function on the neuronal level...and yes, that obviously can still be caused by the physical aspects I have mentioned above, as the T still "fires" and happens, and can get "stuck" perhaps.

Personally, in the KCNQ family = the Kv7's, I am looking harder at Kv7.4 and wondering if any of these companies involved need a nudge in that direction. I'm not 100% convinced any more that Kv3 is the only road to Rome, just because Autifony says so. Our own trial here with Retigabine seems to reinforce that "wondering". Just because I did not respond on a fairly short trial, and have incredibly entrenched T, does not mean that all the others have not had direct and clear "auditory effect" on their T...and pretty rapidly too.

I intend to see if I can get some "nudges" going.

best, Zimichael
 
#1,955
Zimichael said:
Juan Carlos...Well, we all have that "wonder" about how so many people can get blasted by discos and concerts, etc. and think it's "cool" to come out of it with T ringing in their heads...and it just goes away. Then there are the few where it does not, and they end up on places like this TT forum. And then 80% or whatever of those "adapt". And so on...It's the "non adapters" or the "repeat offenders" (with T being the "offender"!) that do things like trying Retigabine.

However, within this T population, I feel quite strongly that "acoustic trauma" induced T, and probably "ototoxic" induced T (where actual hair cell or audile nerve damage seemingly takes place), are different from the fairly wide array of possibilities for T c/o circulatory issues, TMJ, spinal nerve issues, etc. These latter are much more likely to give what I will call "variable" tinnitus. It just makes sense that that would be so. Also, there are plenty of reports of T being reduced or cured after some kind of physical remediation of those issues (craniosacral therapy, spinal adjustment or block, surgery, etc.). Whereas "hard core" sound trauma T seems to not be affected as easily.
This is where the Kv drugs I think will have their heyday. They seemingly go in and deal with the "trauma" aspect of the T function on the neuronal level...and yes, that obviously can still be caused by the physical aspects I have mentioned above, as the T still "fires" and happens, and can get "stuck" perhaps.

Personally, in the KCNQ family = the Kv7's, I am looking harder at Kv7.4 and wondering if any of these companies involved need a nudge in that direction. I'm not 100% convinced any more that Kv3 is the only road to Rome, just because Autifony says so. Our own trial here with Retigabine seems to reinforce that "wondering". Just because I did not respond on a fairly short trial, and have incredibly entrenched T, does not mean that all the others have not had direct and clear "auditory effect" on their T...and pretty rapidly too.

I intend to see if I can get some "nudges" going.

best, Zimichael
Click to expand...


Maybe you are right, only time will give the answer.
If Aut63 cures trauma T as we hope, means that there is no real damage in haircells. Maybe the difference between that cause is just the location of the most hyperexcited neurons, in case of trauma they may be located and super excited in the cochlea (that's why trauma cause use to have more pure tonal T as every part of the labyrinth corresponds to a frequency), then with time the excitement expands a bit to other areas. And with other causes like stress it might be located in any area of the auditory path, that could explain why stress cause T is more like hissing and multitonal and would explain why varies more among day time and stress level. Note also the cases that cuting the audio nerve didnt cure T, that assures that T is not only in the cochlea after some time

Autifony knew of the effect of Retigabine so they could make a "better version" with no side effects of it but instead they decided to go for KV3 and after testing with mice decided go on with phase 1 and 2 and forgot about KV7 so that makes me put a hope on them.
Anyways in some time will know the answer of wich is better as there is a company (http://knoppbio.com/about/?9) focusing in KV7 as I read in Autifony thread, but they are on earlier stage so that will take at least 1 year to get some more info.
In my case im not sure about cause, I went to disco a couple of days in a month as all my life i was doing(with protection), but what changed on the time that T appeared is that i had much more stress than usual besides one month before i had a back/neck contraction, so I have no idea wich of the three is the cause (maybe all combined). I read good things of NAC so now will give a try

Another question I was wondering: Im pretty sure hyper excitability kind of "expands" from cochlea to other auditory path after some time, so it becomes "chronic", but all brain is connected, i wonder why it has never affected other parts of it. Hyperactivity could go for example to the vision area wich is close and cause vision epilepsy, but never read a case of that. Just side effects related to auditory system, like clogged ears, ear pain,H, maybe headache. It seems there is some barreer or the neurons are just different: thats why some KV modulators act just to some parts of the brain, so we are not like computers, as every byte of RAM act exactly the same, therefore different KV modulators act only in some parts of the brain, I guess that's a good thing to treat specific illness like tinnitus without afecting other areas just taking pills and not local meds into the brain as injections (am101). So thats a not bad thing, we are so annoyed with T but it doesnt affect the rest of our health at least while we sleep good, this fact must give us some confidence and lose fear of T.
JC
 
#1,957
Just a little progress update.
I've been using 3x100mg daily for 12 days now.
Annnnnddd.... I'm afraid I'm going to call my initial good days placebo. Or they were just low days.

I can't say my T has improved in any measurable (by me) way.
Maybe the dosage is too low, maybe it needs more time. My pills will run out on Sunday.
If my 300mg order ever gets here, I'm gonna give it another shot. I'm still hopeful but not as excited as before.
 
#1,958
This needs to be said: It's irrelevant if someone does not respond at a low dose. Meaningless. Without significance, clinical or otherwise. A few people seemed to respond at low doses, but aside from Mpt, we have good reason to believe that was pure optimism.

This is a drug that according to the literature starts to have a discernible effect on epileptic seizures at 600mg/day in the most sensitive patients. Most patients respond at 900/day, some go as high as 1200/day. There is no reason we should expect any different results. The drug opens potassium channels to combat seizures and it opens potassium channels to combat tinnitus. Epilepsy is generally considered a more serious illness than tinnitus, but that doesn't mean it is any harder to treat. We're talking about the exact same neurons, after all.

If a woman takes half a birth control pill, she doesn't get half pregnant. We should stop attaching significance to low dose responses, or a lack thereof. If you haven't gone up to a level where you are responding, or to 1200mg/day, you don't know if Retigabine will work for you.

I hope these supply problems clear up. It's frustrating that we have so many people willing and able to make the attempt, but are experiencing setback after setback!
 
#1,959
raymundo2245 said:
I wonder what noise induced T is best treated with? I did it before with lots of patience and determination, i know i can do it again but its just that it was stupid of me to go to a place like that, but oh well, i need to rehabituate, and im gonna do it, it was incredible, it had decreased alot and it wss very loud at first, now its back to the same levek it was at first or maybe its just that my ears got damaged again, since i feel alk the same simptoms, sensetive hearing,depression,not hungry, nausea, when it all was gone and started eating better habituation kicked in, so i guess its just a matter of time, i feel the same crackleling i felt at first, now maybe if i get lucky it will get the same way it wss again, i really hope so..
Click to expand...


Hello raymundo2245, this is way off thread so you can reply to me personally if preferred but can you let me into any tips that helped you to habituate so swiftly and what seems originally with such good results, what did you do that you found really worked for you that you may never have thought off, just really keen to know as the whole process for you went as I think many of us perceive habituation in many different ways ?

Thank you, now back to the main topic.
 
#1,960
@Juan Carlos ...Well, I won't go into detail about your comments above, as indeed all good thoughts, and yes, that "stress" component to getting T is "interesting" to say the least. (A brain-wide glutamate type response perhaps???).

However, one thing that I have zero evidence for but an analogy for...I think it is theoretically possible to have auditory hair cell damage, that triggers a T state, but that the T state can be then be "quasi independent" thereafter. In other words, once it gets going it stays going.
Yes, if you "repair" the hair cells (say with stem cell treatment) their "reactivation" may then jam the T state with new signals and get it to freak out and F' off, etc. However, on an inverse note, I think it is theoretically possible to stop the T signal and still have the damaged or trashed hair cells. A really simple analogy would be phantom limb pain, where showing say a mirror image to the eyes/brain can "shut off" the pain when the brain thinks the limb is "reattached". The "forever firing loop" shuts down! The damage is still there...I'm sure there are other examples.

This I think is the potential for the Kv channels approach. If it were not so, I think it would plain not work. Which it seems to do!
In the end though we are throwing around a bunch of ideas and speculation (which is great), though T has a long history of being a very elusive creature to capture and understand. If a model really hits pay-dirt, it will indeed "pay" big time!

P.S. With your T there are many variables that people forget...Yes your stress for one, but I also wonder if you were taking Ibuprofen for that "back/neck contraction"? (Not discussion for this thread though). Plus genetics...My father had T (WWII), my older bother has T (noise trauma), I have T. Coincidence, or a 'weak link'???

best, Zimichael
 
#1,961
rtwombly said:
This needs to be said: It's irrelevant if someone does not respond at a low dose. Meaningless. Without significance, clinical or otherwise. A few people seemed to respond at low doses, but aside from Mpt, we have good reason to believe that was pure optimism.

This is a drug that according to the literature starts to have a discernible effect on epileptic seizures at 600mg/day in the most sensitive patients. Most patients respond at 900/day, some go as high as 1200/day. There is no reason we should expect any different results. The drug opens potassium channels to combat seizures and it opens potassium channels to combat tinnitus. Epilepsy is generally considered a more serious illness than tinnitus, but that doesn't mean it is any harder to treat. We're talking about the exact same neurons, after all.

If a woman takes half a birth control pill, she doesn't get half pregnant. We should stop attaching significance to low dose responses, or a lack thereof. If you haven't gone up to a level where you are responding, or to 1200mg/day, you don't know if Retigabine will work for you.

I hope these supply problems clear up. It's frustrating that we have so many people willing and able to make the attempt, but are experiencing setback after setback!
Click to expand...

rt...I have to respectfully disagree here.

We are not testing Trobalt for epilepsy. Indeed we are using dosing data based on epilepsy as that is what the manufacturer and research says, so we infer back to that in relation to our suppositions on the Kv7 channels involved.

The fact is we are just "testing" this stuff. In a test you just look at what happens. The theories postulated will either stand up or not. With such small sample sizes as we have here, no matter what we know that results will be very tentative. Anything that happens, or does not happen is relevant. We don't have the luxury of nice big N sample and bell curve to muddle over later.

In this light, I find it highly significant that even a few people have had "results" at low doses (actually, more than a few). Either they are placebo'ing or not. We do not have a double blind, etc., etc. to find out. Personally I don't think it's placebos, or if so we have someone like @undecided backing off and saying so.

Yes, there may be higher dose correlation with T "results", but that does not at all mean that lower dose effects for T should be thrown out the window. They should be noted and absorbed and added to the knowledge base.

Time and more testers (especially long term T people with say 10 years or more) will tell if higher doses make any difference. At this point we just don't know, as no-one has tested Retigabine for T in a trial like this before...just with mice!

Keep an open mind. Very best, and this is not a slap down! Zimichael
 
#1,962
Zimichael said:
However, one thing that I have zero evidence for but an analogy for...I think it is theoretically possible to have auditory hair cell damage, that triggers a T state, but that the T state can be then be "quasi independent" thereafter. In other words, once it gets going it stays going.
Click to expand...

I think this is most probably what is happening. I like the Thanopolous paper on this:
http://www.pnas.org/content/110/24/9980
this paper is awesome too:
http://www.pnas.org/content/109/21/8292.abstract

Take a look at this picture. I think the problem spot for us is the fusiform cell. The afferent parallel fibers from the granule cells would involve all of the non-acoustic trauma causes of T (like TMJ, etc). This would explain how it is possible to modulate your T with neck movements, jaw movements, etc. This would also explain how it is possible to get tinnitus without acoustic trauma.


Image.png


I recommend viewing the short supplemental clip from the Hamann paper above:
http://www.pnas.org/content/suppl/2012/05/04/1116981109.DCSupplemental/sm01.mp4

Basically I think tinnitus can have multiple causes, but for the most part presents the same (hyper-excited fusiform cells in the DCN being the primary root of the problem).
 
#1,963
Zimichael said:
rt...I have to respectfully disagree here.

We are not testing Trobalt for epilepsy. Indeed we are using dosing data based on epilepsy as that is what the manufacturer and research says, so we infer back to that in relation to our suppositions on the Kv7 channels involved.

The fact is we are just "testing" this stuff. In a test you just look at what happens. The theories postulated will either stand up or not. With such small sample sizes as we have here, no matter what we know that results will be very tentative. Anything that happens, or does not happen is relevant. We don't have the luxury of nice big N sample and bell curve to muddle over later.

In this light, I find it highly significant that even a few people have had "results" at low doses (actually, more than a few). Either they are placebo'ing or not. We do not have a double blind, etc., etc. to find out. Personally I don't think it's placebos, or if so we have someone like @undecided backing off and saying so.

Yes, there may be higher dose correlation with T "results", but that does not at all mean that lower dose effects for T should be thrown out the window. They should be noted and absorbed and added to the knowledge base.

Time and more testers (especially long term T people with say 10 years or more) will tell if higher doses make any difference. At this point we just don't know, as no-one has tested Retigabine for T in a trial like this before...just with mice!

Keep an open mind. Very best, and this is not a slap down! Zimichael
Click to expand...

I am with @rtwombly on this one, I don't think we are in any position to judge the effects of the drug until you have a sufficient dose for a sufficient amount of time. Given that @undecided is also not experiencing any side effects, he might need a higher dose. There seems to be different reactions to this drug, note how @Christian78 actually got worse for a while. If nothing happens at 900mg/day, then we can say something about it not working. So far the two people that have gone up to that dosage level have reported great results.

I know you are saying that you should at least feel 'something' at the lower dosages, but I just don't think we know enough to say that this will always be true for everyone. Perhaps there are fine distinctions in the various forms of T that people have (the stable T versus fluctuating T you were talking about) that react differently to this drug. I don't see why it would be the case that any amount of the drug must have some effect on T.

Also wanted to add that I think the Kv7.4 effect might be a key player in all of this. The effects on Kv7.4 require 3 to 4 times as much of the drug to affect it compared to the Kv7.2/3 channels (see the table in the post I had a few days back). Maybe for some people the Kv7.4 channel effect is necessary for change? This might be a possibility.
 
#1,964
locoyeti said:
I think this is most probably what is happening. I like the Thanopolous paper on this:
http://www.pnas.org/content/110/24/9980
this paper is awesome too:
http://www.pnas.org/content/109/21/8292.abstract

Take a look at this picture. I think the problem spot for us is the fusiform cell. The afferent parallel fibers from the granule cells would involve all of the non-acoustic trauma causes of T (like TMJ, etc). This would explain how it is possible to modulate your T with neck movements, jaw movements, etc. This would also explain how it is possible to get tinnitus without acoustic trauma.


View attachment 3502

I recommend viewing the short supplemental clip from the Hamann paper above:
http://www.pnas.org/content/suppl/2012/05/04/1116981109.DCSupplemental/sm01.mp4

Basically I think tinnitus can have multiple causes, but for the most part presents the same (hyper-excited fusiform cells in the DCN being the primary root of the problem).
Click to expand...
I spoke with a very knowledgeable audiologist from AZ recently for an hour and one of the things we talked about was the origin of the tinnitus siginal and it seemed we (mainly him) said the same thing about the dysfunction in the DCN
 
#1,965
Zimichael said:
We are not testing Trobalt for epilepsy. Indeed we are using dosing data based on epilepsy as that is what the manufacturer and research says, so we infer back to that in relation to our suppositions on the Kv7 channels involved.
Click to expand...
I think it's a mistake to make that distinction. What took me a long time to really wrap my brain around is that Retigabine doesn't target any one area of the body or the brain. It affects every part of the nervous system that has the right chemical makeup to respond. It's like how talcum powder clings to moisture, but blows off dry surfaces. Retigabine is the powder, KCNQ channels 2-5 are the moisture.

So when you are taking it, you're treating epilepsy. You're treating everything that the KCNQ2-5 affect. If you're having results, it's because you're taking enough to change the behavior of neurons expressing KCNQ2-5. How much is that? From the big clinical trials and 4 or five years of market evidence, about 600-1200mg per day. That's all we have to go on. I don't think it's particularly relevant that those are levels for epilepsy vs tinnitus. The effect we're looking for is the same: inhibition of hyperactive neurons.

Now, I do agree with you that we should note the effects, but you and others have commented on the lack of efficacy at the doses you've taken and how it's reduced your optimism. That's understandable; I just don't think it's meaningful. If you haven't yet responded, it means you haven't yet responded. It doesn't mean you WON'T.

I know you've had negative effects. That's a bit different. Anybody who has to step back due to side effects has my full sympathy. I'm talking about the mental calculus here. If somebody starts and has minor side effects and no effect at 150/300/450mg, the thinking should be, "I've had some minor side effects. Should I go on?", not, "I've had some minor side effects and no rainbows shot out of the bottle when I cracked it open this morning." A lack of efficacy at low doses is normal. Feeling better at low doses is a fluke. A nice fluke, but a fluke.

Not trying to be argumentative at all. I always enjoy reading your posts. I know you, undecided, and Johno are all stuck without a ready supply anyway. Hope that resolves, and I hope your hyperacusis goes down. For all the success we've had on this thread, we're just getting started. I hope somebody will be able to taper up to a full dose. Until then, all we've got is a theory.
 
#1,967
rtwombly said:
@locoyeti I'd forgotten that Dr. Tz. tied 7.2 and 7.3 to tinnitus. Man, makes me think about getting to yet another doctor to try Retigabine, but even if I got the scrip, would I be able to find the drug anywhere??
Click to expand...

I was just going to go to CVS (local retail pharmacy). If I am not mistaken, the people having procurement issues are trying to get it online. Am I going to have issues at CVS? @Zimichael
 
#1,968
@rtwombly and @locoyeti ...Ha, ha. Just another full days worth of mulling and pondering potential in your posts above. All of which good. That is what this thread is about. However, will do that mulling later as Markku is waiting for me to post my final "report".

Just one point though. I am not saying that efficacy at lower doses is an expectation. I am also not saying that efficacy at higher doses is an expectation - especially for long, long term T like mine. I am just saying there are "observational facts" out there in our current TT trial land, that indeed there have been more than a few reports of "effects" at lowish doses. Period! This is "interesting" as those doses are well below the epilepsy efficacy model of 900 mg/day total, or more.

That's it. I think it is worth taking note of. I make no claim to knowing what will happen re T for someone like me at 900 mg/day for one day, five days, or five weeks. It is pure speculation, though indeed the epliepsy model implies that more "action' may occur. And yes I have no argument with that at all, as the drug is supposedly going to hit the KCNQ's it is associated with whether we like it or not...given the usual "individual/genetic variance" which throws all kinds of confusion into the mixing bowl with such a small "N" number of trialees. More drug load = more saturation of targets. Cool, no problem - as long as the side effects are tolerable. For me 50% more H was not exactly fun.

I hope I cleared that up....Final report coming up.

Best, Zimichael
 
#1,969
Some summary conclusions of my Retigabine trial. (N = 1)

The main question to be addressed with this one month trial, was to see if very long term, 'entrenched' tinnitus (and associated hyperacusis) would react favourably to Retigabine within a short period of time - as has been the case with the majority of other trialees even at doses lower than the recommended target rates for epilepsy. *[See attached table for my actual dose data].

Even though I ultimately had no beneficial reaction or changes to the tone, pitch or volume of my tinnitus (excluding a one day increase), the trail was not a wasted effort. More has been learned.

Here are my conclusions:

- Adding to what other trialees have discovered, it appears to be safe to ramp up dose faster than expected. Certainly faster than Benryu's suggested table, and also the manufacturer's recommendation of no more than 150 mg/week total. However, anyone/everyone is different! [Note Hengist's reaction!].

- Very long term T may not react as favourably as short term T to Retigabine. It may need higher doses and/or more time at those doses. The only conclusion to be certain of here, is that a purely short term, dose dependent exposure of 600 mg/day total, did not have any effect on my tinnitus.

- Hyperacusis was affected negatively by Retigabine. As dose increased hyperacusis increased. Avoidance of noise exposure was rigorously enforced. However, as dose was decreased and tapered off, hyperacusis also decreased and safe exposure to sound is expected to 'normalize' to pre-trial baseline.

- Side effects were less than expected. The initial concern of Urinary Retention was of no issue whatsoever. However, a strong urine "ester smell" and "brown staining" (see separate post) may be something to watch ref. kidneys and bladder if long term use.

- Short term memory aspects can be an issue. Remembering to take the Retigabine consistently required an alarm clock when over about 300 mg/day total. This has not been the case with other medications I have taken in the past.

- Brief periods of fatigue and headaches when changing dose, up or down, were short lived. A matter of hours.

- Supply issues! This could be very problematic. If ordering from online pharmacies make sure to have enough on hand for long "delays" so as to not be caught out of stock at high doses.

I think that's about it.

Best, Zimichael.
 

Attachments

  • My Potiga-Trobalt Dosing Schedule.xlsx
    18.2 KB · Views: 20
#1,972
I haven't heard anything from blue sky but on the website it says my order is "processed" don't think that means much but I think I'll call them tomorrow. The fight is steady but I'm still at a low dose so its not crazy but better then before Ret for sure. Little to No weird central T but I'm also being very careful and limiting my sound exposure by wearing earplugs for almost all my lessons that I teach.
 
#1,973
locoyeti said:
I think this is most probably what is happening. I like the Thanopolous paper on this:
http://www.pnas.org/content/110/24/9980
this paper is awesome too:
http://www.pnas.org/content/109/21/8292.abstract

Take a look at this picture. I think the problem spot for us is the fusiform cell. The afferent parallel fibers from the granule cells would involve all of the non-acoustic trauma causes of T (like TMJ, etc). This would explain how it is possible to modulate your T with neck movements, jaw movements, etc. This would also explain how it is possible to get tinnitus without acoustic trauma.


View attachment 3502

I recommend viewing the short supplemental clip from the Hamann paper above:
http://www.pnas.org/content/suppl/2012/05/04/1116981109.DCSupplemental/sm01.mp4

Basically I think tinnitus can have multiple causes, but for the most part presents the same (hyper-excited fusiform cells in the DCN being the primary root of the problem).
Click to expand...
A great post and find. Basically the firing rate of the fusiform cell is reduced after AOE (acoustic over exposure). Hopefully the drugs being devleoped now (AUT00063, AM102? and others) are now targeting the Kv chanels, so as to make the fusiform cells fire like they did before AOE.
 
#1,975
SteveToHeal said:
A great post and find. Basically the firing rate of the fusiform cell is reduced after AOE (acoustic over exposure). Hopefully the drugs being devleoped now (AUT00063, AM102? and others) are now targeting the Kv chanels, so as to make the fusiform cells fire like they did before AOE.
Click to expand...

Is AM-102 meant to be better than AM-101?
 
#1,976
Danny Boy said:
Is AM-102 meant to be better than AM-101?
Click to expand...
Nobody knows yet what AM102 is. Top secret. Rumor is, it is Auris Medicals Kv modulator for t, to compete with Autifony's AUT00063. It's still in pre-clinical trials tho, so not an option. Only main drug options of this variety available currently are am101, AUT00063(hopefully in the next few weeks) and "TT trial" Retgabine.
 
#1,978
SteveToHeal said:
Nobody knows yet what AM102 is. Top secret. Rumor is, it is Auris Medicals Kv modulator for t, to compete with Autifony's AUT00063. It's still in pre-clinical trials tho, so not an option. Only main drug options of this variety available currently are am101, AUT00063(hopefully in the next few weeks) and "TT trial" Retgabine.
Click to expand...


So it'll be in pill form? Personally, these KV modulators may be the ticket to an actual cure...Well, an actual cure would be to regenerate hair cells which is possible, but who knows how far along that'll be?
 
#1,979
bedouin said:
Yes. Check back in the thread somehere where some guys talk about taking along accompanying documentation to motivate your request. I know it is a big thread so maybe do a search on "prescription" or something. Let me know if you manage to get it on prescription here in the UK.
Click to expand...


Tried looking, can't find it. This stuff would be a lot of help!
 
#1,980
Danny Boy said:
Tried looking, can't find it. This stuff would be a lot of help!
Click to expand...
You will need a prescription from a doctor, either GP oto or neurologist. Well here in Spain i bought some prescription meds without prescription but i guess in UK are more serious than here.

By the way, there a big hope than Autifony med AUT00063 will cure T, and its trials for phase II are going only in the UK, please check the Autifony thread and Autifony website http://autifony.com/autifony-tinnitus-phase-IIa-trial.asp to check if you meet the requirements for the trial. We dont know anyone from the UK that signs up for the trial and it will be a good help to have fresh info about this promising drug.
Aut63 is meant specially for tinnitus and much safer than Retigabine with less side effects, would be great if u can sign in.
 

Log in or register to get the full forum benefits!

Register

Register on Tinnitus Talk for free!

Register Now

Similar threads

I
Reformulated Retigabine (Trobalt): BHV-7000, a Kv7.2 Modulator by Biohaven (Pfizer)
Replies
191
Views
45K
Research News
BB23
BB23
StoneInFocus
Megan Beers Wood Research Updates / Discussion: Cochlear Inflammation & Pain Hyperacusis Mice Model
Replies
7
Views
2K
Hyperacusis and Ear Pain
StoneInFocus
StoneInFocus
MadeleineHope
Role of Patulous Eustachian Tube (& Eustachian Tube Dysfunction in General) in Hyperacusis
Replies
5
Views
2K
Hyperacusis and Ear Pain
Josh59
Josh59
MarkJU
Can General Anesthesia Make Tinnitus and Hyperacusis Worse?
Replies
0
Views
856
Hyperacusis and Ear Pain
MarkJU
MarkJU
EternalRinging
Could Facial Laser Have Adverse Effects on My Tinnitus? Can the General Anesthesia Worsen Tinnitus?
Replies
3
Views
791
Support
MikeB1996
MikeB1996
Top Bottom
Back
Forums
Members
Donate
Menu