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Most of the discussion on this site regarding sodium channel blockers has to do with treating hyperacusis, not tinnitus.

There’s still the Kv7 drugs like XEN-1101 and the Trobalt reformulation. Also Nav1.7 blockers, they seem far away but there’s a lot of money going into them. But yes, generally speaking we remain fucked beyond belief.

I think ebselen’s full effects are poorly understood. Just like benzos. Anybody with ear issues should try it when they can, but it’s tough to say what it will do for anybody that doesn’t have Meniere’s.

Ebselen is known to be pretty safe. It’s the only upcoming drug I’m willing to try immediately upon release. You could order some right now for “research” but I’m not quite brave enough for that.

Read the thread.

Thanks for doing research on something that isn’t your problem. Do you (or anyone) have an opinion on whether ebselen’s ability to treat toxin-induced hyperacusis in mice has any relevance to hyperacusis caused by acoustic trauma? My impression is that the damage is often similar, seeing as most...

It seems I’ve made a fundamental misunderstanding about where the potassium channel drugs do their work. Thank you for the clarification. So there will have to be a top down approach to desensitizing input from the type II fibers if cochlear regeneration doesn’t do the trick. Perhaps there is...

No, I just thought that reducing hyper-excitability in the most common neurotransmitter in the cochlea might have something to do with whatever biochemistry that either caused the initial sensitization or is keeping the fibers sensitized. Edit: Trobalt seemed to only have temporary effects so...

This isn’t expected to have much to do with the... ...correct? Glutamate seems to do everything so...

I don’t understand the nuts and bolts of what sensitization really means for the type II fibers but maybe it’s self-correcting once the OHCs are restored.

XEN-496 is literally just trobalt. I have bad visual snow so I can’t risk taking that stuff, but good luck to the brave souls who do try it. Although I’m barely clinging to life as it is so perhaps I’ll be forced to.

At the end of the day, we KNOW the channel blockers can work for many people, based on Trobalt. So, it is nice to know that XEN-1101 is very likely to work for us. But, I still wouldn't count out SPI-1005 or the regenerative drugs. At the very least, if one of them doesn't work, by process of...

Does all this ATP speculation provide an explanation for how setbacks work?

Read the Ebselen description at the top of page 10. The only hard data available is from the mouse study and the Meniere’s trials. This forum as usual is getting way ahead of itself and speculating on release schedules before we even know if the drug will help us. These questions can’t be...

The only data we have to go on is the phase 2 Meniere’s trial. Its effect was not immediate in that trial, but it was well tolerated with no serious side effects. Symptoms were slowly reduced over the multiple weeks of the trial. So, I imagine it would be something we would take every day (400mg...

I hope so. That would be ideal. A lot of this makes sense intuitively but we just don’t know enough to confirm it. Hyperacusis improves with long periods of rest so something must be going on that calms down over time. Logically that would be some irritant in the cochlea, and SPI-1005 seems to...

Ok, this is what Sound Pharmaceuticals says ebselen (SPI-1005) does: “SPI-1005, a proprietary oral formulation of ebselen, is a small molecule mimic and inducer of glutathione peroxidase (GPx). GPx is the dominant catalytic antioxidant enzyme in the cochlea and is critical for auditory function...

Where do you think this ATP is coming from? I thought it only happened upon initial cell death. Unless damaged yet still living cells are doing it. In which case no upcoming medication would solve the problem unless SPI-1005 can clean ATP up as part of its antioxidant effects? No, this is about...

I hope we have more information soon about how “inflammation” (such a broad term!) relates to tinnitus spikes/hyperacusis. Clearly, many spikes/setbacks are not the result of additional hair cell death. But then why do they happen? Temporary hyperactivity, maybe in the cochlear nerve bushy cells...

“Sound Pharmaceuticals also aims to regenerate cochlear cells, but taking a small interfering RNA approach. The therapeutic agent is SPI-5557, which inhibits p27Kip1, an inhibitor of cyclin-dependent kinase whose deletion in mice leads to proliferation of supporting cells and the regeneration of...

The earlier quote states that the treatment “leads to proliferation of supporting cells and the regeneration of hair cells.” To me that implies the converted support cells are replaced rather than depleted. Perhaps they just think differently from Hough Ear Institute or maybe the method is...

“SPI-1005 is given orally and is being tested in several neurotologic indications including noise induced hearing loss and two types of ototoxicity (hearing loss, tinnitus, dizziness or vertigo): due to aminoglycoside antibiotics (such as tobramycin) and due to platinum-based chemotherapy.“...