Thanks! I guess I have tonal and possibly another type? I have a low pitched hum in my right ear that I can change the frequency of by twitching my face. In my left ear, I have a similar that that I can make go away by twitching my face. I used to be able to make the right side hum go away too, but it's here to stay now...or a treatment comes along.
Brivaracetam — KV3.1 Modulator
- Thread starter Danny Boy
- Start date
MemberI do try my best...I mean the doctors don't even bother? I mean, I found a treatment for hyperacusis yet, doctors who have PHD's haven't? Why? I only had tinnitus for 8 months, yet, they've been researching for years. I actually informed them, a non-profit organisation for hyperacusis and they weren't interested in the slightest! So to be honest, all these charities I don't trust as a cure only means they are out of the job and they can't go hobnobbing with their friends with food paid for by us. So we've had to repurpose epilepsy medication. I'm glad you've found this place and that you love my posts, I will continue the long journey of finding stuff to treat us. Anyway, good luck mate!
ruben ruiz
Member
When is this comming out? And it targets what exactly? As in how would it help us out?
So it might have more side efects since its stronger?? This is a epilepsy med too right?
I sometimes get the feeling that tinnitus research does not attract the best and brightest of scientists. It's just not as trendy as cancer I guess.
Even cancer research is full of fraud. http://edition.cnn.com/videos/us/2015/05/19/lv-griffin-scam-charities-investigation.cnn
I don't trust charities and never donate to them, as I know they don't want to cure cancer...They want to take the money for themselves and don't care. Greed in this world is rife.
Calories
Member
- Mar 30, 2015
- 35
- Tinnitus Since
- March 2015
- Cause of Tinnitus
- B12 Difficiency, Possibly salycilic poising from fenugreek and ginger
Will do buddy.
Wouldn't have a clue about india...They've only ask to licence it in Europe and the US at the moment. They'll expand if it's proven successful.
not true buddy, I said it before ... they emailed me back and said it`s not adresssing the KV 3.1 ...
it`s some ligand thing this adresses ... too tired to look it up but it`s in this thread and I tagged you in it to clarify.
Email them and ask if keppra works on the KV3.1 channels...As Keppra has an unknown mechanism which has been identified as KV3.1. If they say we don't know, then we know they don't have a clue.
unfortunatly i`m not enough informed to understand all medcial and scientific terms ... So in her words from the email..
`Brivaracetam werkt dus als hoge affiniteit SV2A ligand (en niet op potassium kanalen)`
`Brivaracetam works as high affinity SV2A ligand (not on potassium channels)`
"Brivaracetam (BRV) is a pyrrolidine derivative currently being investigated for the treatment of epilepsy (Bialer et al., 2010). It is a novel high-affinity synaptic vesicle protein 2A (SV2A) ligand (Kenda et al., 2004; Gillard et al., 2011). Preclinical studies demonstrated efficacy in a wide range of animal models of partial-onset (focal) and generalized seizures (Matagne et al., 2008) and a higher affinity (>30-fold) for SV2A in human cerebral cortex compared with levetiracetam (LEV) (Gillard et al., 2011)".
edit:
Brivaracetam is a high-affinity synaptic vesicle protein 2A (SV2A) ligand. It is not entirely clear how SV2A affects neuro-transmission, but animal studies suggest that it is potentially a good target for seizure control. Mice deficient in SV2A have seizures (4). Among animal models of epileptogenesis as well as in humans with epilepsy, pathologic reduced SV2A expression is evident (5). In addition, studies find that SV2A binding strongly correlates with antiepileptic potency (6). Interestingly, levetiracetam, which is one of the most commonly used AEDs worldwide, has SV2A binding affinity. Brivaracetam by comparison, has a >30-fold affinity for SV2A than levetiracetam (7) suggesting that brivaracetam may be a very effective AED. As with most AEDs, brivaracetam likely has multiple mechanisms of action. Not only is it an SV2A ligand, it displays inhibitory activity at neuronal voltage-dependent sodium channels (8).
So yes, they don`t know what they speak about themselves ... and actually they don`t even know how it works
...
unfortunatly i`m not enough informed to understand all medcial and scientific terms ... So in her words from the email..
`Brivaracetam werkt dus als hoge affiniteit SV2A ligand (en niet op potassium kanalen)`
`Brivaracetam works as high affinity SV2A ligand (not on potassium channels)`
"Brivaracetam (BRV) is a pyrrolidine derivative currently being investigated for the treatment of epilepsy (Bialer et al., 2010). It is a novel high-affinity synaptic vesicle protein 2A (SV2A) ligand (Kenda et al., 2004; Gillard et al., 2011). Preclinical studies demonstrated efficacy in a wide range of animal models of partial-onset (focal) and generalized seizures (Matagne et al., 2008) and a higher affinity (>30-fold) for SV2A in human cerebral cortex compared with levetiracetam (LEV) (Gillard et al., 2011)".
edit:
Brivaracetam is a high-affinity synaptic vesicle protein 2A (SV2A) ligand. It is not entirely clear how SV2A affects neuro-transmission, but animal studies suggest that it is potentially a good target for seizure control. Mice deficient in SV2A have seizures (4). Among animal models of epileptogenesis as well as in humans with epilepsy, pathologic reduced SV2A expression is evident (5). In addition, studies find that SV2A binding strongly correlates with antiepileptic potency (6). Interestingly, levetiracetam, which is one of the most commonly used AEDs worldwide, has SV2A binding affinity. Brivaracetam by comparison, has a >30-fold affinity for SV2A than levetiracetam (7) suggesting that brivaracetam may be a very effective AED. As with most AEDs, brivaracetam likely has multiple mechanisms of action. Not only is it an SV2A ligand, it displays inhibitory activity at neuronal voltage-dependent sodium channels (8).
So yes, they don`t know what they speak about themselves ... and actually they don`t even know how it works
It'll work on the KV3.1 channels, as it's just a more potent version of keppra. To be honest, it's funny how they don't know how their own drug works.
yes but even Keppra doesn`t work on these kv channels specifically .. Keppra is something of which they don`t know how it exactly works but they see it influencing different kinds of ion channels ... where did you ever read keppra is a kv3.1 channel modulator?
Abstract
Levetiracetam (LEV) is a prominent antiepileptic drug that binds to neuronal synaptic vesicle glycoprotein 2A protein and has reported effects on ion channels, but with a poorly defined mechanism of action. We investigated inhibition of voltage-dependent Ca(2+) (Ca(V)) channels as a potential mechanism through which LEV exerts effects on neuronal activity.
http://www.ncbi.nlm.nih.gov/pubmed/20065495
Experimental and simulation studies on the mechanisms of levetiracetam-mediated inhibition of delayed-rectifier potassium current (KV3.1): contribution to the firing of action potentials.
Huang CW1, Tsai JJ, Huang CC, Wu SN.
Author information
Abstract
Levetiracetam (LEV) is an S-enantiomer pyrrolidone derivative with established antiepileptic efficacy in generalized epilepsy and partial epilepsy. However, its effects on ion currents and membrane potential remain largely unclear. We investigated the effect of LEV on differentiated NG108-15 neurons. In these cells treated with dibutyryl cyclic AMP, the expression level of the K(V)3.1 mRNA was elevated. With the aid of patch clamp technology, we found that LEV could suppress the amplitude of delayed rectifier K(+) current (I(K(DR))) in a concentration-dependent manner with an IC(50) value of 37 microM. LEV (30 microM) shifted the steady-state activation of I(K(DR)) to a more positive potential by 10 mV, without shifting the steady-state inactivation of I(K(DR)). Neither Na(+), nor erg (ether-a-go-go-related)-mediated K(+) and ATP-sensitive K(+) currents were affected by LEV (100 microM). LEV increased the duration of action potentials in current clamp configuration. Simulation studies in a modified Hodgkin-Huxley neuron and network unraveled that the reduction of slowly inactivating I(K(DR)) resulted in membrane depolarization accompanied by termination of the firing of action potentials in a stochastic manner. Therefore, the inhibitory effects on slowly inactivating I(K(DR)) (K(V)3.1-encoded current) may constitute one of the underlying mechanisms through which LEV affect neuronal activity in vivo.
Danny boy you really doing amazing work here. I got t at the same time as you.. I hear it in quiet places and but when outside, it largely fades into the background. when working on the computer, I play low volume bird chirping sounds which mostly mast the t. I have buzzing (power line) type of t. Just knowing (thanks to you) that there are things that help like trobalt, keppra, hopefully brivaracetem has made me feel less powerless against t. Looking forward to autofiny. Thank you.
Btw, where did you find information that Brivaracetam is kv3.1 modulator? I quickly red the articles trough and didn't find any exact references.
Or are you only assuming that it is kv3.1 modulator because it is Keppras cousin?
Well, when nills contacted them, they didn't even know keppra works on the KV3.1 channels. So I am assuming as they would have the same function. This is only because they lost the patent to keppra and it's a generic drug now. So I would assume since they have the same function that it works in the same way.
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