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Fasoracetam

theGirlWithBlueHair

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Does anybody have any knowledge/info/advice for how to dose and how many times a day to take fasoracetam? Information on the web is very limited and scattered and I would like feedback from people who have actually used the substance.
 

kleinerkiffer

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I think you'd get more replies over at Neurosience and Pharmacology discussion. Do you want me to move the thread ?
 

kleinerkiffer

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OD -> N&PD

If no one replies by tomorrow/ the day after tomorrow tell a mod to move it back :)
 
Last edited:

Cosmic Trigger

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Does anybody have any knowledge/info/advice for how to dose and how many times a day to take fasoracetam? Information on the web is very limited and scattered and I would like feedback from people who have actually used the substance.
I used to to help getting off Phenibut. I used 10mg at a pop 3x per day.
 

Cotcha Yankinov

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^Yes I think 10mg is a good starting dose and then proceed up to 30mg, but people take closer to 100mg.
 

theGirlWithBlueHair

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Was it sublingual? And does it help with the cognitive effects? I'm talking about the cognitive problems that baclofen causes because I take it medically. So if I wanted to study...if I take fasoracetam, would it temporarily reverse the effects so I could I study better? I wouldn't be taking it alone. I also have aniractam, sulbitiamine, huperzine a, cdp choline (which I take twice a day), oxiracetam, dimethylaminoethanol (DMAE -which I hear conflicting things about (is this a good supplement or not?) -), adrafinil, and hordenine ( which I take three times a day (I know it's not technically a nootropic, but it's sold as one).

The baclofen and gabapentin I take really affect cognition and memory (gabapentin affects a neurotransmitter called thrombospondin which is responsible for the formation of neuronal synapsis and memory and plasticity and long term potentiation) - not many people know about this, but it really affects the ability to study and remember things.

This is the reason it gets the nickname Morontin. And it doesn't help that I take topiramate for migraines. I had my dose dramitcally lowered. But Topamax has the nickname Dopamax and it definitely deserves it - it affects the AMPA glutamate receptors and kainate glutamate receptors - both of which are mainly involved in long term potentiation. The ampakine racetams work on AMPA receptors, so they kind of work the opposite way of Topamax, which I'm getting off of.

I'd appreciate feedback.
 

Ligaturd

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I've got 5 grams of this sitting around, I've only tried it once and I got really worked up and anxious on it. I'm not sure if this reaction was psychosomatic however. Reading that it upregulated GABA b by possibly being an antagonist, I envisioned getting the opposite reaction of agonism at GABA b and it's possible that I made it a reality. I have read of others getting this reaction as well. I plan to try it on its own though. It isn't very optimal conditions when you take a somewhat new and not very well studied compound in a cocktail with many other compounds.

It has the opposite effect at GABA b of baclofen but from what I have read, those taking it with GABA b agonists have experienced potentiation of the GABA b agonist that they are taking. YMMV of course.
 

theGirlWithBlueHair

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I take 20mg of baclofe 3 times a day. So you're saying that when I want to study and stuff, taking the fasoracetam won't temporarily reverse the cognitive-hampering effects of the baclofen for it's duration but make them worse? It won't have a nootropic effect?
 

Cotcha Yankinov

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I think it's weird that fasoracetam helped reduce a memory or something deficit induced by baclofen in mice when some of the other drugs were more AMPAkines and that sort of stuff failed to reverse the baclofen induced deficit, and I think they tested acetylcholinergic as well. So one might assume that fasoracetam is indeed a GABAb antagonist but it's hard to say for sure. But worrying about baclofen when you're on Topiramate might not be the right direction.
 

theGirlWithBlueHair

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I think it's weird that fasoracetam helped reduce a memory or something deficit induced by baclofen in mice when some of the other drugs were more AMPAkines and that sort of stuff failed to reverse the baclofen induced deficit, and I think they tested acetylcholinergic as well. So one might assume that fasoracetam is indeed a GABAb antagonist but it's hard to say for sure. But worrying about baclofen when you're on Topiramate might not be the right direction.
That's what I have the ampakines for as they antagonize topiramate's stupefying effect. But I don't seem to get this effect, only when I take sodium channel blockers with it concurrently. I was on Vimpat briefly for pain, but it caused me to start forgetting words midsentence, not being able to think, just being dumb as fuck, which is what the topiramate is known for. So I stopped the lacosamide, and the symptoms disappeared.

So I think it just potentiated the topiramate. But otherwise it doesn't display those effects in me.

And GABA B agonists are known for impairing cognition and learning, and this is why I bought the fasoracetam, because baclofen does this to me.
 

asecin

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what about aniracetam, isnt it also gaba b antagonist since i was reading one report of a person trying both fasoracetam and aniracetam saying they felt similar but i cannot find good literature to explain anything in specific about aniracetam action of effect. as it is usual for most racetams, literature is so scarce...
 

theGirlWithBlueHair

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No. They feel similar in some regards because they are both AMPAkines and positively modulate the AMPA glutamate receptor
 

shugenja

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That's what I have the ampakines for as they antagonize topiramate's stupefying effect. But I don't seem to get this effect, only when I take sodium channel blockers with it concurrently. I was on Vimpat briefly for pain, but it caused me to start forgetting words midsentence, not being able to think, just being dumb as fuck, which is what the topiramate is known for. So I stopped the lacosamide, and the symptoms disappeared.

So I think it just potentiated the topiramate. But otherwise it doesn't display those effects in me.

And GABA B agonists are known for impairing cognition and learning, and this is why I bought the fasoracetam, because baclofen does this to me.
Bacopa Monnieri reverses both downregulation and upregulation of GABAa and GABAb receptors (multiple subtypes) in a pilocarpine induced mouse model of epilepsy.

Gene expression of GABAAά1, GABAand GABA, where showed significant down regulation (p < 0.001) in the cerebral cortex of the epileptic rats compared to the control. Gene expression of GABAAά5 receptor subunit showed significant up regulation compared to the control. Treatment using Bacopa monnieri, Bacocide-A and Carbamazepine reversed the changes to near control (Figures (Figures1,1, ,2,2, ,33 and and44).

"GABAB, and GAD65 mRNA were significantly down regulated compared to the control. Treatment using Bacopa monnieri, Bacoside-A and Carbamazepine were reversed the changes to near control (Figures (Figures5,5, ,66 and and77)."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306740/

Bacopa monniera ameliorates amnesic effects of diazepam qualifying behavioral-molecular partitioning.


http://www.ncbi.nlm.nih.gov/pubmed/18585439


It seems that Bacopa exerts a significant homeostatic effect on the GABA receptor complex, upregulating downregulated receptors and vice versa.

There is also evidence in the literature it does the same thing for serotonin

http://www.ncbi.nlm.nih.gov/pubmed/21129470 (upregulation of Tryp hydroxylase, SERT)

I'm still looking for the citation for downregulation of 5HT1a and upregulation of 5HT2c by bacopa.
 

Ligaturd

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what about aniracetam, isnt it also gaba b antagonist since i was reading one report of a person trying both fasoracetam and aniracetam saying they felt similar but i cannot find good literature to explain anything in specific about aniracetam action of effect. as it is usual for most racetams, literature is so scarce...
Aniracetams metabolite N-Anisoyl-GABA is a gaba receptor agonist (not sure about selectivity) but it modulates glutamate levels. It simultaneously has nootropic effects and anxiolytic effects. That combined with Coluracetam pretty much temporarily got rid of my anxiety and depression when I was in the midst of a psychotic break. It's definitely in my top 3 racetams but no, it isn't an antagonist.

Fasoracetam is theorized to be an antagonist as it is supposed to upregulate GABA b, but it also has anxiolytic effects which seems counter intuitive to me. A GABA a antagonist would most likely excitatory damage, prevent any regulation of glutamate activity, cause extreme anxiety and probably even psychosis.
 

Limpet_Chicken

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Girlwithbluehair, have you tried any selective AMPAkines?

I ask because I intend to at least trial sunifiram/DM-235, a 'true' AMPAkine, in the sense of not having some indistinct mechanism of action like E.g piracetam and known mechanism, elucidated by and characterised with electrophysiological studies under patch-clamp conditions.

BUT, I am not going to start it before getting on memantine, and my fucking doctors have for years been content to let me rot more or less. They know memantine itself (tried it for quite some time in combination with galantamine, and the memantine quite literally was the difference between functioning, between being able to not go so hungry because I can't even make food on my bad days, I'd just stand there, in front of it, staring at the wall, unable to make myself move and do it, despite being desperately hungry. My short term, and working memory, as well as ability to consolidate and retain long-term memory is shot, and of recent times my semantic memory has been going too. As has my executive functioning been gone for the most part for many years. My mother has MS, and dementia, and they have destroyed her. I am physically capable of movement unlike her. But now as of recently she was taken into hospital, and most likely she will not live much longer.

But I have watched her. For years and years and years, watched her slowly ROT, decaying like a piece of fucking meat, she doesn't (or didn't. Don't know if she is ever getting out of hospital, we think it unlikely and if she does it will have to be palliative nursing as end of life care because we cannot do it. The sooner she drops dead the fucking better, sound mean? because its not, its far far from it, because the reaper's scythe will be a mercy for her when finally it severs her thread of life, if 'life' came close to what shes stick in now, forced continuation of existence is more accurate.)

Shes turned into a bipedal (not that the legs or anything else WORKS mind you) mammalian cabbage, and I am NOT going to allow that to happen to me. If it means getting permission from the person who holds my life in her hands, to blow my brains out while I still can then so be it. But I'd sooner, far, far, far infinitely sooner, work on what I can while I can to reverse this shit. But I can't find the memantine nor get the precursor dimethyladamantanol or dimethyladamantanyl chloride to produce memantine for myself. And cannot buy it either.

Since GABAb agonism induces a lessening of glutamate release, how about partial negative allosteric modulation? could this be responsible.
 

asecin

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Aniracetams metabolite N-Anisoyl-GABA is a gaba receptor agonist (not sure about selectivity) but it modulates glutamate levels. It simultaneously has nootropic effects and anxiolytic effects. That combined with Coluracetam pretty much temporarily got rid of my anxiety and depression when I was in the midst of a psychotic break. It's definitely in my top 3 racetams but no, it isn't an antagonist.

Fasoracetam is theorized to be an antagonist as it is supposed to upregulate GABA b, but it also has anxiolytic effects which seems counter intuitive to me. A GABA a antagonist would most likely excitatory damage, prevent any regulation of glutamate activity, cause extreme anxiety and probably even psychosis.

so it modulates glutamate, but how long lasting is that? since i stopped it, i had rebound depression so im not really sure how to approach it now. it seems to help as long as you take it and even then, i built tolerance. so depression was unavoidable. also, can you please help me out here, does tianeptine work on glutamate in similar mechanism because both aniracetam and tianeptine feel similar somehow, cannot explain it but i assume modulation of glutamate?
 

Cotcha Yankinov

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Glutamate unfortunately is really good at compensating via long term potentiation and such, typically when you use GABA-A agonists the glutamate downstream of that compensates and that is a major issue when it comes to tolerance/withdrawal.
 

Ligaturd

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what about aniracetam, isnt it also gaba b antagonist since i was reading one report of a person trying both fasoracetam and aniracetam saying they felt similar but i cannot find good literature to explain anything in specific about aniracetam action of effect. as it is usual for most racetams, literature is so scarce...
so it modulates glutamate, but how long lasting is that? since i stopped it, i had rebound depression so im not really sure how to approach it now. it seems to help as long as you take it and even then, i built tolerance. so depression was unavoidable. also, can you please help me out here, does tianeptine work on glutamate in similar mechanism because both aniracetam and tianeptine feel similar somehow, cannot explain it but i assume modulation of glutamate?

I used it for 2 months straight and never had any sort of withdrawal or anything of that sort. Theoretically it should be possible but I haven't heard of it being reported, typically when you stop GABAergics after becoming dependant on them you will experience a glutamate rebound effect.

According to this it does modulate glutamate levels: http://www.tianeptine.com/glutamate.html

I never really looked into tianeptine, I assumed it exhibited most of its effects through Serotonin reuptake enhancement and MOR agonism. Interesting.
 
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