hGH isn't the only thing that can make you taller.

[js.rm.atp]

Growth Hormone isn't the only known substance that can make you taller.

So what else can make you taller? (Perhaps even exceeding your genetic limit)

And no I'm not talking about pth analogs

And definetely not stuff that increases bone density or improves mineralization like Romosozumab or Strontium ranelate.

I'm talking pharmaceuticals that drive pure chondrocyte proliferation and growth plate activity.

Quick context if you didn't know:

There's 2 pathways of growth.

1. Via osteoblasts. These cause bone modeling which is helpful for bones like the carniofacial ones as they don't have a growth plate (except for the ramus).
In short these cause more bonemass.

2. Via chondrocytes in the growth plates. These grow and divide like almost every other cell in your body to cause growth. Chondrocytes specifically form cartilage which then later turns into solid bone through ossification.
In short these cause longitudinal growth.

The compounds listed below only affect the 2. pathway.

1. Infigratinib (or other FGFR3 inhibitors)

The Fibroblast Growth Factor Receptor 3 (FGFR3) is a kinase tyrosine type receptor and also one of the main receptors that decreases chondrocyte proliferation when being activated.

Here's a bit on a kinase receptor: It works by a molecule (mainly FGF1, 2, 4, 8, 9 and 18 in this case) binding to it and thereby causing autophosphorylation, which activates it. This is very simplified but keep this in mind for later.

So when it is activated through the said autophosphorylation, that sends a signal via MAPK and ERK, essentially slowing down chondrocytes proliferation.

Now by inhibiting this receptor, which is exatcly what Infigratinib does, it prevents it from being activated.

So in short: Inhibit the receptor that stunts growth -> one factor of growth limitation is removed -> more growth.

But obviously you cant just magically grow 10cm taller just by doing this because there are many many other factors which will be mentioned later.

As said there are also other FGFR3 inhibitors: Rogaratinib, Fexagratinib, Zoligratinib.

And just like with GH (if you aren't GH deficient), if your FGFR3 isn't overly active, this won't do much for you.

2. CNP analogs

2.1 Vosoritide (BMN-111)

Vosoritide is a synthetic C-type Natriuretic Peptide (CNP) analog.

It works by binding to the Natriuretic Peptide Receptor B (NPR-B), which is an enzyme with guanylyl cyclase activity.

NPR-B when bound to by Vosoritide or other CNP analogs, the guanylyl cyclase domain is activated and converts GTP into cyclic guanosine monophosphate (cGMP).

So we got cGMP and this will play a number of roles within the growth plate.

First of all it activates Protein Kinase G-type II (PKG II), which inhibits RAF-1 (a key protein involved in autophosphorylation).

By inhibiting this Protein you essentially block the signal from the activated FGFR3 to MAPK and ERK, meaning these can't suppress chondrocyte proliferation anymore.

2.2 TransCon CNP

TransCon CNP again, binds to the Natriuretic Peptide Receptor B (NPR-B).

The main difference between TransCon CNP and other CNP analogs like Vosoritide is that TransCon CNP has a very long lasting half life (up to a week) and therfore it stimulates the NPR-B constantly meaning cGMP release at all times.

To illustrate this is comparable to cjc ipa without dac (normal CNP analogs) to cjc ipa with dac (TransCon CNP).

2.3 ______

There are other CNP analogs such as BMN-333, CNP-ELP, (GIn⁶,¹⁴)CNP-38, etc.

These aren't really worth noting because they're only used in animal trials or stage 1 human trials and are not as strong as the ones already listed.

3. SAG (Smoothened Agonist)

First of all you have to know what Indian HedgeHog (IHH) pathway does so here is a brief explaination:

The IHH is a signal protein produced by prehypertrophic chondrocytes, which binds to the Patched 1 receptor (PTCH1) on neighbouring, specifically premature chondrocytes.

When the PTCH1 receptor is not bound to, it inhibits Smoothened (SMO) but when bound, this inihibition is given up on.

Now the molecule Smoothened Agonist (SAG) does what IHH would usually do: bind to the PTCH1 receptor.

But it does this by itself, completely bypassing IHH.

Now Smoothened (which is no longer inhibited) activates Gli1 and 2, which activate genes that trigger the release of Parathyroid Hormone related Proteins(PTHrP's).

Now you don't have to rely on Smoothened Agonists or IHH modulators, you can just take PTHrP's as they are, for example Abaloparatide.

Anyway, PTHrP's bind to the Parathyroid Hormone type 1 Receptor (PTH1R), which causes delayed hypertrophy.

Delayed hypertrophy means an extention of the lifetime of chondrocytes, thereby giving them more time to divide (form more cartilage).

So in short, SAG through a number of signals and activations causes chondrocyte proliferation and delayed growth plate closure.

4. IGF-1

Now this is like the most basic thing ever because everybody knows IGF-1 causes growth but I'm still gonna explain how it works.

When Growth Hormone (GH) binds to the Growth Hormone Receptor (GHR), JAK2 phosphorylates, which activates STAT5.

STAT5 enters the nucleus and upregulates genes involved in IGF-1 production.

Now IGF-1, which is now circulating in your body, binds to the IGF-1 Receptor (IGF1R Kinase receptor btw the way) on chondrocytes, leading to the phosphorylation of Insulin Receptor Subtrate 1 (IRS-1).

IRS-1 is an adaptor protein that activates PI3K, which then activates AKT.

AKT through a number of activations and inhibitions including TCS1, TSC2 and RHEB, essentially activtes mTORCI, which strongly promotes chondrocyte proliferation, protein synthesis (creating proteins).

In this case, mTORCI promotes the synthesis of Extracellular Matrix (ECM) proteins (these make up your cartilage) and the hypertrophy of these proteins (hypertrophy = growth).

Another thing AKT does is increase Vasuclar Endothelial Growth Factor (VEGF / this, like the name says promotes the formation of new blood vessels) and AKT also deactivates FOXO.

FOXO detects stress within the cell, potentially leading to apoptosis (self destruction) but now that FOXO is inactive, this won't happen.

This isn't necessarily a good thing tho because apoptosis is there for a reason, prevent cell mutations (cancer).

So in short: IGF-1 leads to new cartilage and the growth of said cartilage, as well as condrocyte proliferation and new blood vessel formation.

5. HIF-1 alpha stabilizers

This has been just way too much biology and chemistry these past few days and HIF-1 alpha stablizers, BMP and WNT agonists are on a whole nother level so I'm gonna leave it up to you to research these if you care.

Now for the stuff you should not be doing

1. Cjc1295 + ipamorelin (or any other ghrp)
This simply doesn't cause much growth, you're way better of just taking GH.

2. Mk677
If you want bloat and insulin resistance, go on take it.

3. IGF-1 lr3 (if your goal is height)
This is very good for muscle but not for height as it is not picked up by IGF1BP's, which carry normal IGF1 onto chondrocytes.

The worst part about these research chems

They are research chemicals meaning they aren't sold anywhere. But if you do find a way to get them lmk. First time making a good thread kinda nervous

 

[Monicaa]

you can get everything if you just look good enough.

 

[7evenvox22]

edit:
Did read, good thread.
But most of these compounds are literally impossible to source

 

[Grievous]

High effort but wouldn't work

 

[Grievous]

High effort but wouldn't work

Where'd u get the idea for this thread
Out of interest

 

[Stacyslayerᛉ]

not mentioning Aromatase inhibitors must be a crime

 

[infraorbidal]

Growth Hormone isn't the only known substance that can make you taller.

So what else can make you taller? (Perhaps even exceeding your genetic limit)

And no I'm not talking about pth analogs

And definetely not stuff that increases bone density or improves mineralization like Romosozumab or Strontium ranelate.

I'm talking pharmaceuticals that drive pure chondrocyte proliferation and growth plate activity.

Quick context if you didn't know:

There's 2 pathways of growth.

1. Via osteoblasts. These cause bone modeling which is helpful for bones like the carniofacial ones as they don't have a growth plate (except for the ramus).
In short these cause more bonemass.

2. Via chondrocytes in the growth plates. These grow and divide like almost every other cell in your body to cause growth. Chondrocytes specifically form cartilage which then later turns into solid bone through ossification.
In short these cause longitudinal growth.

The compounds listed below only affect the 2. pathway.

1. Infigratinib (or other FGFR3 inhibitors)

The Fibroblast Growth Factor Receptor 3 (FGFR3) is a kinase tyrosine type receptor and also one of the main receptors that decreases chondrocyte proliferation when being activated.

Here's a bit on a kinase receptor: It works by a molecule (mainly FGF1, 2, 4, 8, 9 and 18 in this case) binding to it and thereby causing autophosphorylation, which activates it. This is very simplified but keep this in mind for later.

So when it is activated through the said autophosphorylation, that sends a signal via MAPK and ERK, essentially slowing down chondrocytes proliferation.

Now by inhibiting this receptor, which is exatcly what Infigratinib does, it prevents it from being activated.

So in short: Inhibit the receptor that stunts growth -> one factor of growth limitation is removed -> more growth.

But obviously you cant just magically grow 10cm taller just by doing this because there are many many other factors which will be mentioned later.

As said there are also other FGFR3 inhibitors: Rogaratinib, Fexagratinib, Zoligratinib.

And just like with GH (if you aren't GH deficient), if your FGFR3 isn't overly active, this won't do much for you.

2. CNP analogs

2.1 Vosoritide (BMN-111)

Vosoritide is a synthetic C-type Natriuretic Peptide (CNP) analog.

It works by binding to the Natriuretic Peptide Receptor B (NPR-B), which is an enzyme with guanylyl cyclase activity.

NPR-B when bound to by Vosoritide or other CNP analogs, the guanylyl cyclase domain is activated and converts GTP into cyclic guanosine monophosphate (cGMP).

So we got cGMP and this will play a number of roles within the growth plate.

First of all it activates Protein Kinase G-type II (PKG II), which inhibits RAF-1 (a key protein involved in autophosphorylation).

By inhibiting this Protein you essentially block the signal from the activated FGFR3 to MAPK and ERK, meaning these can't suppress chondrocyte proliferation anymore.

2.2 TransCon CNP

TransCon CNP again, binds to the Natriuretic Peptide Receptor B (NPR-B).

The main difference between TransCon CNP and other CNP analogs like Vosoritide is that TransCon CNP has a very long lasting half life (up to a week) and therfore it stimulates the NPR-B constantly meaning cGMP release at all times.

To illustrate this is comparable to cjc ipa without dac (normal CNP analogs) to cjc ipa with dac (TransCon CNP).

2.3 ______

There are other CNP analogs such as BMN-333, CNP-ELP, (GIn⁶,¹⁴)CNP-38, etc.

These aren't really worth noting because they're only used in animal trials or stage 1 human trials and are not as strong as the ones already listed.

3. SAG (Smoothened Agonist)

First of all you have to know what Indian HedgeHog (IHH) pathway does so here is a brief explaination:

The IHH is a signal protein produced by prehypertrophic chondrocytes, which binds to the Patched 1 receptor (PTCH1) on neighbouring, specifically premature chondrocytes.

When the PTCH1 receptor is not bound to, it inhibits Smoothened (SMO) but when bound, this inihibition is given up on.

Now the molecule Smoothened Agonist (SAG) does what IHH would usually do: bind to the PTCH1 receptor.

But it does this by itself, completely bypassing IHH.

Now Smoothened (which is no longer inhibited) activates Gli1 and 2, which activate genes that trigger the release of Parathyroid Hormone related Proteins(PTHrP's).

Now you don't have to rely on Smoothened Agonists or IHH modulators, you can just take PTHrP's as they are, for example Abaloparatide.

Anyway, PTHrP's bind to the Parathyroid Hormone type 1 Receptor (PTH1R), which causes delayed hypertrophy.

Delayed hypertrophy means an extention of the lifetime of chondrocytes, thereby giving them more time to divide (form more cartilage).

So in short, SAG through a number of signals and activations causes chondrocyte proliferation and delayed growth plate closure.

4. IGF-1

Now this is like the most basic thing ever because everybody knows IGF-1 causes growth but I'm still gonna explain how it works.

When Growth Hormone (GH) binds to the Growth Hormone Receptor (GHR), JAK2 phosphorylates, which activates STAT5.

STAT5 enters the nucleus and upregulates genes involved in IGF-1 production.

Now IGF-1, which is now circulating in your body, binds to the IGF-1 Receptor (IGF1R Kinase receptor btw the way) on chondrocytes, leading to the phosphorylation of Insulin Receptor Subtrate 1 (IRS-1).

IRS-1 is an adaptor protein that activates PI3K, which then activates AKT.

AKT through a number of activations and inhibitions including TCS1, TSC2 and RHEB, essentially activtes mTORCI, which strongly promotes chondrocyte proliferation, protein synthesis (creating proteins).

In this case, mTORCI promotes the synthesis of Extracellular Matrix (ECM) proteins (these make up your cartilage) and the hypertrophy of these proteins (hypertrophy = growth).

Another thing AKT does is increase Vasuclar Endothelial Growth Factor (VEGF / this, like the name says promotes the formation of new blood vessels) and AKT also deactivates FOXO.

FOXO detects stress within the cell, potentially leading to apoptosis (self destruction) but now that FOXO is inactive, this won't happen.

This isn't necessarily a good thing tho because apoptosis is there for a reason, prevent cell mutations (cancer).

So in short: IGF-1 leads to new cartilage and the growth of said cartilage, as well as condrocyte proliferation and new blood vessel formation.

5. HIF-1 alpha stabilizers

This has been just way too much biology and chemistry these past few days and HIF-1 alpha stablizers, BMP and WNT agonists are on a whole nother level so I'm gonna leave it up to you to research these if you care.

Now for the stuff you should not be doing

1. Cjc1295 + ipamorelin (or any other ghrp)
This simply doesn't cause much growth, you're way better of just taking GH.

2. Mk677
If you want bloat and insulin resistance, go on take it.

3. IGF-1 lr3 (if your goal is height)
This is very good for muscle but not for height as it is not picked up by IGF1BP's, which carry normal IGF1 onto chondrocytes.

The worst part about these research chems

They are research chemicals meaning they aren't sold anywhere. But if you do find a way to get them lmk. First time making a good thread kinda nervous

Bro wtf these are impossible to source

 

[js.rm.atp]

Where'd u get the idea for this thread
Out of interest

Was looking into what causes dwarfism and eventually found out about all these pharmaceuticals and I didnt wanna gatekeep them cuz they could change my or someone elses life so I just worte this thread

 

[Grievous]

Was looking into what causes dwarfism

Yeah but u should've been able to figure that it wouldn't work unless ur a dwarf
these methods only work if there's already something inhibiting ur growth like in dwarfs not in regular people if u tried it on a regular person it would trigger ur bodies regulatory mechanisms

 

[js.rm.atp]

Yeah but u should've been able to figure that it wouldn't work unless ur a dwarf
these methods only work if there's already something inhibiting ur growth like in dwarfs not in regular people if u tried it on a regular person it would trigger ur bodies regulatory mechanisms

Ye I forgot to add that FGFR3 inhibitors wont do much if your FGFR3 isnt overly active and also for CNP analogs if youre not cGMP deficient

 

[ce10098]

molecule

 

[1up]

First time making a good thread kinda nervous

nice thread