MemberI don't think money would speed up the process. Even the biggest pharma companies with loads of money still have to follow trial procedure and timelines. Drugs just take years to get from concept to market. We're going to have to be patient. 
Autifony Therapeutics Phase II Study for AUT00063, for the Treatment of Hearing Loss and Tinnitus
- Thread starter attheedgeofscience
- Start date
Neramexane
From Wikipedia, the free encyclopedia
Neramexane
Systematic (IUPAC) name
1,3,3,5,5-pentamethylcyclohexanamine
Identifiers
CAS Registry Number 219810-59-0
ATC code None
PubChem CID: 6433106
ChemSpider 4938294
UNII 856DX0KJ84
Chemical data
Formula C11H23N
Molecular mass 169.307 g/mol
SMILES[show]
InChI[show]
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Neramexane is a drug related to memantine,[1] which acts as an NMDA antagonist[2] and has neuroprotective effects.[3] It is being developed for various possible applications, including treatment of tinnitus,[4][5] Alzheimer's disease,[6] drug addiction[7] and as an analgesic.[8] Animal studies have also suggested antidepressant[9] and nootropic[10] actions, so there are a wide range of potential applications this drug may be used for. It also acts as a nicotinic acetylcholine receptor antagonist.[11]
A clinical trial found that doses of 50mg and above safely improved tinnitus scores over 16 weeks.
So what happened to this drug!?
Founder
From a neurogical and functionnal (auditory system) point of view there is NO FREAKING DIFFERENCE between acute vs chronic T. if the drugs acts on the synaptic transmission, you could have had T. for 3 days or 300 years, it won't make a difference. Only plasticity cause a certain inertia.
First of all, excuse me my ignorance in brain chemistry. But I see that neramexane is a NMDA antagonist, much like esketamine (AM101), and this one is not intended for chronic T, but only for the initial stages where the famous and worshipped potassium channels are still not locked. I mean, the difference seems clear enough to understand the failure of this drug.
By the way, does anybody know about a good book about T, in terms of physiology at a cell or molecular level? Or any paper or collection of papers to start with?
Edit. I've seen the Autifony powerpoint and some things are really nice. In the competition landscape, it looks like the other pharma companies are focused on the NMDA receptors, with AM101, neramexane, gacyclidine and caroverine. I understand that those are good news for new sufferers, since they will have access to a wide variety of drugs intended at this acute stage. And it looks like the Kv modulator approach of Autifony could be a huge success (or a miserable failure, but nevertheless if this drug makes phase III most people will at least try it, as has happened with Retigabine).
Then, the impressive p < 0.001 (statistically significant differences) of the spontaneus activity rate reduction induced by AUT00063. I mean, this is the first time I see a graph with some objective data about the effectivity of this drug. This is probably for an in vitro assay, but man, the drug works. This plus the reports of some people in the clinical trial thread are good news.
And... they have additional backup Kv3.1 modulators. I know how research works, papers don't get published without solid evidence, less in the biomedical field, and if the current research is pointing in the right direction, we should be at least hopeful.
By the way, does anybody know about a good book about T, in terms of physiology at a cell or molecular level? Or any paper or collection of papers to start with?
Edit. I've seen the Autifony powerpoint and some things are really nice. In the competition landscape, it looks like the other pharma companies are focused on the NMDA receptors, with AM101, neramexane, gacyclidine and caroverine. I understand that those are good news for new sufferers, since they will have access to a wide variety of drugs intended at this acute stage. And it looks like the Kv modulator approach of Autifony could be a huge success (or a miserable failure, but nevertheless if this drug makes phase III most people will at least try it, as has happened with Retigabine).
Then, the impressive p < 0.001 (statistically significant differences) of the spontaneus activity rate reduction induced by AUT00063. I mean, this is the first time I see a graph with some objective data about the effectivity of this drug. This is probably for an in vitro assay, but man, the drug works. This plus the reports of some people in the clinical trial thread are good news.
And... they have additional backup Kv3.1 modulators. I know how research works, papers don't get published without solid evidence, less in the biomedical field, and if the current research is pointing in the right direction, we should be at least hopeful.
"Great", so t. is mainly gonna be stopped in his root, and we (old timers) will be left on autifony, or SF34 (btw what are those guys doing beside scientific articles?!). After that (if aut and sf fails) in 5 years no one will be interested to invest BIG money in condition that has already been cured in acute stage. T. is gonna be past condition, with far less new suffers as most of them is gonna be cured in acute stage.
Realy "great" to have that in a mind...
From the Phase II results of AM101, it looks like it substantially improves T "only" in a 62% of the cases. The rest progresses into chronic t, whatever this means. Sum the current base of chronics and the newcomers and voilà, lots of money to make. If there's money, there will be someone ready to exploit it. It's sad, but also good for us.
And there will be also people who won't even visit an ENT after a trauma, and will only figure out that there was a solution when it's too late.
Btw... science is mostly about making papers. A paper is always an innovation, an advancement. Then, there is the translational medicine that makes money from papers, such as the pharma guys.
Sorry if I look too optimistic, I try to be realistic and I am fully aware that we're still in the early stages.
And there will be also people who won't even visit an ENT after a trauma, and will only figure out that there was a solution when it's too late.
Btw... science is mostly about making papers. A paper is always an innovation, an advancement. Then, there is the translational medicine that makes money from papers, such as the pharma guys.
Sorry if I look too optimistic, I try to be realistic and I am fully aware that we're still in the early stages.
Don't forget 10 % of them had their tinnitus worsened, so in the future many new sufferers will hesitate trying AM101
That why I am bit "selfish", and do not wish big success rate for AM and OTO, just because of us...
"Selfish" wish here again, shorter frame after trauma that AM and OTO will work (less >3 months) will be better for us also...
Here's the thing - what if AM101 etc fail ? What if AUT63 and/or SF34 succeeds ? What if they all fail ? What if they all succeed ? We don't have a crystal ball, all we can do is watch and wait.
I think we're on the cusp of some great stuff with regards to T treatment. There is a phenomenal amount of money to be made from drugs that address both new onset T and chronic T, I don't think this fact is lost on pharma.
I think we're on the cusp of some great stuff with regards to T treatment. There is a phenomenal amount of money to be made from drugs that address both new onset T and chronic T, I don't think this fact is lost on pharma.
- Jan 3, 2015
- 635
- Tinnitus Since
- 04/21/2014
- Cause of Tinnitus
- Sensorineural hearing loss right ear.
I think the Russians are onto something, if their entire head transplant surgery, is successful? Just make sure to order you new head, without Tinnitus! };-)
You don't need to wait.
This link takes you to their own page and you will find all the questions asked, and all the answers that they provided, and that was back on July 16th as well.
That doesn't include everything (and we already have those answers posted here on TT before they were posted onto their FB), they still have several unanswered questions from our members to which my previous post and their response from the other day continues to apply.
So some new answers to pending questions will be coming.
First, not between 8 and 12 months, it is 6 to 18 months.
No one said that it is a cure for all type of t. (even autifony) but for the most, where problem is between hair cells and brain it is suppose to be a cure. There are different causes of t. but AUT63 is targeting consequence in the brain.
Second, What doctor, where, and when? U are stating things without any reference or any proof, it is not fair to many members that are searching right info here on TT.
Lloyd Carter
Member
Yes, we hear the "T is only considered chronic after one year!" line, but we just don't understand exactly when it moves form the ear to the brain. And it might happen at different times for different people. If AUT works, it will probably have varied responses from users, just like Trobalt. This will be affected by a wide range of things.
I highly doubt that Autifony will work only on T ranging 6-18 months. That's just the time frame they chose for Phase IIA. I fully expect Phase IIB to include a wider range of dates. I think most people on this forum would agree that their T is relatively similar at the 6-18 month mark as it is 4 or 5 years later (assuming no new noise exposure). Some have random spikes, but most are not permanent. Meaning, hopefully, Autifony will work just as well for anyone with chronic T, no matter how long it's been there.
I highly doubt that Autifony will work only on T ranging 6-18 months. That's just the time frame they chose for Phase IIA. I fully expect Phase IIB to include a wider range of dates. I think most people on this forum would agree that their T is relatively similar at the 6-18 month mark as it is 4 or 5 years later (assuming no new noise exposure). Some have random spikes, but most are not permanent. Meaning, hopefully, Autifony will work just as well for anyone with chronic T, no matter how long it's been there.
My ENT, who "specialized" in T, believed T becomes "chronic" once the potassium channel gates cease to repolarize. Every brain is different, so there is no timeframe. However, if you have T for a month or more from a single event, like noise trauma, there's a good chance it's not going away (although it could). Now, by repolarizing the gates, the T goes away (or is greatly reduced), regardless of how long they've been "stuck". Again, just his theory. Unfortunately, he passed away unexpectedly recently, so he won't get to see the results of Aut
For all we know, it's all in the brain.
The thing about chronicity is that it might be very hard to undo the tinnitus related neuronal network if it has been established for years on end. It becomes part of its ''normal'' function.
Lloyd Carter
Member
Maybe, but the positive results some long-time T sufferers have had from Trobalt shows that it IS possible. Just time for researchers to figure out how!
My ENT, who "specialized" in T, believed T becomes "chronic" once the potassium channel gates cease to repolarize. Every brain is different, so there is no timeframe. However, if you have T for a month or more from a single event, like noise trauma, there's a good chance it's not going away (although it could). Now, by repolarizing the gates, the T goes away (or is greatly reduced), regardless of how long they've been "stuck". Again, just his theory. Unfortunately, he passed away unexpectedly recently, so he won't get to see the results of Aut
If your ENT knows about potassium channels he is light-years ahead of his peers.
No doubt! I'd say 99% of ENT''s are T clueless. His practice was based around the E in ENT though. More audiology than anything. He had Meniere's and chronic T, so it was a point of focus for him.
Want to share some information that I found on the internet. Could be of importance for oure future chances of getting a cure. It is an interesting presentation that autifony used in some sort of acquisition: link
Especially the sheet below seems important for the pipeline of all drugs that are currently under development:
Fingers crossed for aut-0063 or Caroverine or oto-311...
Especially the sheet below seems important for the pipeline of all drugs that are currently under development:
Fingers crossed for aut-0063 or Caroverine or oto-311...
Attachments
OTO311 is not gonna be useful for us (it's just for acute stage),
Caroverine has already been in use, without results https://www.tinnitustalk.com/threads/tinnex-caroverine.46/page-5
So, Keep all your hopes just for AUT63
- Jul 21, 2013
- 842
- Tinnitus Since
- 01/2013
- Cause of Tinnitus
- Acoustic trauma from headphones
It's likely that the longer the "tinnitus" has been created in the brain, the longer you'd have to take drugs to give your brain to go back to a semi-normal state.My ENT, who "specialized" in T, believed T becomes "chronic" once the potassium channel gates cease to repolarize. Every brain is different, so there is no timeframe. However, if you have T for a month or more from a single event, like noise trauma, there's a good chance it's not going away (although it could). Now, by repolarizing the gates, the T goes away (or is greatly reduced), regardless of how long they've been "stuck". Again, just his theory. Unfortunately, he passed away unexpectedly recently, so he won't get to see the results of Aut
I agree. I feel it'll be a lifetime of meds to keep it surppressed, which is ok with me.
That's ok with me too. One thing I really hope for is that it will help prevent spikes as well. If I could go back to going out in loud places (still wearing earplugs of course) and not have to worry about a spike then this drug would be the holy grail for me.
- Jul 21, 2013
- 842
- Tinnitus Since
- 01/2013
- Cause of Tinnitus
- Acoustic trauma from headphones
For us I'm assuming this is what we should expect.
Looking to the future, the only way I could see true silence being achieved would be to repair 1) ear, 2) auditory nerve, and 3) drugs to help the parts of the brain that are stuck (potassium channel modulators + potential other drugs)
Eventually the neurons would work themselves out for the most part in that scenario and you'd at a point be able to take no drugs and have minimal tinnitus, at least I hypothesize.
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