37 replies to this topic

[FunSponge]

I can't find anything in the search bar, I'm been told its a new compound coming out that can fully repair brain damage and that there's a group buy been arranged, if someone knows about it please post a link.

[FunSponge]

Sorry I meant HA - FGL.

[William Sterog]

What Is HA-FGL?
HA-FGL can be most briefly described as a polysaccharide covalently bound to a peptide. The polysaccharide is hyaluronate. Hyaluronate is a ubiquitous, endogenously present carbohydrate that is used much like scaffolding in the body. It controls inflammation and extracellular remodeling, and growth.

FGL is a sequence of amino acids bound together that copies the sequence of amino acids found in the powerful growth factor called NCAM, which stands for Neural cell adhesion molecule. By copying the amino acid sequence, it can replicate any relationship with receptors that it may interact with.

NCAM and polysialylatic acid bind together to control the sticking together of neurons, and can great neurogenesis in far-reaching brain regions through sticking neurons together to make a chain that can transport neural precursor cells [R].

It uses a hyaluronate size about twice the size of Injuv’s hyaluronate. It’s 10Kda in size and has 35% of its active regions (that bind with CD44) replaced with amide joiners to attach FGL. This does mean it loses some of the sites that are used to be absorbed.

https://wholisticresearch.com/ha-fgl/

[William Sterog]

Side effects of the FGL peptide do exist. In young rats on high doses (around 100mg Human equivalent dose) every other day for two weeks, huge brain loss was found, despite improving memory. The dosage was high, higher than other studies, and personally is a bizarre dosage to choose. This widespread apoptosis was completely blocked when administered with Amyloid plaques, a well-known cause and consequence of the Alzheimer’s pathology. It seems that these plaques interfere with apoptosis.

Interesting and terrifying.

[FunSponge]

Iv heard about this, hopefully that can be avoided with smaller doses, it seeks to be a high risk high reward compound.

[gintrux]

Also hyper interested in this substance. Can anyone share their reports if you had tried it?

[Rorororo]

Side effects of the FGL peptide do exist. In young rats on high doses (around 100mg Human equivalent dose) every other day for two weeks, huge brain loss was found, despite improving memory. The dosage was high, higher than other studies, and personally is a bizarre dosage to choose. This widespread apoptosis was completely blocked when administered with Amyloid plaques, a well-known cause and consequence of the Alzheimer’s pathology. It seems that these plaques interfere with apoptosis.

Interesting and terrifying.

 

https://www.alzforum...-memory-rodents

 

 

 

They report that FGL treatment stimulates activity-dependent delivery of glutamate receptors to synapses, leading to a long-term enhancement of synaptic transmission.

 

There is also a relationship with amlyoid plaques and glutamate. I don't think it was a coincidence that apoptosis was blocked when administered with Amloyoid plaques.

 

Source:https://www.ncbi.nlm...les/PMC6582288/

 

 

 

 

Also hyper interested in this substance. Can anyone share their reports if you had tried it?

 

I would stay the hell away from this drug...its really dangerous increasing glutamate! It will fry the OPs brain since he already has high levels of glutamate. 

 

 

Edited by Rorororo, 02 June 2020 - 07:33 PM.

[WholisticResearch]

https://www.alzforum...-memory-rodents

 

 

There is also a relationship with amlyoid plaques and glutamate. I don't think it was a coincidence that apoptosis was blocked when administered with Amloyoid plaques.

 

Source:https://www.ncbi.nlm...les/PMC6582288/

 

 

 

 

 

I would stay the hell away from this drug...its really dangerous increasing glutamate! It will fry the OPs brain since he already has high levels of glutamate. 

I agree with with your general points. It would be dangerous for OP to take HA-FGL, and he certainly shouldn't. 

However, FGL doesn't increase glutamate, FGL (L) isn't considered dangerous, and it has been tested to be safe on healthy individuals, and increasing glutamate isn't inherently dangerous, but it sure can be!

FGL increases the amount of phophorylated AMPA receptors via PKC, via FGFR1. This is not the same as increasing the amount of, or even merely the activity of, glutamate. It is a very precise, specific  phenomena, that the animal kingdom has given itself because it needs it to help itself learn better, whilst it uses the neural migratory system (with NCAM, where FGL is derived from). Activating FGFR1 actually increases inhibitory neuron development and activity. I hope this doesn't sound like im glorifying FGL, as it's a very tricky compound to get right, and im sure there will be better compounds in the future. However it is probably the strongest ampakine peptide known to the scientific community at the moment.

 

But no matter how safe FGLL/FGL turn out to be, those lessons can't be applied to HA-FGL. 

[Rorororo]

I agree with with your general points. It would be dangerous for OP to take HA-FGL, and he certainly shouldn't. 

However, FGL doesn't increase glutamate, FGL (L) isn't considered dangerous, and it has been tested to be safe on healthy individuals, and increasing glutamate isn't inherently dangerous, but it sure can be!

FGL increases the amount of phophorylated AMPA receptors via PKC, via FGFR1. This is not the same as increasing the amount of, or even merely the activity of, glutamate. It is a very precise, specific  phenomena, that the animal kingdom has given itself because it needs it to help itself learn better, whilst it uses the neural migratory system (with NCAM, where FGL is derived from). Activating FGFR1 actually increases inhibitory neuron development and activity. I hope this doesn't sound like im glorifying FGL, as it's a very tricky compound to get right, and im sure there will be better compounds in the future. However it is probably the strongest ampakine peptide known to the scientific community at the moment.

 

But no matter how safe FGLL/FGL turn out to be, those lessons can't be applied to HA-FGL. 

 

To be honest, I just googled HA-FGL and saw the article that FGL increases activity dependent glutamate. 

 

I don't know much about FGL to comment on the rest.  However, I am trying to advice OP to think rationally at this time.  If the OP already has high glutamate levels at his baseline then FGL should increase glutamate. 

[Rorororo]

Wait a minute, didn't someone say rats lost a major portion of their brains with FGL?

 

Then the article stated FGL increases activity dependent glutamate?

 

 

It sure sounds like excitotoxicity to me

[gintrux]

Ordering some FGL. What's the recommended dosage to start with? Intramuscular os subcutaneous injection?

[gintrux]

Guys, FGL was already clinically tested for safety on humans.... In 2007

 

https://www.research...lthy_Volunteers

 

 

 

The FG loop peptide (FGL(L)), a novel mimetic of the neural cell adhesion molecule (NCAM), is in clinical development for neurodegenerative disorders such as Alzheimer's disease. Preclinical studies in rats, dogs and monkeys have demonstrated exposure in plasma and cerebrospinal fluid after parenteral or intranasal administration of FGL(L), with no systemic toxicity. This article reports on the results of the first administration of FGL(L) in humans. To determine the tolerability, safety and pharmacokinetics of ascending, single intranasal doses of FGL(L) 25, 100 and 200mg in healthy subjects. In an 8-day, open-label, phase I study, 24 healthy male volunteers (mean age 42 [range 24-55] years) received single intranasal doses of FGL(L) (25, 100 and 200mg) in accordance with an ascending dose, sequential-cohort design. All three intranasal doses of FGL(L) were well tolerated and there were no clinical notable abnormalities in ECG recordings, vital signs or laboratory tests. Three subjects (13%) reported five adverse events. A transient (<3 minutes) burning sensation in the nose was reported in two subjects at the 200mg dose level while runny eyes (<2 minutes) were experienced in one subject at 25mg. These events had an onset immediately following intranasal administration, and a relationship to FGL(L) was suspected. One of the latter subjects who had experienced a burning sensation in the nose also experienced dizziness, vomiting and headache with onset >2 days after single-dose administration of FGL(L); no relationship to the study drug was suspected. Quantifiable plasma concentrations of FGL(L) were observed up to 1 hour after intranasal administration of the 100mg dose and up to 4 hours after the 200mg dose (plasma FGL(L) concentrations were undetectable at all timepoints for the 25mg dose). Increasing doses of FGL(L) were associated with higher systemic exposures: mean C(max) 0.52 ng/mL and 1.38 ng/mL (100mg and 200mg, respectively); mean AUC(24) 1.27 ng x h/mL and 4.05 ng x h/mL (100mg and 200mg, respectively). Intranasal administration of FGL(L) (25, 100 and 200mg) was well tolerated in healthy male volunteers, with no safety concerns and a pharmacokinetic profile that was generally dose related. Further studies are currently being planned to evaluate the effects of FGL(L) in patients with Alzheimer's disease.

 

[FunSponge]

Gintrux can you pm me or post a link if you have a source.

[WholisticResearch]

It's not excitotoxicity, it's apoptosis that causes the problems in the studies. It's mechanism doesn't actually lend itself to excitotoxicity damage easily (apparently) because it only increases glutamate-like if there is coordinated glutamate activity happening at that moment anyway, according to researchers.
It may even help epilepsy if given with BDNF-like compounds. FGL could still lead to excitotoxicity of course, and should be a big concern with overdoses, and extended use. 

HA-FGL will be released earliest 18th July. 

The term  "FGL" refers to a 15 amino acid sequence that on it's own doesn't work much at all. This is because tyrosine kinase receptors exist often as dimers, meaning two agonists are needed, to trigger each receptor in the dimer complex, and trigger autophosphorylation. The drug used in the preclinical human study is a dimerized version of FGL, called FGL (L), and apparently only works intranasally at 250mg lol. It's really really expensive, and is only obtainable from compounding pharmacies like TMC.

Probably the most practical version of FGL is FGLd. It uses a simple lysine backbone, easily made from many peptide labs and attaches four monomers on at their n-terminus. It doesn't work as effectively as FGL (L) at neurite outgrowth, and HA-FGL probably won't be as effectively as FGL (L) either in terms of neurite outgrowth, i would think. 



What people get from CanLabs and other places is the normal, pretty inactive monomer, which is cheap.  The monomer has some good reviews though, which is abit confusing but I would imagine some people have higher baseline brain-FGF levels. I still recommend people go out and try FGL monomer as there aren't that many reviews and it could still work, i guess.

 

[Rorororo]

It's not excitotoxicity, it's apoptosis that causes the problems in the studies. It's mechanism doesn't actually lend itself to excitotoxicity damage easily (apparently) because it only increases glutamate-like if there is coordinated glutamate activity happening at that moment anyway, according to researchers.
It may even help epilepsy if given with BDNF-like compounds. FGL could still lead to excitotoxicity of course, and should be a big concern with overdoses, and extended use. 

HA-FGL will be released earliest 18th July. 

The term  "FGL" refers to a 15 amino acid sequence that on it's own doesn't work much at all. This is because tyrosine kinase receptors exist often as dimers, meaning two agonists are needed, to trigger each receptor in the dimer complex, and trigger autophosphorylation. The drug used in the preclinical human study is a dimerized version of FGL, called FGL (L), and apparently only works intranasally at 250mg lol. It's really really expensive, and is only obtainable from compounding pharmacies like TMC.

Probably the most practical version of FGL is FGLd. It uses a simple lysine backbone, easily made from many peptide labs and attaches four monomers on at their n-terminus. It doesn't work as effectively as FGL (L) at neurite outgrowth, and HA-FGL probably won't be as effectively as FGL (L) either in terms of neurite outgrowth, i would think. 



What people get from CanLabs and other places is the normal, pretty inactive monomer, which is cheap.  The monomer has some good reviews though, which is abit confusing but I would imagine some people have higher baseline brain-FGF levels. I still recommend people go out and try FGL monomer as there aren't that many reviews and it could still work, i guess.

 

I haven't read the studies but I am sure guess it will be linked to excitotoxicity. 

 

Also, for HA-FGL not FGL

 

According to your website you advertise HA-FGL under this description:

 

"How Does HA-FGL Compare to Other Nootropic Peptides? It's one of a kind. It's a strong glutamatergic that also grows dopamine neurons, and alters factors ..."

 

The one guy got the OP interested in it again....It will cause further damage to the OPs state.

 

Then your defense against FGL not HA-FGL (which you sell) is casting doubt on the issue that HA-FGL wont be risky btw.  I know you have a business and want to make a living but this is a person's health here....

[WholisticResearch]

Funsponge, don't take ha-fgl. There are plenty of other options.
Roro, I have agreed with your recommendation that OP does not take ha-fgl. It would be an awful idea. I will now commend you for giving what I consider is the correct advise regarding OP's decision to not take ha-fgl.

 

I COMMEND YOU

 

Great. Now we have that out the way, I will now breifly look over your accusations that I would prioritise financial earnings over the quality of life and safety of an individual, which is usually considered pretty rude when my comments above would give of evidence of the contrary. 

just, btw, the protein that causes the apoptosis is GSK3B, and does cause greater excitatory signalling, but has many other responsibilties to do with apoptosis. The problem is only related to an excitatory chemical, not because of it's excitatory effects. According to the researchers at least. 

Do you mean "casting doubt on the issue that it will be risky" ? 
If that's right, then let me be clear.

HA-FGL is nothing like FGL in many ways, and seperate evaluations should take place for each compound. They are very different, and do not think that just because FGL (L) is okay (Obviously the monomer is fine) that HA-FGL will be similiar in any way. That's pretty clear. 

[Rorororo]

Funsponge, don't take ha-fgl. There are plenty of other options.
Roro, I have agreed with your recommendation that OP does not take ha-fgl. It would be an awful idea. I will now commend you for giving what I consider is the correct advise regarding OP's decision to not take ha-fgl.

 

I COMMEND YOU

 

Great. Now we have that out the way, I will now breifly look over your accusations that I would prioritise financial earnings over the quality of life and safety of an individual, which is usually considered pretty rude when my comments above would give of evidence of the contrary. 

just, btw, the protein that causes the apoptosis is GSK3B, and does cause greater excitatory signalling, but has many other responsibilties to do with apoptosis. The problem is only related to an excitatory chemical, not because of it's excitatory effects. According to the researchers at least. 

Do you mean "casting doubt on the issue that it will be risky" ? 
If that's right, then let me be clear.

HA-FGL is nothing like FGL in many ways, and seperate evaluations should take place for each compound. They are very different, and do not think that just because FGL (L) is okay (Obviously the monomer is fine) that HA-FGL will be similiar in any way. That's pretty clear. 

 

They almost have the same name.  I, myself, got confused.  Granted, I googled it for a couple of seconds then linked it.  I think it can be fair to say that it can cause confusion between HA-FGL and FGL. Especially, when someone isn't paying close attention. 

[WholisticResearch]

Yes that is pretty scary. Getting the two muddled up would be especially bad considering the different dosage scales, one being milligrams the other being a couple micrograms.

 

Hopefully in the future we'll deal with things have wider dosage windows. 
 

Edited by WholisticResearch, 08 June 2020 - 11:59 PM.

[gintrux]

Fuck, I just ordered some FGL from canlab. But will try anyway.

 

Which accessible vendor has FGL (L)? Anyone willing to reship from TMC to me in Europe?

[gintrux]

So if the dosage for FGL (L) is up to 200mcg (from that study above), what could be the dosage for FGL (15 chain amino acid)? I got some from canlab. ROA intranasally or would subcutaneous work? The latter is easier for me.

[WholisticResearch]

The dosage for the normal 15mer I don't think has ever been clarified.
I'm pretty sure it doesn't have any published in vivo data. There were some unpublished data that they collected, that I think informed them that it isn't detectabley effective, so they quickly dimerised and dendrimised it. They probably anticipated it wouldn't work. The term "the FGL peptide" refers to a huge variety of different versions of the 15 amino acid sequence, and some studies wrongly name the drug that they're studying.

The intranasal dosage for FGLL is 200 MILLIGRAMS. This costs around £250 if you buy £125,000 of FGLL. It's incredibly expensive.   If you wanted to have just one intranasal dose made, custom synth, it'd probably cost around £1300+. 

Now, my instinct would be to have 10mg in one go of the monomer, but there are some reports of 2mg being too much and preventing sleep. So, 1mg at a time until I feel something. 

Intranasal hasn't got any data for the monomer, and likely degrades super quickly, so subcutaneous is the best option. 

Don't forget to update us!

[FunSponge]

You guy's knew I probably have high glutamate, how did you know that and why didn't you recommend I take nac?

I read an article that says huffing gasoline depletes gluthione and wrecks the gaba / glutamate balance, nearly all major psychiatric disorders have low gluthione in common, I got depression and psychosis while I was addicted to huffing so maybe the only thing Iv been suffering from for 20 year's is low gluthione.

My psychiatrists say what's wrong with me is a chemical change in the brain, you would think they would do some research to know what exactly that change is instead they just give me anti psychotics that don't work, been on nac a week, feeling relatively clear headed, getting some relief from it, let's hope it's not placebo.

Edited by FunSponge, 23 June 2020 - 10:04 AM.

[FunSponge]

I copy pasted from this https://www.ncbi.nlm...les/PMC2442441/ The majority of acute behavioural effects appear to be underpinned by changes in receptor and/or ion channel activity (for example, GABAA, glycine and 5HT3 receptor activation, NMDA receptor inhibition), although nonspecific interactions can also arise at high concentrations.

I have glycine ordered, Iv read sarcosine also works to unlock NMDA receptors and I already have that.

Here another copy and paste.
NMDA receptors can be activated (unlocked) by binding with an assortment of neurotransmitters, including:

Glutamate
Aspartate
Glycine
D-serine

Edited by FunSponge, 23 June 2020 - 10:52 AM.

[Rorororo]

You can take bacopa, black seed oil for gaba 

 

NMDA - I have no clue, look up how to reverse PCP damage 

 

5ht3 - no clue

 

glycerin no clue

 

 

I would imagine your damage comes akin to PCP.  I would look up how to reverse damage to that.

Edited by Rorororo, 24 June 2020 - 02:59 AM.

[FunSponge]

You can take bacopa, black seed oil for gaba

NMDA - I have no clue, look up how to reverse PCP damage

5ht3 - no clue

glycerin no clue


I would imagine your damage comes akin to PCP. I would look up how to reverse damage to that.

It says NMDA can be activated with glycine, glutamate, I barely understand what NMDA is or 5ht3 is, I'm just trying to fix what might be wrong.

Does pcp contain solvents?, it says touline depletes gluthione which disrupts the gaba / glutamate balance, I know people also loose there minds from pcp but I don't know if it's the same thing, embalming fluid probably contains chemicals maybe solvents.

The link I posted is about the damage caused directly from solvents.

Edited by FunSponge, 24 June 2020 - 12:30 PM.

[Rorororo]

From wiki on Toluene:

 

 

 

Similar to many other solvents such as 1,1,1-trichloroethane and some alkylbenzenes, toluene has been shown to act as a non-competitive NMDA receptor antagonist and GABA_A receptor positive allosteric modulator.^[31] Additionally, toluene has been shown to display antidepressant-like effects in rodents in the forced swim test (FST) and the tail suspension test (TST),^[31] likely due to its NMDA antagonist properties.

 

 

I believe the main damage here is a large amount of NMDA antagonism that caused the damage.  Try searching for DXM or PCP damage and how to reverse it.  

 

 

These might be a help:

https://www.longecit...ociation/page-2

&

https://www.longecit...sychosis/page-1

Edited by Rorororo, 24 June 2020 - 01:50 PM.

[FunSponge]

From wiki on Toluene:

Do you actually read anything I write before replying?

I posted a link to a study on the nuero chemical changes caused by huffing solvents, it says to take glycine and glutamate to activate NMDA receptors, by glutamate does it mean nac?, I'm taking 3000mg daily and have glycine ordered, I must have thrown out the sarcosine.

I barely have the cognition to understand half of any of it but if I can follow the recommendations I should be alright.



I believe the main damage here is a large amount of NMDA antagonism that caused the damage. Try searching for DXM or PCP damage and how to reverse it.


These might be a help:
https://www.longecit...ociation/page-2
&
https://www.longecit...sychosis/page-1

[Rorororo]

 

From wiki on Toluene:

Do you actually read anything I write before replying?

I posted a link to a study on the nuero chemical changes caused by huffing solvents, it says to take glycine and glutamate to activate NMDA receptors, by glutamate does it mean nac?, I'm taking 3000mg daily and have glycine ordered, I must have thrown out the sarcosine.

I barely have the cognition to understand half of any of it but if I can follow the recommendations I should be alright.



I believe the main damage here is a large amount of NMDA antagonism that caused the damage. Try searching for DXM or PCP damage and how to reverse it.


These might be a help:
https://www.longecit...ociation/page-2
&
https://www.longecit...sychosis/page-1

 

 

 

Yes, I read them....

 

I suggest looking into NSI 189 and Gastrodin:

https://www.ncbi.nlm...les/PMC3181613/

 

Then I suggest looking into Clemastine for meylin

 

https://pubmed.ncbi....h.gov/26791223/

 

Gastrodin should help your gaba\glutamate balance then you have NSI 189 to generate new neurons.  The problem is migration; you can look up P21.  

 

Then you will repair your meylin with clemastine.

 

 large doses ~3g of taurine and ~5g of creatine throughout the day will also help expedite things. 

 

Then 7,8 DHF is proven to help lead damage.

 

This is all I have to suggest to look up...again, I am not a doctor and this might be contradicting...its your body and health and its your discretion. Just make sure you research anything that you want to take and talk to an actual doctor. 

 

If I had your problem I would take 7,8 DHF, Clemastine, gastrodin, taurine and creatine.

Then when things improve, I would look into NSI-189 and P21. 

 

NAC might be good but I don't know know too much about it.  I know its an amino acid so I dont think it can hurt? I could be wrong though. 

Edited by Rorororo, 28 June 2020 - 07:28 PM.

[FunSponge]

Cheers Man.
I honestly don't have the cognition to read anything or fully understand any of this, nac is a precursor to gluthione which balances gaba / glutamate in the brain, the study says solvent abuse depletes it permanently, I'm also taking glycine to unlock NMDA receptors, whatever that means, also taking complex b vitamin / magnesium / Zinc / omega 3 fish oil and 250mg Dihexa weekly.

I'm not well enough to come up with another battle plan, there's probably other stuff I could be taking for 5ht3 and I don't even have a fucking clue what that is.

I'd love it if the only thing Iv been suffering from for the past 20 years was a gaba / glutamate imbalance, I would happily wrap my mouth around a penis if it were true, something so simple that can actually be fixed with nac.

Edited by FunSponge, 29 June 2020 - 05:39 PM.

[Rorororo]

Cheers Man.
I honestly don't have the cognition to read anything or fully understand any of this, nac is a precursor to gluthione which balances gaba / glutamate in the brain, the study says solvent abuse depletes it permanently, I'm also taking glycine to unlock NMDA receptors, whatever that means, also taking complex b vitamin / magnesium / Zinc / omega 3 fish oil and 250mg Dihexa weekly.

I'm not well enough to come up with another battle plan, there's probably other stuff I could be taking for 5ht3 and I don't even have a fucking clue what that is.

I'd love it if the only thing Iv been suffering from for the past 20 years was a gaba / glutamate imbalance, I would happily wrap my mouth around a penis if it were true, something so simple that can actually be fixed with nac.

 

 

The glycerine concerns me.  Look here:

 

https://pubmed.ncbi....h.gov/24690269/

 

 

 

Chronic inhalation of both types of gasoline (a single daily 30-min session of 1/5 LC50 for 60 days) caused a significant increase in the aspartic and glutamic acid concentrations of the hippocampus without affecting the levels of GABA or glycine.

 

 

I wouldn't touch anything with NMDA but thats just me...I dont know too much to say for certain though. I would be more concerned with lowering your glutamate. Gastrodin will help with this. 

 

Look here for lowering glutamate with gastrodin:

 

https://www.ncbi.nlm...les/PMC5801292/

 

https://pubmed.ncbi....h.gov/27188468/

 

Your dihexa dose is way too high too...I would honestly lower it if you want to keep taking it...... I wouldnt though...

Edited by Rorororo, 30 June 2020 - 04:02 AM.