https://investors.otonomy.com/presentations
So, results are out for Phase 1.
Not actually sure how good/bad/trivial the results are?
So, results are out for Phase 1.
Not actually sure how good/bad/trivial the results are?
I think these results were discussed on this thread a few page back! When they came out in the summer. Check out page 11 of this thread.https://investors.otonomy.com/presentations
So, results are out for Phase 1.
Not actually sure how good/bad/trivial the results are?
Ooh, ok! Sorry, completely missed that.I think these results were discussed on this thread a few page back! When they came out in the summer. Check out page 11 of this thread.
OTO-313 is Gacyclidine. Like Ketamine it is an NMDA antagonist (though it's closer to PCP than Ketamine apparently) but given intratympanically in this case.Anyone know if OTO-313 has any similarities to Ketamine? All I understand is that they both act on NMDA receptors.
They both antagonize NMDA receptors meaning they reduce the receptor activity. Beyond that I don't know.Anyone know if OTO-313 has any similarities to Ketamine? All I understand is that they both act on NMDA receptors.
The only thing I could find on this is with alcohol, which has small NMDA blocking properties, and with very long term use, or withdrawal there is an upregulation of Glutamate receptors.To the medically inclined people here - would blocking NMDA activity in the ear result in upregulation of Glutamate, and presumably trigger homeostatic adjustment in the long term?
I see, thanks! Hopefully chronic sufferers won't have to rely on this medication longer term.The only thing I could find on this is with alcohol, which has small NMDA blocking properties, and with very long term use, on withdrawal this is an upregulation of Glutamate receptors.
I suspect if this is an issue here it would be more of a long term use issue rather than a single dose of OTO-313.
Interestingly, the molecule itself is very similar.Anyone know if OTO-313 has any similarities to Ketamine? All I understand is that they both act on NMDA receptors.
OTO-313 is for tinnitus and showed positive results in its Phase I/II trial. It would probably be your best bet of the two.Would OTO-313 or OTO-413 help with chronic tinnitus in someone without hearing loss?
I think we will widely know more after all the medicines are hopefully available as at the moment we cannot exactly pinpoint what treats tinnitus and this will vary and/or be made clearer consequently after the treatments become available.OTO-313 is for tinnitus and showed positive results in its Phase I/II trial. It would probably be your best bet of the two.
OTO-413 is speculated to help, since tinnitus is due to cochlear damage. If your tinnitus is due to synapse damage it would possibly help, if it's due to something else (like hair cell damage) it wouldn't help.
We may know more after Tinnitus Talk interviews Otonomy early next year.
There is a lot more evidence that this treatment will assist than many of the previously examined treatments.I am a little confused. Is this not really good news for us? I have not been on this forum for long, so I guess people have been let down by a lot of 'treatments' and this might just be another one of those, but it seems like there is some clinical evidence that it can help.
I think many here are discouraged that OTO-313 appears to be only for acute tinnitus.I am a little confused. Is this not really good news for us? I have not been on this forum for long, so I guess people have been let down by a lot of 'treatments' and this might just be another one of those, but it seems like there is some clinical evidence that it can help.
I think some are discouraged by OTO-313 being only for acute tinnitus because they are not aware of the subsequent clinical trials for chronic tinnitus, nor is there any information and/or data relating to chronic tinnitus.I think many here are discouraged that OTO-313 appears to be only for acute tinnitus.
Although the next clinical trial in the first quarter of 2021 will be accepting chronic tinnitus sufferers.
That's a misunderstanding based on misinformation recycling on the internet.I think many here are discouraged that OTO-313 appears to be only for acute tinnitus.
If tinnitus is exacerbated by excess Glutamate in and around the cochlea, causing things to act hyperexcited and fire erratically, why would this therapy be limited to acute cases? I have never read anything that suggests that this ceases to be the case as time goes on, or else by the same logic, wouldn't the tinnitus soften and/or abate? I am not an expert, but conceptually it seems ambiguous as to why this would only be helpful to chronic cases.That's a misunderstanding based on misinformation recycling on the internet.
Otonomy is currently exploring if, and under what circumstances, OTO-313 might be helpful.
Until we know more, until Otonomy itself knows more, no need to get discouraged.
It wouldn't be necessarily. The Glutamate surge affects everyone acutely and is a more variable factor chronically.If tinnitus is exacerbated by excess Glutamate in and around the cochlea, causing things to act hyperexcited and fire erratically, why would this therapy be limited to acute cases? I have never read anything that suggests that this ceases to be the case as time goes on, or else by the same logic, wouldn't the tinnitus soften and/or abate? I am not an expert, but conceptually it seems ambiguous as to why this would only be helpful to chronic cases.
The only thing I can think of is that somehow the brain internalizes the erraticism of the ear over time, but this is quite an abstract concept and I'm not sure there is concrete evidence.
Indeed.But this would be another good question for Otonomy...
I spoke with Otonomy a couple of weeks ago, and they had no real information other than Q1 of 2021. I was advised to keep checking the "latest news" section on their homepage.Does anyone know when the next clinical trial is going to start?
Doubtful.This is a shot in the dark, but... I've had mild tinnitus since 2016 where after a week I habituated. I experienced a significant worsening about six months ago. Could this somehow pass as acute tinnitus? I'd really like to apply for their Phase 2 as they've extended the timeframe to 1 year.
That's an interesting thought. Especially if it was another noise injury, you could reasonably assume your cochlear NMDA receptors are overstimulated again. You could always apply and ask.This is a shot in the dark, but... I've had mild tinnitus since 2016 where after a week I habituated. I experienced a significant worsening about six months ago. Could this somehow pass as acute tinnitus? I'd really like to apply for their Phase 2 as they've extended the timeframe to 1 year.
Could this somehow pass as acute tinnitus?
Doubtful.
The duality of man.Yes.