J147 (IQ boosting) (High-IQ) (Mid Effort) (GTFIH)

Rigged

Rigged

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New drug never been posted hooray
im russian so dont expect everything to be grammatically correct negroids
Also always DO YOUR OWN RESEARCH

J147, derived from curcumin with structural modifications for enhanced central nervous system bioavailability and mitochondrial affinity, interacts primarily with mitochondrial ATP synthase, particularly targeting daATP5A subunit. This interaction moderates mitochondrial membrane potential and cellular ATP levels, important for neuronal metabolic stability and helps against excitotoxic stress

By diminishing ATP synthase activity, regulates mitochondrial membrane potential, important in maintaining neuronal metabolic stability. This helps protect cells under bioenergetic stress by maintaining ATP levels through alternative metabolic pathways, increased glycolytic flux, important in neurons where ion homeostasis deregulation contributes to Alzheimers pathogenesis

It enhances neuroprotective pathways and neuroplasticity through upregulation of brain derived neurotrophic factor (BDNF). This involves secondary signaling cascades activated via mitochondrial biogenesis promoters and sirtuin pathways, especially SIRT1, cuz its affects in neural longevity and stress resistance. Enhanced BDNF expression promotes synaptic plasticity and resilience, helping memory and learning

It affects amyloid precursor protein (APP) processing, reducing amyloidogenic cleavage of APP which results in accumulation of beta amyloid plaques, a mark of Alzheimer's pathology. This modification is partly achieved by changing activity of secretase enzymes, primarily beta secretase 1 (BACE1), potentially via changes in enzyme expression or cellular localization

It has an anti-inflammatory effect within the central nervous system by modulating microglial activity, the brain's immune cells. This is achieved by downregulating pro-inflammatory cytokines and upregulating anti-inflammatory cytokines, mediated through NF-kB signaling pathways. Changing microglial activation reduces the neuroinflammatory response, important in slowing neurodegeneration in Alzheimers

Its lipophilicity and molecular weight are optimized for penetration across the blood brain barrier, issue for many neurotherapeutic agents. Once in the brain, It accumulates in regions like the hippocampus and cerebral cortex, related to Alzheimer’s pathology, where it executes its neuroprotective actions

- Animal Models: Doses in rats are from 1 to 30 mg/kg, orally
- Human dose based on animal studies, uses a conversion method based on body surface area. Animal data suggests a range of 1 to 30 mg/kg for rodents:

FDA gives a conversion factor to convert animal doses to human doses based on body surface area. It's 12.3 for rodents.

- Dosing Range: If converting these from animal models to human use, you could consider a starting dose somewhere within this range, 0.08mg/kg - 2.44mg/kg
- Dosing Schedule: Typically, this would be taken once daily.

The math is hypothetical and uses a basic method for conversion. Actual doses would need to be decided through actual studies and not org posts

- Known Side Effects: Minimal sides in animals. Cant be fully certain about sides in humans

Lost in the tundras of mumbai

@PsychoDsk
@ThugggButt
@dannydipss
@iabsolvejordan
@CrackyLolra
@Snake.0359
@the_nextDavidLaid
@bululu_87
@wannaimprove
@mathis
 

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Reactions: pentamogged9000, iam good boy, 5.5psl and 11 others
@Clavicular since u said ion post enough
Also since u said everything i post is water and that i should kill myself
 
  • JFL
  • +1
Reactions: PseudoMaxxer and NoseProphecy
Htn, 5’6 (over 😔), Top 5 IQ, Low Inhib
 
Good thread op I will read later but I saved it
 
  • Love it
Reactions: Rigged
why the fuck you format like this

not clicking through all that
 
  • +1
Reactions: aestheticsrespecter
I should add like a subway surfer clip somewhere in the post idk if ppl here have enough attention span to read
 
  • JFL
  • +1
Reactions: iam good boy and Deleted member 30843
why the fuck you format like this

not clicking through all that
Literally skip all the science and just go to doses gng its not that hard
 
  • +1
Reactions: NoseProphecy
I can fact check that anyone that's 5'6 is extremely intelligent and good looking so I would pay attention to what op is saying
 
  • JFL
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Reactions: Rigged and NoseProphecy
Literally skip all the science and just go to doses gng its not that hard
what if i want to read the science before taking random jew substances?
 
  • +1
Reactions: xegigi
what if i want to read the science before taking random jew substances?
Then you have tap your screen once to read the Science
 
Good thread op I will take it and report on the results!
 
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Reactions: NoseProphecy and Rigged
I’ve seen some studies where Curcumin decreases iGF1 , would this do the same thing ?
 
I’ve seen some studies where Curcumin decreases iGF1 , would this do the same thing ?
Theoretically, could possibly affect IGF-1 levels cuz of similarities to curcumin, since like u said its known to downregulate IGF-1 via inhibition of the PI3K/Akt signaling pathway

Just in theory could lower igf by 10-30%, so i guess not ideal if ur younger, but if ur older with closed plates itd be a good thing to add to the stack
 
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Reactions: gigell
Theoretically, could possibly affect IGF-1 levels cuz of similarities to curcumin, since like u said its known to downregulate IGF-1 via inhibition of the PI3K/Akt signaling pathway

Just in theory could lower igf by 10-30%, so i guess not ideal if ur younger, but if ur older with closed plates itd be a good thing to add to the stack
I agree , thank for your research
 
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Reactions: Rigged
by doing this, and increasing my IQ, i can now read women's minds which doesnt help at all since now i know that all of them find me repulsicve :feelswhy::feelswhy::feelswhy::feelswhy:
 
  • JFL
Reactions: hoursk and Rigged
bump
high effort
 
New drug never been posted hooray
im russian so dont expect everything to be grammatically correct negroids
Also always DO YOUR OWN RESEARCH

J147, derived from curcumin with structural modifications for enhanced central nervous system bioavailability and mitochondrial affinity, interacts primarily with mitochondrial ATP synthase, particularly targeting daATP5A subunit. This interaction moderates mitochondrial membrane potential and cellular ATP levels, important for neuronal metabolic stability and helps against excitotoxic stress

By diminishing ATP synthase activity, regulates mitochondrial membrane potential, important in maintaining neuronal metabolic stability. This helps protect cells under bioenergetic stress by maintaining ATP levels through alternative metabolic pathways, increased glycolytic flux, important in neurons where ion homeostasis deregulation contributes to Alzheimers pathogenesis

It enhances neuroprotective pathways and neuroplasticity through upregulation of brain derived neurotrophic factor (BDNF). This involves secondary signaling cascades activated via mitochondrial biogenesis promoters and sirtuin pathways, especially SIRT1, cuz its affects in neural longevity and stress resistance. Enhanced BDNF expression promotes synaptic plasticity and resilience, helping memory and learning

It affects amyloid precursor protein (APP) processing, reducing amyloidogenic cleavage of APP which results in accumulation of beta amyloid plaques, a mark of Alzheimer's pathology. This modification is partly achieved by changing activity of secretase enzymes, primarily beta secretase 1 (BACE1), potentially via changes in enzyme expression or cellular localization

It has an anti-inflammatory effect within the central nervous system by modulating microglial activity, the brain's immune cells. This is achieved by downregulating pro-inflammatory cytokines and upregulating anti-inflammatory cytokines, mediated through NF-kB signaling pathways. Changing microglial activation reduces the neuroinflammatory response, important in slowing neurodegeneration in Alzheimers

Its lipophilicity and molecular weight are optimized for penetration across the blood brain barrier, issue for many neurotherapeutic agents. Once in the brain, It accumulates in regions like the hippocampus and cerebral cortex, related to Alzheimer’s pathology, where it executes its neuroprotective actions

- Animal Models: Doses in rats are from 1 to 30 mg/kg, orally
- Human dose based on animal studies, uses a conversion method based on body surface area. Animal data suggests a range of 1 to 30 mg/kg for rodents:

FDA gives a conversion factor to convert animal doses to human doses based on body surface area. It's 12.3 for rodents.

- Dosing Range: If converting these from animal models to human use, you could consider a starting dose somewhere within this range, 0.08mg/kg - 2.44mg/kg
- Dosing Schedule: Typically, this would be taken once daily.

The math is hypothetical and uses a basic method for conversion. Actual doses would need to be decided through actual studies and not org posts

- Known Side Effects: Minimal sides in animals. Cant be fully certain about sides in humans

Lost in the tundras of mumbai

@PsychoDsk
@ThugggButt
@dannydipss
@iabsolvejordan
@CrackyLolra
@Snake.0359
@the_nextDavidLaid
@bululu_87
@wannaimprove
@mathis
So basically, it can be used for both focusing and stress management?
 
New drug never been posted hooray
im russian so dont expect everything to be grammatically correct negroids
Also always DO YOUR OWN RESEARCH

J147, derived from curcumin with structural modifications for enhanced central nervous system bioavailability and mitochondrial affinity, interacts primarily with mitochondrial ATP synthase, particularly targeting daATP5A subunit. This interaction moderates mitochondrial membrane potential and cellular ATP levels, important for neuronal metabolic stability and helps against excitotoxic stress

By diminishing ATP synthase activity, regulates mitochondrial membrane potential, important in maintaining neuronal metabolic stability. This helps protect cells under bioenergetic stress by maintaining ATP levels through alternative metabolic pathways, increased glycolytic flux, important in neurons where ion homeostasis deregulation contributes to Alzheimers pathogenesis

It enhances neuroprotective pathways and neuroplasticity through upregulation of brain derived neurotrophic factor (BDNF). This involves secondary signaling cascades activated via mitochondrial biogenesis promoters and sirtuin pathways, especially SIRT1, cuz its affects in neural longevity and stress resistance. Enhanced BDNF expression promotes synaptic plasticity and resilience, helping memory and learning

It affects amyloid precursor protein (APP) processing, reducing amyloidogenic cleavage of APP which results in accumulation of beta amyloid plaques, a mark of Alzheimer's pathology. This modification is partly achieved by changing activity of secretase enzymes, primarily beta secretase 1 (BACE1), potentially via changes in enzyme expression or cellular localization

It has an anti-inflammatory effect within the central nervous system by modulating microglial activity, the brain's immune cells. This is achieved by downregulating pro-inflammatory cytokines and upregulating anti-inflammatory cytokines, mediated through NF-kB signaling pathways. Changing microglial activation reduces the neuroinflammatory response, important in slowing neurodegeneration in Alzheimers

Its lipophilicity and molecular weight are optimized for penetration across the blood brain barrier, issue for many neurotherapeutic agents. Once in the brain, It accumulates in regions like the hippocampus and cerebral cortex, related to Alzheimer’s pathology, where it executes its neuroprotective actions

- Animal Models: Doses in rats are from 1 to 30 mg/kg, orally
- Human dose based on animal studies, uses a conversion method based on body surface area. Animal data suggests a range of 1 to 30 mg/kg for rodents:

FDA gives a conversion factor to convert animal doses to human doses based on body surface area. It's 12.3 for rodents.

- Dosing Range: If converting these from animal models to human use, you could consider a starting dose somewhere within this range, 0.08mg/kg - 2.44mg/kg
- Dosing Schedule: Typically, this would be taken once daily.

The math is hypothetical and uses a basic method for conversion. Actual doses would need to be decided through actual studies and not org posts

- Known Side Effects: Minimal sides in animals. Cant be fully certain about sides in humans

Lost in the tundras of mumbai

@PsychoDsk
@ThugggButt
@dannydipss
@iabsolvejordan
@CrackyLolra
@Snake.0359
@the_nextDavidLaid
@bululu_87
@wannaimprove
@mathis
If u r high iq I just wanna ask what religion r u?
 
hell yeah, new shit, did read

although j do have a few concerns. is this a temporary boost like piracetam or long term like neuropeptides? i would assume tha latter because of the bdnf but cant be too certain. is this a relatively new drug?
 
diminishing ATP synthase activity,
Just fuck up your body's ability to do anything theory.

Don't trust this shit guys, you do not want to reduce ATP synthesis, You NEED this stuff.
 
ah yes, new research chemical that could have massive unforeseen side effects

sounds legit
 
  • Hmm...
Reactions: hoursk
Too unsafe, zero human trials
 
Don't take substances that increase IQ

Intelligence is a curse

Be stupid and happy
 
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Reactions: Rigged
good thread but this drug seems too dangerous
on one hand it reduces alz, on the other it causes alz from the beta-amyloid protein fragments? (if i read that right)
also, decrease atp synthesis is extremely dangerous, u should def avoid even if it gives benefits

ketamine is better for bdnf at this point
 
If u r high iq I just wanna ask what religion r u?
Tbh idrk, religion was originally faith, faith is just hope, so i hope religion is true because religion is beautiful some of them, but i dont specifically worship and spread anything around
 
  • +1
Reactions: Deleted member 45780
hell yeah, new shit, did read

although j do have a few concerns. is this a temporary boost like piracetam or long term like neuropeptides? i would assume tha latter because of the bdnf but cant be too certain. is this a relatively new drug?
yeh long term, its fairly new
 
Just fuck up your body's ability to do anything theory.

Don't trust this shit guys, you do not want to reduce ATP synthesis, You NEED this stuff.
The idea is not to inhibit ATP production entirely but to regulate it in a way that supports neuronal health and prevents overexcitation that can lead to cellular damage
 
ah yes, new research chemical that could have massive unforeseen side effects

sounds legit
Cant say till u try it since its new, if u die or go blind or something lmk so i can add it to the guide thx
 
tldr? how many iq points wouled this increase and whats the reason to belive that?
 
Too unsafe, zero human trials
yep but if u think the drug is cope or something like that just cause no trials (yet) is dumb
 
Yea obviously its dangerous but i just was telling him most of his threads were water so atleast its original
Im 4/6 on non water threads rn 😔 well get that sh up
 
yep but if u think the drug is cope or something like that just cause no trials (yet) is dumb
agreed, I dont think its cope just risky
 
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Reactions: Rigged

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