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I thought high iq n*****s were open minded?

genio

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Its insulting when both of these n*****s call me low iq for believing something then proceed to have the most low iq, childish debate of all time when even if im wrong, im debating to try to figure out what’s effective for height
Like son youre not high iq enough to insult my curiosity

@Acumenis @matiasheanolikeswomen
 
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Its insulting when both of these n*****s call me low iq for believing something then proceed to have the most low iq, childish debate of all time when even if im wrong, im debating to try to figure out what’s effective for height
Like son youre not high iq enough to insult my curiosity

@Acumenis @matiasheanolikeswomen
did you try maybe pinning testosterone for height
 
see us 80iq people dont have to deal with this
u have 30 seconds to reply
what compounds are best to activate the mtorc1 pathway
and how many pathways u have to activate to active sox2, and which compound blocks lex-9
 
u have 30 seconds to reply
what compounds are best to activate the mtorc1 pathway
and how many pathways u have to activate to active sox2, and which compound blocks lex-9
n***a he doesnt heightmax chill on my boy
 
u have 30 seconds to reply
what compounds are best to activate the mtorc1 pathway
and how many pathways u have to activate to active sox2, and which compound blocks lex-9
I’ll treat this as a biology/mechanism question rather than a “what should I take” question. “LEX-9” isn’t a standard pathway name I recognize, so I’m going to verify what that could refer to before answering that part.
 
I’ll treat this as a biology/mechanism question rather than a “what should I take” question. “LEX-9” isn’t a standard pathway name I recognize, so I’m going to verify what that could refer to before answering that part.
n***a doesnt study heightmaxxing bro
 
For mTORC1 activation, the main “clean” biological inputs are:

1. Leucine / EAAs / whey protein — strongest normal nutrient signal. Leucine activates mTORC1 through leucine sensors like Sestrin2/LRS → Rag GTPases → lysosomal mTORC1 recruitment.

2. Arginine — activates mTORC1 through CASTOR1 and lysosomal SLC38A9, and can also affect the TSC2–Rheb side of the pathway.

3. Methionine / SAM — also part of amino-acid sensing for mTORC1; leucine, arginine, and methionine are described as potent/rapid activators.

4. HMB — leucine metabolite; activates mTORC1, but not exactly through the same Sestrin2/Rag route as leucine.

5. Insulin / IGF-1 / growth factors — activate the PI3K–AKT → TSC2 inhibition → Rheb → mTORC1 arm. This is powerful but not something to mess with casually.

6. Lab-only direct activators: MHY1485 and 3BDO are research compounds used to activate mTOR/mTORC1/autophagy-related signaling in cells/animals, not normal supplements. 3BDO was reported to activate MTOR via FKBP1A.

For SOX2, there is no fixed number of pathways you “have to activate.” SOX2 is a transcription factor/gene inside a bigger stemness network, not a single on/off pathway. Depending on the cell type, SOX2 can be pushed by things like EGFR–STAT3, AKT/FoxO1, OCT4/SOX/NANOG circuitry, Notch/Wnt/TGF-β balance, and epigenetic state. A SOX2 review notes EGFR/STAT3 can increase SOX2 promoter activity, AKT can affect SOX2 through FoxO1, and multiple miRNAs/lncRNAs also regulate SOX2.

For small molecules: RepSox / E-616452, a TGF-β/ALK5 inhibitor, is famous because it can replace Sox2 function in some reprogramming systems by inducing Nanog — but that is in cell-culture reprogramming, not “take this and activate SOX2 in your body.” Other reprogramming cocktails often include stuff like CHIR99021 for Wnt/GSK3β inhibition, VPA for HDAC inhibition, forskolin for cAMP, etc., but these are experimental stem-cell tools.

About “LEX-9”: I don’t think that’s a standard pathway name. The closest things I found are:

LeX9 / Lewis X analog — a glycan/ligand in binding studies, not a pathway you “block.”
LHX9 — a transcription factor. If you meant LHX9, I don’t see a well-established small-molecule blocker. In studies, they usually reduce it with knockdown/siRNA/shRNA, not a simple compound. One gastric cancer study showed LHX9 knockdown reduced PKM2/glycolysis-related signaling and malignant cell behavior.

Also important: SOX2 + mTORC1 activation is not automatically “good.” SOX2 is heavily tied to stemness/cancer-stem-cell behavior, and mTORC1 overactivation is linked with growth, metabolism, aging, and cancer risk. In glioma models, mTOR inhibition reduced SOX2/SOX9-mediated stem-cell activity.
 
For mTORC1 activation, the main “clean” biological inputs are:

1. Leucine / EAAs / whey protein — strongest normal nutrient signal. Leucine activates mTORC1 through leucine sensors like Sestrin2/LRS → Rag GTPases → lysosomal mTORC1 recruitment.

2. Arginine — activates mTORC1 through CASTOR1 and lysosomal SLC38A9, and can also affect the TSC2–Rheb side of the pathway.

3. Methionine / SAM — also part of amino-acid sensing for mTORC1; leucine, arginine, and methionine are described as potent/rapid activators.

4. HMB — leucine metabolite; activates mTORC1, but not exactly through the same Sestrin2/Rag route as leucine.

5. Insulin / IGF-1 / growth factors — activate the PI3K–AKT → TSC2 inhibition → Rheb → mTORC1 arm. This is powerful but not something to mess with casually.

6. Lab-only direct activators: MHY1485 and 3BDO are research compounds used to activate mTOR/mTORC1/autophagy-related signaling in cells/animals, not normal supplements. 3BDO was reported to activate MTOR via FKBP1A.

For SOX2, there is no fixed number of pathways you “have to activate.” SOX2 is a transcription factor/gene inside a bigger stemness network, not a single on/off pathway. Depending on the cell type, SOX2 can be pushed by things like EGFR–STAT3, AKT/FoxO1, OCT4/SOX/NANOG circuitry, Notch/Wnt/TGF-β balance, and epigenetic state. A SOX2 review notes EGFR/STAT3 can increase SOX2 promoter activity, AKT can affect SOX2 through FoxO1, and multiple miRNAs/lncRNAs also regulate SOX2.

For small molecules: RepSox / E-616452, a TGF-β/ALK5 inhibitor, is famous because it can replace Sox2 function in some reprogramming systems by inducing Nanog — but that is in cell-culture reprogramming, not “take this and activate SOX2 in your body.” Other reprogramming cocktails often include stuff like CHIR99021 for Wnt/GSK3β inhibition, VPA for HDAC inhibition, forskolin for cAMP, etc., but these are experimental stem-cell tools.

About “LEX-9”: I don’t think that’s a standard pathway name. The closest things I found are:

LeX9 / Lewis X analog — a glycan/ligand in binding studies, not a pathway you “block.”
LHX9 — a transcription factor. If you meant LHX9, I don’t see a well-established small-molecule blocker. In studies, they usually reduce it with knockdown/siRNA/shRNA, not a simple compound. One gastric cancer study showed LHX9 knockdown reduced PKM2/glycolysis-related signaling and malignant cell behavior.

Also important: SOX2 + mTORC1 activation is not automatically “good.” SOX2 is heavily tied to stemness/cancer-stem-cell behavior, and mTORC1 overactivation is linked with growth, metabolism, aging, and cancer risk. In glioma models, mTOR inhibition reduced SOX2/SOX9-mediated stem-cell activity.
n***a used ai
 
I’ll treat this as a biology/mechanism question rather than a “what should I take” question. “LEX-9” isn’t a standard pathway name I recognize, so I’m going to verify what that could refer to before answering that part.
I mean let 7
and for questioning my intelligence
what are all the 191 amino acids in hgh (in correct order)
 

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