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Frequency Therapeutics — Hearing Loss Regeneration

#12,481
Lucifer said:
Thanks for this patorjk.

Do you have a website link where I can view how many shares do the CEO and Co-Founder have and how many shares they have sold?

I wonder what could be the reason why Christopher Loose is not selling his shares every 2 weeks. Maybe the results have been looking positive and knows he will make a lot of money when FX-322 comes out in the market and wants to maximise his rate of return on his investment.
Click to expand...
I use eTrade, which has a tab for that info. However, you can also get the info from the SEC website and Frequency Therapeutics' own website (though it's less user friendly):

https://www.sec.gov/edgar/searchedgar/companysearch.html
https://investors.frequencytx.com/sec-filings

Those sites will show the trades as they happen. I'm not sure if there's a way to look up current company ownership without deducing it from the trading information.

My guess is that Chris just wanted to diversify himself and thought the stock would climb and spike after September, so he setup a 10b5-1 plan. When the results got delayed he was probably unable to get out of it.
 
#12,482
100Hz said:
Yeh it seems pretty obvious now doesn't it that there has to be an OHC there for the extra ribbons synapses to even happen (for type IIs). With the ATP / dead hair cell route though, only based on a few diagrams I've found and I'm trying to find more to help back it up, it appears that type II afferents connect (I wouldn't say synapse exactly), to support cells as well as actual hair cells, I wonder if this is the case then could type IIs be susceptible to ATP via support cells as well, or does it takes a functioning OHC to actually begin transmission of the signal. Your other theories above are also very interesting.

Here's one of the diagrams showing the type II connecting to a support cell:

View attachment 42161
Click to expand...
If all the hair cells were dead, noxacusis would not be possible without the type 2 fibers.

This is very different from tinnitus where you can remove the whole cochlea and still have "phantom cochlea."
 
#12,483
100Hz said:
Yeh it seems pretty obvious now doesn't it that there has to be an OHC there for the extra ribbons synapses to even happen (for type IIs). With the ATP / dead hair cell route though, only based on a few diagrams I've found and I'm trying to find more to help back it up, it appears that type II afferents connect (I wouldn't say synapse exactly), to support cells as well as actual hair cells, I wonder if this is the case then could type IIs be susceptible to ATP via support cells as well, or does it takes a functioning OHC to actually begin transmission of the signal. Your other theories above are also very interesting.

Here's one of the diagrams showing the type II connecting to a support cell:

View attachment 42161

In other words if all hair cells were dead, yet all type IIs sensitized, would there even be a mechanism / pathway for a pain signal anymore.
Click to expand...
This conversation Juan and I have been having seems to support that theory:

Screenshot_20201215-105252_Chrome.jpg
 
#12,484
FGG said:
If all the hair cells were dead, noxacusis would not be possible without the type 2 fibers.
Click to expand...
Every theory seems to lead back to needing to take care of the sensitized type IIs above all else for noxacusis. The only other hope I've got is that ATP leakage is playing a huge part in it and can be stopped somehow.

I know that this set of circumstances would probably be so unlikely anyway, but if say all the sensitized type II connected OHCs were damaged to a point where they would be flagged for repair, then say that all healthy OHCs type IIs had not been sensitized either from an external ATP source or by them being maximally stimulated, if FX-322 did fix up all the damaged OHCs that would mean no more excess ATP (unless it came from yet somewhere else, gap junctions etc.). If you ticked all those boxes would sensitized type IIs but without the presence of excess ATP behave themselves at last? It's an insane amount of conditions to meet, just wonder hypothetically what it might take to nullify the effects of sensitized type IIs without having to need something like XEN or RL-81.
 
#12,485
100Hz said:
Every theory seems to lead back to needing to take care of the sensitized type IIs above all else for noxacusis. The only other hope I've got is that ATP leakage is playing a huge part in it and can be stopped somehow.

I know that this set of circumstances would probably be so unlikely anyway, but if say all the sensitized type II connected OHCs were damaged to a point where they would be flagged for repair, then say that all healthy OHCs type IIs had not been sensitized either from an external ATP source or by them being maximally stimulated, if FX-322 did fix up all the damaged OHCs that would mean no more excess ATP (unless it came from yet somewhere else, gap junctions etc.). If you ticked all those boxes would sensitized type IIs but without the presence of excess ATP behave themselves at last? It's an insane amount of conditions to meet, just wonder hypothetically what it might take to nullify the effects of sensitized type IIs without having to need something like XEN or RL-81.
Click to expand...
I know it removes the ear's natural protection but once FX-322, OTO-413, and SPI-1005 come out, couldn't one just have the Tensor Tympani and stapedius muscles destroyed? They seem to be the main cause for a lot of people's hyperacusis, at least for me it is.

I mean with the new hair cells and synapses from FX-322 and OTO-413, the ability to regenerate them as necessary and with the extra protection from SPI-1005 I feel like those 2 muscles would be totally useless if they're still malfunctioning because of sensitized type 2 afferents after those 3 treatments.
 
#12,487
100Hz said:
Every theory seems to lead back to needing to take care of the sensitized type IIs above all else for noxacusis. The only other hope I've got is that ATP leakage is playing a huge part in it and can be stopped somehow.

I know that this set of circumstances would probably be so unlikely anyway, but if say all the sensitized type II connected OHCs were damaged to a point where they would be flagged for repair, then say that all healthy OHCs type IIs had not been sensitized either from an external ATP source or by them being maximally stimulated, if FX-322 did fix up all the damaged OHCs that would mean no more excess ATP (unless it came from yet somewhere else, gap junctions etc.). If you ticked all those boxes would sensitized type IIs but without the presence of excess ATP behave themselves at last? It's an insane amount of conditions to meet, just wonder hypothetically what it might take to nullify the effects of sensitized type IIs without having to need something like XEN or RL-81.
Click to expand...
I think reducing excess ATP leakage from damaged neighboring hair cells and gap junction leakage from inflammation would likely at least reduce the problem but noxacusis is so very multi factorial.
 
#12,488
frpp said:
I know it removes the ear's natural protection but once FX-322, OTO-413, and SPI-1005 come out, couldn't one just have the Tensor Tympani and stapedius muscles destroyed? They seem to be the main cause for a lot of people's hyperacusis, at least for me it is.

I mean with the new hair cells and synapses from FX-322 and OTO-413, the ability to regenerate them as necessary and with the extra protection from SPI-1005 I feel like those 2 muscles would be totally useless if they're still malfunctioning because of sensitized type 2 afferents after those 3 treatments.
Click to expand...
Why would the middle ear be causing noxacusis; I thought it was cochlear. I assume the tensor tympani is spasming in order to protect the inner ear as a result of damage sustained to the cochlea.
 
#12,489
weab00 said:
Why would the middle ear be causing noxacusis; I thought it was cochlear. I assume the tensor tympani is spasming in order to protect the inner ear as a result of damage sustained to the cochlea.
Click to expand...
The noise threshold for the tensor tympani to react is drastically lowered or almost non existent in people with TTTS so it will spasm either constantly or some even at the slightest sound (talking or even breathing for me) and it causes a lot of nerve pain and migraines.

It's definitely related to some form of cochlear damage but, in the case of TTTS hyperacusis, if you cut those muscles oftentimes it stops since there's nothing left to signal to spasm.
 
#12,490
weab00 said:
Why would the middle ear be causing noxacusis; I thought it was cochlear. I assume the tensor tympani is spasming in order to protect the inner ear as a result of damage sustained to the cochlea.
Click to expand...
It's more likely that we need FX-322 or OTO-413 to fix the underlying issues in the ear. If we're lucky Ebelsen may help us with pain hyperacusis and that should be out soon once they release results in April 2021.
 
#12,491
frpp said:
The noise threshold for the tensor tympani to react is drastically lowered or almost non existent in people with TTTS so it will spasm either constantly or some even at the slightest sound (talking or even breathing for me) and it causes a lot of nerve pain and migraines.

It's definitely related to some form of cochlear damage but, in the case of TTTS hyperacusis, if you cut those muscles oftentimes it stops since there's nothing left to signal to spasm.
Click to expand...
Aren't you then exposing your inner ear to more sound by removing the protective layer?
 
#12,495
#12,496
Lucifer said:
Is this loan for their new building or is it actually for their pivotal trials? Wouldn't they already have enough money to complete their pivotal trial because of Astellas Pharma?
Click to expand...
Looks like they need to buy more equipment ASAP. The equipment can either be used to prepare for the pivotal, or make current equipment available for the pivotal; or both.

Cash on hand will go to operations first: paying people, keeping the lights on, paying for trials. So, they're leveraging equity with a short-term loan to buy equipment.
 
#12,497
#12,498
frpp said:
The noise threshold for the tensor tympani to react is drastically lowered or almost non existent in people with TTTS so it will spasm either constantly or some even at the slightest sound (talking or even breathing for me) and it causes a lot of nerve pain and migraines.

It's definitely related to some form of cochlear damage but, in the case of TTTS hyperacusis, if you cut those muscles oftentimes it stops since there's nothing left to signal to spasm.
Click to expand...
I still hope that this threshold would recover over time once the underlying lying cochlear problems were fixed. If it didn't though then yeh cutting it would be a last resort.
 
#12,500
weab00 said:
If there's anyone that's going to parse through a 34 page investor report, it's Diesel.
Click to expand...
Just doing what I can. I hope we all hang in there long enough to get this stuff and go back into the world. These little details I hope keep us all positive while we wait.
 
#12,501
weab00 said:
Yeah, we don't want "hair-like cells," give me some damn new born stereocilia.
Click to expand...
I mean if they work which Rinri Therapeutics stated they do and increased hearing by 40% in preclinical models and if some people don't have any or enough support cells to fully restore hearing, these could work quite nicely, especially for filling in any gaps.
 
#12,503
frpp said:
I mean if they work which Rinri Therapeutics stated they do and increased hearing by 40% in preclinical models and if some people don't have any or enough support cells to fully restore hearing, these could work quite nicely, especially for filling in any gaps.
Click to expand...
Isn't it the case that most people theoretically should benefit from FX-322 and actually as a result not need what Rinri Therapeutics is working on since their medicine is for people with actual nerve issues and often this is not necessarily accompanied with hair cell loss?
 
#12,504
Diesel said:
I hope we all hang in there long enough to get this stuff and go back into the world. These little details I hope keep us all positive while we wait.
Click to expand...
Definitely seeing all of this as positive moment on Frequency Therapeutics' part. I can't imagine all of this funding being pumped their way if negative results were coming in at any capacity.
 
#12,505
FGG said:
This makes me wonder if CIs would actually help noxacusis in this case because they destroy the sensory cells where the electrodes are placed.
Click to expand...
This reminded me of a person who said her hyperacusis got so much better after CIs.

But from what I read, they avoid destroying your existing cochlear tissue as far as possible.
 
#12,506
frpp said:
The noise threshold for the tensor tympani to react is drastically lowered or almost non existent in people with TTTS so it will spasm either constantly or some even at the slightest sound (talking or even breathing for me) and it causes a lot of nerve pain and migraines.

It's definitely related to some form of cochlear damage but, in the case of TTTS hyperacusis, if you cut those muscles oftentimes it stops since there's nothing left to signal to spasm.
Click to expand...
100Hz said:
I still hope that this threshold would recover over time once the underlying lying cochlear problems were fixed. If it didn't though then yeh cutting it would be a last resort.
Click to expand...
Just to add, I believe this does naturally happen anyway as noise tolerance does tend to recover after each setback, even if it takes months it does generally seem to be an upward trend until the next setback. I hope that a permanent / manageable fix to the underlying issue would mean a permanent fix for this as it would just continue to get better. I appreciate that some sufferers may take much longer or maybe appear to not heal at all though, but based on my condition and of a lot of others I've read about it does seem to work this way, maybe some people just need so much more time for this to settle and having that underlying damage fixed would finally allow that to happen.
 
#12,507
tbuzz89 said:
Definitely seeing all of this as positive moment on Frequency Therapeutics' part. I can't imagine all of this funding being pumped their way if negative results were coming in at any capacity.
Click to expand...
That's why I believe FX-322 works. Why would Astellas Pharma give them so much funding to go through the clinical trials otherwise? You wouldn't want to invest that much money if you knew it was going to fail.
sssing said:
This reminded me of a person who said her hyperacusis got so much better after CIs.

But from what I read, they avoid destroying your existing cochlear tissue as far as possible.
Click to expand...
This is why I have hope that FX-322 should resolve both pain and loudness hyperacusis.
 

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