1565 replies to this topic

[megatron]

Got the letter today; seized by customs :(

[renfr]

Got the letter today; seized by customs :(

Tough luck for you!
Maybe you should get it from someone in the EU, Norway is part of the EEA therefore it shares a single market with the EU (http://en.wikipedia....n_Economic_Area).

[peakplasma]

My sunifiram was delivered today, just minutes after my apartment office closed. Ill try my first dose tomorrow morning.

also, someone on reddit posted this:


"Sunifram's combines two mechanisms with respect to AMPAr. One increases channel open frequency via allosteric modulation, the other gates the channel as a direct agonist.
The body has mechanisms to very rapidly remove excess glutamate that are required to prevent glutamatergic exitotoxicity, which is why relevant ion-channel modulators like Piracetam are not neurotoxic.
If the channel is forced to remain open whilst there is already excess stimulation (Sunifram does both these things by binding as a ligand to two different AMPA receptor sites), leading to a greater threshold of glutamatergic activity within the cell, there would be a greater potential for toxicity than either mode of action alone.
The massive Ca++ influx should result in excitotoxic damage, as Sunifram bound as a direct agonist directly gates the ion channel and makes it open, passing unregulated bucketloads of calcium into the cell, and killing it in the process. AMPARs are expressed to a high extent within the prefrontal cortex and hippocampus, which as is well known, are involved in rational higher cognitive function, learning and memory, as well as in the striatum, where they interact with DA receptors.
I would definitely not fuck around with this drug."

I can't really make any sense of it, could anyone verify (or hopefully disprove) this claim?

Do you know which study suggests it is a direct agonist?

There is definitely some cause for concern regarding excitotoxicty since at least one AMPAkine has been shown to be cytotoxic in rats. However, I didn't read anything to suggest that Sunifiram is any more damaging than any other racetam.

[megatron]

Got the letter today; seized by customs :(

Tough luck for you!
Maybe you should get it from someone in the EU, Norway is part of the EEA therefore it shares a single market with the EU (http://en.wikipedia....n_Economic_Area).

I know I think I'll just wait for PRL 8-53 and NSI-189.

[OpaqueMind]

I'm a bit worried about the possibility of excitotoxicity too. Some more digging unearthed this which was in reply to a question on the ADD forum of Bluelight;

The way the ligand gates the channel dictates more the behaviour than potency.

A good example would be barbiturates vs benzos at GABAa allosteric sites. Benzos increase the efficacy of GABA, as do barbs, but while the benzos increase frequency of channel opening, whilst the barbs cause the channel open time to lengthen, resulting in increased current flux per opening, rather than more openings with average current passing. The body can compensate for an overly large dose of a benzo by releasing less GABA, but with the way barbs gate the channel, it can do far, far less about it, explaining the increased toxicity of barbs over benzos (and why whilst tolerance can build to the high or sedation, the LD-50 doesn't rise, as it does with say, an opiate, where a user can eventually build up such a monster monkey on his back that grams of H a day can be survived)

Incidentally, barbs are AMPA antagonists in addition to their GABAergic effects, unusual mode of doing it too, by getting into the ion channel, then stabilizing the receptor in an agonist-bound, desensitized state, sort of locking itself in there (the AMPA receptors structure is formed of subunit tetramers, and closes around the ligand like the shell of a bivalve mollusc)

Synergy between those AMPAkines that increase channel open frequency, and those that increase open times will be possible, most likely, the two effects seeing as they are occuring seperatly of each other in different ligands, suggests that seperate binding sites mediate the two effects.

A further action that some AMPAkines produce, is that they inhibit desensitization of the receptor, normally AMPARs desensitize very quickly on agonist binding of glutamate (although some exogenous direct agonists have very different desensitization kinetics) which allows for more efficient signalling before the receptor desensitizes.

However, weather its a good thing, may be another matter entirely. As has been stated, glutamatergic overactivation is dangerous, producing excitotoxicity. It looks like most AMPAkines are pretty safe, and don't appear to be excitotoxins, but its important to be careful. Combining one that increases channel open frequency, with one that gates the channel in a manner analogous to barbs at GABAaRs would of course produce a synergistic effect, weather or not its safe or not, I do not know. But the parallel between benzos and barbs should be born in mind, the body has mechanisms where excess glutamate can be very rapidly removed* but if the channel is forced to remain open whilst there is already excess stimulation, or a greater threshold of glutamatergic activity going on, I think there would be a greater potential for toxicity than either mode of action alone.

Also to remember, is that an allosteric modulator binds at a seperate site than the neurotransmitter agonist, in the case of the AMPAr, there are four sites per receptor that bind glutamate, a direct agonist will activate the receptor and cause influx of calcium, sodium and potassium, way too much Ca++, as there is a fine threshold and balance between enough, somewhat better, and extra crispy, which is why there is needed such an efficient, rapid removal system.

The body can't do that in the case of a direct agonist, reducing the level of glutamate released is going to have minimal effect at best,when a potent, artificial agonist gets in there and starts toasting neurons, but in the case of an allosteric positive modulator, the chance to reduce the effect, seeing as how PAMs have no effects on their own, unless the actual orthosteric agonist is bound, then quick lessening of released glutamate should be acheivable.

and

As far as direct agonism resulting in excitotoxicity, its the massive Ca++ influx, that results in excitotoxic damage, and like I said, an agonist directly gates the ion channel and makes it open, passing unregulated bucketloads of calcium into the cell, and making kentucky-fried brain cell while its at it. AMPARs are expressed to a high extent within the prefrontal cortex and hippocampus, which as is well known, are involved in rational higher cognitive function, learning and memory, as well as in the striatum, where they interact with DA receptors, I would guess, mediating the neuroplastic alterations seen in chronic stimulant (ab)use.

Now a few comments by one dude on Bluelight is by no means a definitive declaration of effects, but since he seems to know his stuff (I know little of the 3-pound universe, but this would be some needlessly complex jibber-jabber otherwise) it alarmed me a little.

On the wikipage for sunifiram, it says both that it acts as a 'positive allosteric modulator of AMPA receptors' and 'as an agonist of AMPA receptors'. Yet the paper reference for both of these is the same. As far as I can tell, nowhere in that paper does it directly indicate that either of these MoAs is true. However it does say that Sunifiram caused the reversal of AMPA antagonism, which may indicate something of the mechanism to someone who understands more than I. I wonder, does it necessarily take an agonist to reverse antagonistic effects on a receptor?

I think maybe someone with little to no knowledge of it's actual MoA has been messing with the Wiki page. I don't remember the MoA being outlined in a seperate section before. As well as this, one of the references of this new info is a website that actually sells the nootropic, and not an actual study.

So, I'm pretty confused to say the least. Has it been verified anywhere else that Sunifiram is an AMPA agonist? And if it was, would this MoA then override the defense mechanism that pumps Ca++ out of the neuron/synapse in order to prevent excitotoxicity?

Hopefully someone more in the know with regards to Neurochemistry can shed some light on the subject. I would assume that the people who developed this drug, being at least partially aware of its mechanism, would not actively put out something that causes excitotoxicity. But hey, you never know.

Edited by OpaqueMind, 20 April 2013 - 05:50 PM.

[OpaqueMind]

Oh and I slept fine last night after taking Sunifiram yesterday, even better than usual (which ain't great), which was was strange (but welcome) given the amount of reports of insomnia. My nervous systems effed up yo.

[OpaqueMind]

Hmmm but this paper reports that

The most potent compounds of both series, DM232 (unifiram) and DM 235 (sunifiram) respectively (Chart 1), were able to revert memory impairment induced by scopolamine and other amnesing agents (Ghelardini et al. 2002a, 2002b); however, no significant interaction with receptor or channels known to be involved in the modulation of the cholinergic system had been evidenced, (Ghelardini et al. 2002b) and therefore, the mechanism of action of these compounds remained to be clarified.

I assume that 'no significant interaction' means that they detected neither agonist nor antagonist properties. Although thats talking about the cholinergic system, I'm not sure of the relation of that one to the AMPA one. This paper was published 10 years ago though, do we have an updated profile of Sunifiram's effects?

Sorry for the multi posts, forgot you could simply add to your previous ones.

So, one more guy on another site said that

This class of compound has very low toxicity, for instance in the mice the compound can be injected in 1000 times the active dose, without any colateral symptom, such as loss of motor coordination or difference in motility.

He didn't provide a source, but I doubt he pulled it fresh out of his arse. We noot people have a certain integrity about us (well some of us do ). Has anyone seen a study that reported on this? I couldn't find any on PubMed.

If it's true, does that mean that it's not excitotoxic? I mean, I imagine that mass glutamate overload and subsequent destruction of vast swathes of the brain is fatal, or at least causes visible symptoms. They probably even checked for it by looking inside their brains after the test subjects died. So if what this guy says is right then we're all good

Edited by OpaqueMind, 20 April 2013 - 06:31 PM.

[Adaptogen]

The statement said that there were no negative side effects at 1000 times the (lowest) active dose. This was in one of the pdfs that Isochroma posted

[Dissolvedissolve]

I assume that 'no significant interaction' means that they detected neither agonist nor antagonist properties. Although thats talking about the cholinergic system, I'm not sure of the relation of that one to the AMPA one. This paper was published 10 years ago though, do we have an updated profile of Sunifiram's effects?

If it's true, does that mean that it's not excitotoxic? I mean, I imagine that mass glutamate overload and subsequent destruction of vast swathes of the brain is fatal, or at least causes visible symptoms. They probably even checked for it by looking inside their brains after the test subjects died. So if what this guy says is right then we're all good

Statements regarding the cholinergic system are not directly relevant to AMPA. AMPA is a subtype of glutamate receptor.

Ghelardini et al. uses up to .1 mg/kg in rats, which yields <2 mg for a 70 kg human via allometric scaling. Romanelli et al. 2006 goes up to 10 mg/kg in rats, which gets us to 150 mg in a 70 kg human, again via allometric scaling. But the fact that there are no overt signs of excitotoxicity does not mean excitotoxicity was not occurring. And it's not like they're using the equivalent of, say, grams of sunifiram. That's only around 10-20x the "therapeutic dose" that many people here are using.

Also some interesting info:

Our data provide experimental evidence supporting the proposition that the long-lasting synaptic enhancements produced by unifiram are similar to the hippocampal LTP, that represents a model for a cellular mechanism related to learning and memory (61). Unifiram, through unknown mechanism(s), might enhance either the release of putative neurotransmitters such as glutamate, as already demonstrated for FK960, a putative cognitive enhancer in the hippocampus (22), or the response to glutamate at postsynaptic level probably on AMPA receptors
[...]

The amelioration of memory processes induced by unifiram and sunifiram is obtained without any induction of side effects. Both compounds, at the highest effective doses, did not impair motor coordination, as revealed by the rota-rod test, nor modify spontaneous motility, as indicated by the Animex apparatus and the hole board test. Furthermore, unifiram and sunifiram, at a dose 1000-times higher than the minimal effective dose, are still devoid of any alteration of behavioral parameters.

→ source (external link)

Keep in mind the minimal effective dose they are talking about is far, far lower than anyone on this forum has used - I believe it's .001mg/kg in rats. It's equivalent to well under 1 mg in humans. So you cannot say there's a 1000x therapeutic ratio with any degree of confidence. Even if we say that 5 mg is effective in humans, that would require sunifiram to be capable of being ingested in the multiple grams range. (I am obviously not suggesting anyone experiment with such a dose.)

Based on the first mechanism mentioned - ie glutmate release - there is potential for excitoxicity. If it just enhances response to glutamate, that would be better.

Edited by Dissolvedissolve, 20 April 2013 - 07:49 PM.

[MizTen]

Since I've stopped taking sunifiram every day:

After three days off, I still have vision improvement. Not the HD nearly psychedelic effects as at first, but I now sit nearly 6 inches further away from my computer screen (I have never been able to do that before) and night driving is much improved. This is huge for me.

There also continues increased energy during the day, (though not so much as before) and a higher tolerance for stress. This at a time when there is significant unwelcome stress.

The other major effect is that I have regained my dream recall after years of it being gone. The dreams are incredible, with themes of healing and power, along with full body sensory enhancement.

I really hesitated to post, partly because some here did not get much effect or even any and partly because my experience seems kind of over the top and I really don't know what to think.

Maybe I got the freshest Sunifiram from NSN, I was one of the first to receive my order. Maybe my demographic being different than most others here is causing these effects. Maybe my practices of meditation and shamanism have somehow combined with Sunifiram to cause my current brain changes.

I totally do not feel that I am losing it, nor does anyone around me think I am. My brain seems to be operating at a higher level somehow. Even though there is no euphoria now.

I am baffled, worried a bit that this will go away or that Sunifiram has somehow broken something.

Edited by MizTen, 20 April 2013 - 10:55 PM.

[OpaqueMind]

Damn, it's annoying that all we can really go on is speculation. Still, after the single dose I had yesterday morning, benefits are still very apparent. Eloquence is up, vision is very, very 3d and clear. Because of this I feel myself in context far more, that is, I have greater situational awareness. I also find myself making far more connections between ideas than usual. I remember reading that the effects are semi-permanent. That'd be awesome. I think i'ma take some more tomorrow morning, not too much as I'm cautious now, but the residual effects are too great to pass up enhancing further.

Have people found that the effects accumulate over doses?

Also, MizTen, if you dont mind saying, do you have any neurological abnormalities that may have contributed to your profound reaction?

[peakplasma]

I really hesitated to post, partly because some here did not get much effect or even any and partly because my experience seems kind of over the top and I really don't know what to think.

Your experiences with Sunifiram have been my favorite reads. They are very detailed and articulate; so please do keep posting!

[OpaqueMind]

I doubt you've broken something, sounds more like you've fixed it to me :P

Meditation may well play its part. I've found Sunifiram and meditation to synergise quite potently.

Edited by OpaqueMind, 20 April 2013 - 11:14 PM.

[renfr]

I will not say anything about semi-permanent effects of Sunifiram because I've experienced significant changes in terms of cognition very recently but these are probably due to other changes in my lifestyle that happened recently but if effects can be permanent or very long-lasting this is really worth it.
I would like to see where it was said that it could be permanent, maybe were you referring to LTP potentiation?

Though this looks great, there's still the risk of excitotoxicity.

[Rethar]

I noticed something a bit strange on the 5th day of taking sunifiram. I hadn't slept the night between day 4 and 5 so I was tired, and then I watched a TV show when I noticed that the sounds I were hearing felt like they were too loud and that it was irritating me. After I got some sleep, when I woke up I still had this effect. It almost felt like I was getting too much stimulation from the sounds or something. I hadn't experienced anything like this on the previous days.

[MizTen]

Damn, it's annoying that all we can really go on is speculation. Still, after the single dose I had yesterday morning, benefits are still very apparent. Eloquence is up, vision is very, very 3d and clear. Because of this I feel myself in context far more, that is, I have greater situational awareness. I also find myself making far more connections between ideas than usual. I remember reading that the effects are semi-permanent. .... Have people found that the effects accumulate over doses? Also, MizTen, if you dont mind saying, do you have any neurological abnormalities that may have contributed to your profound reaction?

I hope the effects are permanent! I have no neurological abnormalities that I'm aware of, other than the stuff that science and modern life inflict on us: ADD, PTSD, tinnitus, possible mitochondrial damage from chemotherapy, possible heavy metal accumulation, heavy exposure to pesticides, etc. I am in my mid-fifties, so maybe aging alone has caused some damage which led to the awesome response for me. But then my experience might kind of indicate that this may heal the brain.

I noticed something a bit strange on the 5th day of taking sunifiram. I hadn't slept the night between day 4 and 5 so I was tired, and then I watched a TV show when I noticed that the sounds I were hearing felt like they were too loud and that it was irritating me. After I got some sleep, when I woke up I still had this effect. It almost felt like I was getting too much stimulation from the sounds or something. I hadn't experienced anything like this on the previous days.

Yes, I have the same sound increase, as well as a temporary increase in tinnitus after I took my first dose. My tinnitus runs at low normal most of the time now, since I started Sunifiram. It was very loud before Sunifiram. But sound sensitivity is still there post-Sunifiram.

... Your experiences with Sunifiram have been my favorite reads. They are very detailed and articulate; so please do keep posting!

That's great, thanks. Especially the articulate part!

I doubt you've broken something, sounds more like you've fixed it to me :P Meditation may well play its part. I've found Sunifiram and meditation to synergise quite potently.

I do kind of suspect that something did get fixed. It is very enticing now to figure out how to use my best personal practices to fix more with the help of Sunifiram. On the one hand, I am afraid there is a dark side, or that all the good changes will all evaporate, on the other hand, I start thinking that this could be the cure for some intractable brain disorders... and here we are as willing volunteers in some major medical breakthrough.

Edited by MizTen, 21 April 2013 - 01:19 AM.

[Passion]

I do kind of suspect that something did get fixed. It is very enticing now to figure out how to use my best personal practices to fix more with the help of Sunifiram. On the one hand, I am afraid there is a dark side, or that all the good changes will all evaporate, on the other hand, I start thinking that this could be the cure for some intractable brain disorders... and here we are as willing volunteers in some major medical breakthrough.

This grand feeling of a drug that has transformed life itself and cured all possible mental ailments or inefficiencies sounds very familiar to me. It's the same feeling I had the first few weeks I was on Piracetam. I immediately wanted to share this incredible breakthrough with everyone I trusted because it was such an incredible feeling. Unfortunately, as weeks passed by, the effect started dying off and I was left with a very sense of disillusionment that has left me lurking these forums, looking for the holy grail ever since. Now instead of producing this effect, the Piracetam would produce quite the opposite effect (regardless of dosage).

After stopping for a long time, I found that the effect comes back a little bit but fades pretty quickly. The same goes for the other racetams I've tried.

My Question to you is this:
Is Sunifiram your first exposure to a racetam or have you already been through the racetam honeymoon period, only now to see it revived by Sunifiram? I really want to believe your testimony here but I'm tired of wasting money and time on new substances which fail at the same point piracetam does.

[violetechos]

He didn't provide a source, but I doubt he pulled it fresh out of his arse. We noot people have a certain integrity about us (well some of us do ). Has anyone seen a study that reported on this? I couldn't find any on PubMed.

If it's true, does that mean that it's not excitotoxic? I mean, I imagine that mass glutamate overload and subsequent destruction of vast swathes of the brain is fatal, or at least causes visible symptoms. They probably even checked for it by looking inside their brains after the test subjects died. So if what this guy says is right then we're all good

Hey opaque - check this out. I'm sure this is the study he is referencing. Never forget about the deepweb! Found this via scirus.com :
Novel nootropic drug sunifiram improves cognitive deficits via CaM kinase II and protein kinase C activation in olfactory bulbectomized mice

http://www.sciencedi...166432812008443

CaM kinase II being calcium (the allosteric activation he was reffering to) and the protein kinase C activation (agonism) ... This is a stab in the dark but i'm guessing CaM kinase slows down calcium processing , and the protein kinase C activation increases turnover of calcium. This system is connected to glutamate .

From what I understand most other nootropics do one or the other, but not both at once.A large amount of the neuroprotection derived from nootropics comes from calcium channel inhibition (analous to gabapentin and thc , yes?)

Interesting to note this study used glycine inhibitors, so it may be possible to extrapolate the results to sunifiram + noopept as well...

Can someone please post or link me to the full version of this abstract? I am trying to pull apart the mechanism of action for this one...

I like how the sunifiram feels, but the weird experiences I has the first few days taking it freaked me out. Twitching... pain reactions, itching,cramps,twitching on bottom of foot (intense),slight confusion, bordering mania . Yeah....Dose was below 10mgs too . Way below.

That redditor is probally on to something.We as a community need to be more careful. Someone is gonna end up frying their brain the frack out one day and its not gonna be pretty...Tardive diskinesia,depression, memory destruction... The glutamate system is nothing to mess around with!

I'd need to see the full paper to extrapolate more... Isochroma, wanna help? lulz :P

Edited by lenses, 21 April 2013 - 06:56 PM.

[Isochroma]

Novel nootropic drug sunifiram improves cognitive deficits via CaM kinase II and protein kinase C activation in olfactory bulbectomized mice.pdf

lenses: The reactions you describe are nervious reactions, not caused by Sunifiram.

Panic tends to induce more panic and that just keeps growing on forums like this.

It's time to get realistic and take the energy you are putting into worry and use it for experimentation.

[renfr]

He didn't provide a source, but I doubt he pulled it fresh out of his arse. We noot people have a certain integrity about us (well some of us do ). Has anyone seen a study that reported on this? I couldn't find any on PubMed.

If it's true, does that mean that it's not excitotoxic? I mean, I imagine that mass glutamate overload and subsequent destruction of vast swathes of the brain is fatal, or at least causes visible symptoms. They probably even checked for it by looking inside their brains after the test subjects died. So if what this guy says is right then we're all good

Hey opaque - check this out. I'm sure this is the study he is referencing. Never forget about the deepweb! Found this via scirus.com :
Novel nootropic drug sunifiram improves cognitive deficits via CaM kinase II and protein kinase C activation in olfactory bulbectomized mice

http://www.sciencedi...166432812008443

CaM kinase II being calcium (the allosteric activation he was reffering to) and the protein kinase C activation (agonism) ... This is a stab in the dark but i'm guessing CaM kinase slows down calcium processing , and the protein kinase C activation increases turnover of calcium. This system is connected to glutamate .

From what I understand most other nootropics do one or the other, but not both at once.A large amount of the neuroprotection derived from nootropics comes from calcium channel inhibition (analous to gabapentin and thc , yes?)

Interesting to note this study used glycine inhibitors, so it may be possible to extrapolate the results to sunifiram + noopept as well...

Can someone please post or link me to the full version of this abstract? I am trying to pull apart the mechanism of action for this one...

I like how the sunifiram feels, but the weird experiences I has the first few days taking it freaked me out. Twitching... pain reactions, itching,cramps,twitching on bottom of foot (intense),slight confusion, bordering mania . Yeah....Dose was below 10mgs too . Way below.

That redditor is probally on to something.We as a community need to be more careful. Someone is gonna end up frying their brain the frack out one day and its not gonna be pretty...Tardive diskinesia,depression, memory destruction... The glutamate system is nothing to mess around with!

I'd need to see the full paper to extrapolate more... Isochroma, wanna help? lulz :P

The danger here is excitotoxicity, that's why everyone who is going to take racetams or experimental RCs should use an antioxidant in conjunction to avoid extreme excitotoxic situations.
Many studies shows that using an antioxidant can lessen or even totally suppress damage that could be caused.

[peakplasma]

To be clear, none of the studies suggest AMPA agonism and this latest 2013 paper reveals GLYCINE or NMDAR activation with partial AMPA activity to explain the 2003 results regarding reversal of the “kynurenate test”.

Amelioration of cognitive deficits mediated by sunifiram was associated with stimulation of glycine-binding site of NMDAR.
The amelioration of acquisition of memory by sunifiram was partly mediated through activation of "-amino-3-hydroxy-5-methyl-4-isoxazolepropionate type glutamate receptor (AMPAR) [12].

This latter quote [12] refers to the 2003 paper (AMPA-Receptor Activation is involved...).

The paper goes on to discuss 3 different hypotheses to explain the possible mechanisms:

- One possible explanation to the DM-induced AMPA mediated reversal of the “kynurenate test” is that AMPA receptors might influence NMDA receptors function, by directly modulating their activity.
- Another possible explanation considers that, once slices are exposed to 100 μM NMDA, a release of endogenous glutamate occurs in the biophase that might induce AMPA receptor desensitisation
- Finally, it could be proposed that DM232 and DM235 might influence the AMPA-induced release of neurotransmitters others than noradrenaline, which might in turn facilitate NMDA receptor functions

In later papers, you will frequently find statements referencing this 2003 paper AMPA receptor involvement but without any apparent direct interaction and so the mechanism remains unknown.

There is evidence that AMPA receptors are involved in the cognition enhancing effect of these compounds. [12] However, a direct interaction of 1 and 2 with nicotinic or AMPA receptors in vitro has not been proven yet.

[abelard lindsay]

So I've been taking Sunifram about once a week and Zembrin/CILTEP. I took Suni on Friday night and then the next day I had the usual CILTEP crash. I took Zembrin/CILTEP and 350mg NALT to fix it and then said, what the heck (for science!) and took another 350mg NALT.

So I'm sitting in bed that night and I'm rewinding through the day with these picture perfect flashbulb memories of things that happened. It's like I'm there experiencing every little subtle detail of events in sequential order. It's not just vague memories or fragments I'm remembering. I remember the amount on the bill and the tip and total and how I wrote it in on the receipt, which I wasn't trying to remember at the time. I remember people's individual comments at dinner, their expressions. I remember getting out of my car and looking at the moon and where it was in the sky. It's as crystal clear as a movie that I've watched 100s of times. I had trouble sleeping so I watched a whole bunch of Stanford crypto class videos and can remember them in vivid detail. I'm posting this on the Sunifram board because yesterday's experience was on a much more intense level then even the previous week when I was also taking Zembrin/CILTEP.


Anyway... I think I finally got what I've been looking for as far as the LTP stuff goes. Going to try the double NALT thing again today.

[health_nutty]

So I've been taking Sunifram about once a week and Zembrin/CILTEP. I took Suni on Friday night and then the next day I had the usual CILTEP crash. I took Zembrin/CILTEP and 350mg NALT to fix it and then said, what the heck (for science!) and took another 350mg NALT.

What is your Sunifiram dosing schedule? Only once a week?

What is your current full regimen?

[abelard lindsay]

So I've been taking Sunifram about once a week and Zembrin/CILTEP. I took Suni on Friday night and then the next day I had the usual CILTEP crash. I took Zembrin/CILTEP and 350mg NALT to fix it and then said, what the heck (for science!) and took another 350mg NALT.

What is your Sunifiram dosing schedule? Only once a week?

What is your current full regimen?

I take 25mg Zembrin + 10mg Forskolin + 1500mg L-Phenylalanine in the morning + 200mg caffeine + 50mg p5p. The last two are probably not as important. At about 2pm I take 350mg of N-Acetyl-L-Tyrosine and 200mg caffeine , as I always start to get sleepy about this time and the NALT+ Caffeine wakes me up. Yesterday I didn't take Zembrin in the morning and was sleepy until I took the NALT. I then took the usual stack a few hours afterwards. I take 5-10mg of Suni about once a week, usually about 4 hours before bed. I don't trust Suni 100 percent yet. I had a bad time with Coluracetam so I'm more cautious now with new 'racetams. It seems from what I've been reading on this thread that the effects persist for several days so maybe this was the previous days Suni + Zembrin synergistically potentiating LTP.

[Q did it!]

Hey Isochroma-Reborn do you know when New Star Nootropics will or may start carrying Coluracetam and Unifraim? Need to stock up on Coluracetam before I run out. I have been dosing only 10mg of Coluracetam every other day so I can make the Coluracetam last me a few years but would like to take it twice a day at 10mg . Hopefully it will come to market and others can try this remarkable drug. It really alters your vision/processing power for the good!

Back to Sunifiram now.
I have been testing it on and off I must say it has the chemical is a strange one. It works better if combined wit physical activity. The first two too three see to have the greatest impact that are very noticeable. Dosing Sunifiram as the stimulant seems to work well with the CILTEP stack. Really makes your mid like a sponge, and Lectures are looked foreword to and enjoyed. Also memory is improving significantly though working memory is impaired/lowered slightly .

Have not tried yet the stack with Zimbrin. Wondering if just adding Kanna non-extract at moderate dosages say 100mg -200mg may have the same affects and at a better price tag.

Cannot wait too but combine PRL-8-53 with my revised stack to see what I can achieve

Edited by Q did it!, 21 April 2013 - 09:32 PM.

[Reformed-Redan]

Can anyone else attest to the effects mentioned by abelard lindsay?

One case doesnt make a rule.

[abelard lindsay]

Can anyone else attest to the effects mentioned by abelard lindsay?

One case doesnt make a rule.

It appears I'm the only one who's tried Zembrin/Ciltep/Suni . Seems the cost of Zembrin is putting a lot of people off trying it.

[Q did it!]

Can anyone else attest to the effects mentioned by abelard lindsay?

One case doesnt make a rule.

It appears I'm the only one who's tried Zembrin/Ciltep/Suni . Seems the cost of Zembrin is putting a lot of people off trying it.

I do fully intend to give Zimbrin a try but will have to wait tell mid next month to do so sadly due to cost.

[health_nutty]

Can anyone else attest to the effects mentioned by abelard lindsay?

One case doesnt make a rule.

It appears I'm the only one who's tried Zembrin/Ciltep/Suni . Seems the cost of Zembrin is putting a lot of people off trying it.

I'm taking Ciltep/Suni, but I'm only using 5mg Forskolin / 50mg of Luteolin twice a day (have been for a while).

Yes, the cost of Zembrin is the issue

Very amazing results! I hope your stack continues to work for you.

Btw, what issue did you have with colouracetam?

[abelard lindsay]

Btw, what issue did you have with colouracetam?

I got an ACH overload that lasted a couple of days. I had to take benadryl (anti-cholinergic) to deal with it. Not super fun.