SciFluor Receives US Patent for KCNQ2/3 Activator to Treat Epilepsy and Neurological Disorders

http://www.pharmabiz.com/NewsDetails.aspx?aid=86103&sid=2

 

Excellent work spotting that, @OptimusPrimed. I had read many moons ago that SciFluor was interested in Retigabine, but had no idea if they would be able to follow up. So for the record there are now two safer versions of RTG/EZG that should be entering the testing phases soon. Neat that they specifically cited an indicator of the toxicity problem being absent from their new version.

 

SciFluor Life Sciences LLC has just recently increased its capital by 30 million dollars:

http://finance.yahoo.com/news/scifluor-life-sciences-raises-30-060000299.html

On the company's homepage, the drug candidate SF0034 is not specifically mentioned to be a derivative of Trobalt, but it is simply stated that the compound is a selective KCNQ2/3 activator (= Kv7.2/3 channels):

However, in the news just released as well as the financial sources I normally rely on for obtaining drug pipeline information, it is now confirmed to be a "potassium channel Kv7.2 (KCNQ2) and KCNQ3 modulator and a fluorinated derivative of Ezogabine." [Ezogabine = Retigabine = Trobalt]

Just before x'mas I was in contact with a researcher who shared with me the following development:

www.tinnitustalk.com/threads/retigabine-trobalt-potiga-%E2%80%94-petition-to-the-ata.6896/page-4#post-80103

I therefore cannot help but wonder if there is any connection between the research of SciFluor and the researcher who provided me with the information above. I tried to contact SciFluor about two months ago (as I already back then had tracked down the information which has now been officially released a few days ago i.e. that the compound in question specifically is a derivative of Trobalt). The reason I did that was to learn more about any anticipated trial timeline and whether that timeline would be accelerated as the compound is a chemical derivative (and not a completely new development - and hence perhaps allowing the trial to proceed in a speedier fashion). However, SciFluor has not come back with an answer (which is not unusual for pharmas - it's about "50/50" in my experience). I will try to contact the company via an "alternative route" in the very near future to see if I can get an answer that way instead. I will also try to get more information as to whether the compound will be geared towards tinnitus (as well as epilepsy) in their future trials (something which is not entirely clear to me).

attheedgeofscience
05/MAY/2015.

 

Thanks @OptimusPrimed for the digging and @attheedgeofscience for the unique and priceless information once again.

Too bad that even tho this would cure T instantly, it is couple of years away from the drug store shelves but progress is progress.

 

Excellent! Retigabine is, without a shadow of doubt from having read the experiences of people on this forum, a very good foundation on which further research can provide fruits.

 

this is kind of crazy excessive optimism. Retigabine clearly does not cure tinnitus. Among the small sample size of people on here who have tried it, there has been a nonzero group of people who saw no benefit whatsoever.

 

Well my point was that this drug will be several years away even if it works. I don't see any "crazy excessive optimism" in there

 

If you research almost all user experiences of treatments on the net over the last ten years, like I have done, you will come to the conclusion that retigabine is the only substance that has shown a series of positive results.

Granted, it is far from perfect, with unpleasant side effects making it unsuitable for long term use, which I am guessing, a tinnitus drug will need to be taken. For some it is ineffective.

Further research and modification of retigabine has got to be a good thing.

 

@attheedgeofscience Want to thank you for always bring us up to date ...You are a true asset to our forum God Bless

 

Just a brief "mini-update" adding a bit more information and also addressing a few of the comments further up (re: efficacy). The following post from the ATA-petition thread has a pdf-document included as an attachment file:

www.tinnitustalk.com/threads/retigabine-trobalt-potiga-%E2%80%94-petition-to-the-ata.6896/page-8#post-103579

Not many people opened it (just 28 in a period of a month or so) despite alerts being sent internally on TinnitusTalk. However, those who did open it may have noticed that the introduction reads as follows:



In the above excerpt, I have specifically underlined a couple of sentences. The attentive reader will know why. There are a number of professors who reviewed the thesis, and while Team Trobalt does not disclose sources, I can at least say that none of the professors mentioned are behind the quote in this post of mine that I referred to yesterday:

www.tinnitustalk.com/threads/retigabine-trobalt-potiga-%E2%80%94-petition-to-the-ata.6896/page-4#post-80103

However, the paper is still very relevant due to affiliations and the last line "In vivo and in vitro testing is underway to determine efficacy" provides a clue as to why that is.

I should also mention that the summary of what tinnitus is (see pages 17-19) is first rate. You will not find many family-, ENT-, or neurologist- physicians in the world who can account for the description of tinnitus as provided in this document.

Those who are interested in chemistry (and tinnitus) will appreciate the document very much, I am sure. As pertains to efficacy, I should mention that Trobalt is a so-called dirty-drug (= wide spectrum MoA). I have tracked down a few testimonials in relation to this, and there seems to be differences of opinion (at the professor-level) as to whether a high selectivity compound is better than a dirty drug for the treatment of tinnitus. I can, however, say that one professor mentioned that he/she considered Kv7.x-channels to be more important than Kv3.x-channels in relation to the treatment of symptoms of tinnitus.

In relation to SF0034, I can specifically mention the following:

Anyway, I have now shared what I know. I will update the forum if I learn more from SciFluor Life Sciences LLC.

attheedgeofscience
06/MAY/2015.

 

I don't disagree with that; perhaps I misunderstood what you were saying. I was just responding to " even tho this would cure T instantly".

I totally agree with you that this is a fascinating avenue of exploration which should be aggressively pursued with money, resources and large-sample studies.

I'm not totally convinced that Kv3.1 channel drugs are necessarily more efficient at signal suppression than benzos, and I'm far from convinced that they are any safer in their current form (trobalt). In my case, benzos completely eliminate my tinnitus... two weeks on Klonopin or Valium drops the volume to a point where I have to plug my ears in a quiet environment to hear any internal noise. But, I won't take benzos long-term ever again, and I won't take trobalt or AUT0063 until a lot more people have done it with positive results and without going blind or having their dicks turn blue.

 

I didn't know that Trobalt is/was a Kv3.1-channel drug.

[Notice the missing question mark at the end of my sentence above...].

 

fine, "KvX.x channel drug". I'm definitely not sold on the safety or efficiency of specifically targeted Kv3.1 channel drugs, since they do not exist in the wild.

You have used brackets in an odd way, did you mean to use parentheses?

 

Can you explain this a bit please?

`specifically targeted Kv3.1 channel drugs, since they do not exist in the wild`

 

ATOES's cute comment to me was a challenge to my classification of Trobalt as a "Kv3.1 channel drug". He is quite correct, it is not a Kv3.1 channel drug, it is a non-specific Kv channel drug which exerts action at a significant number of channels.

So, my comment in response which you are questioning, was an admission that I was wrong on that point, combined with an assertion that we don't know much about what a Kv3.1 specific drug would do in the human body, because as far as I know there are not any drugs presently in wide circulation which act on that specific channel and nowhere else.

 

Doesnt Keppra act on the Kv3.1 channel?

 

Keppra's mechanism is not fully understood, but it certainly is not a drug which acts only on the Kv3.1 channel.

Wikipedia says

 

@Team Trobalt has managed to get hold of a senior representative from SciFluor Life Sciences LLC. We have drafted a number of questions and we expect to have some kind of feedback on that within a week's time. Exactly how much feedback we will get, we don't know, but we can say that we will at least receive a reply to our inquiry. For sure.

Below a bit more info on SF0034 that I have tracked down. Here an excerpt from one of the pdf-files:



attheedgeofscience
12/MAY/2015.

 

Let's hope this translates with less side effects.

 

So with all of this information, is there any guess as to when an improved version of Retagabine will be available? Or at least put into clinical trials? I figure it is almost definitely too early for info like that, but I'm seriously considering trying Retagabine....

 

If it really works, 4-5 years. And I may be optimistic... Clinical Trials are really slow. :/

 

It's most likely going to be trialed for epilepsy first. Trials are not even underway so most likely more then 5 years.

 

I hope our greek friend Dr. Thanos Tzounopoulos will bring change to that. (PS I hope i`m connecting the correct pieces here - anyone correct me if i`m wrong please)

http://www.audres.pitt.edu/people/tzounopoulos.php

Current Research
Mechanisms of synaptic plasticity have traditionally been ascribed to higher-order sensory processing areas such as the cortex, whereas early sensory processing centers have been considered largely hard-wired. However, recent results from our lab and human studies have revealed remarkable evidence for cellular and behavioral mechanisms for learning and memory in early stages of sensory processing. We are investigating the cellular mechanisms underlying synaptic and intrinsic plasticity in sensory systems and in their role for normal and pathological sensory processing. Our current studies are focusing on the role of zinc as a novel neurotransmitter in the brain. In collaboration with chemist Dr. Lippard of MIT, a pioneer in the development of zinc chelators and sensors, we are currently assessing the dynamics and the functional role of synaptically-released zinc in the brain with novel tools.

A second area of our research focuses on tinnitus and its underlying cellular and molecular mechanisms. Based on our recent findings on the molecular mechanisms underlying the induction of tinnitus and in collaboration with the medicinal chemist Dr. Peter Wipf of the University of Pittsburgh, we are developing and testing novel specific Kv7.2/3 agonists for preventing the triggering of tinnitus. Moreover, our current tinnitus-related studies are aimed towards understanding the neuronal mechanisms that underlie the maintenance of tinnitus.

A third area of our research focuses on the circuit, synaptic and intrinsic mechanisms via which cortical (A1) projection neurons mediate top-down modulation of auditory processing in normal and disease states.

 

"We are developing and testing novel specific KV7.2/3 for preventing the triggering of tinnitus." So does this mean that this medication would be used only to prevent tinnitus, but not to treat an existing condition? Sorry if that's a dumb question, I'm not the best at deciphering the exact meaning in some of these scientific journals/reports....

 

We don't know that. I don't even think people who wrote the article know exactly.

 

This is very fascinating news...The more the merrier I say! Thanks for sharing!

 

Hm, let's just hope Autifony show some positive results. Everyone seems to be negative about Autifony lately, I hope they prove us wrong.

 

It's because no one is reporting tremendous results, just like AM-101. If the pills do indeed work, and the proposed mechanism of action is somewhat right - then you may expect some ''jackpots'' full recovery. The closest thing to a full recovery we're seen reported is for trobalt. It's hard to not be cynical when some forum dudes find a drug already on the market that reportedly seems to work better than anything in clinical trials already. Makes you wonder what the f*** are the researchers doing.

 

We know the KV7 channels are decreased when tinnitus first starts...So really as soon as you get tinnitus you should get trobalt as it can hopefully lower it to an acceptable level or get rid of it...Who knows? Nobody so far has taken it within 48 hours of having tinnitus.

 

If I'm not mistaken I've recently read about a study on animals with Retigabine (active compound in Trobalt) and showed that animals treated with it didn't develop tinnitus in the same extent as the control group when subjected to loud noise.