About fghrh3 [GTFIH HEIGHTMAXXERS]

[duduboy]

I saw a claim that erdafitinib and TYRA-300 are only relevant for patients who have dwarfism with elevated FGFR3, and that in erdafitinib trials, 67% of patients experienced grade 3 adverse events. Is that accurate? My understanding is erdafitinib is actually approved for FGFR3 altered urothelial (bladder) cancer, not dwarfism, while TYRA-300 is being studied for both cancer and achondroplasia. is that right, and does the 67% grade 3+ AE figure match whats been reported in erdafitinib's clinical trials?

Tagging the height maxx guys I know:
@Zagro @ihatemySOST @Dolorous @enchanted_elixir

 

[enchanted_elixir]

I saw a claim that erdafitinib and TYRA-300 are only relevant for patients who have dwarfism with elevated FGFR3, and that in erdafitinib trials, 67% of patients experienced grade 3 adverse events. Is that accurate? My understanding is erdafitinib is actually approved for FGFR3 altered urothelial (bladder) cancer, not dwarfism, while TYRA-300 is being studied for both cancer and achondroplasia. is that right, and does the 67% grade 3+ AE figure match whats been reported in erdafitinib's clinical trials?

Tagging the height maxx guys I know:
@Zagro @ihatemySOST @Dolorous @enchanted_elixir

This is the first time I heard this drug, but what I would say is that, for height growth, is probably just going along with the growth hormone, protein, and aromatase inhibitors. now I am not going to say that fibroblast growth factor 23 is useless, it is useful because it helps contribute to making new cartilage which will turn into bone but I think it’s a waste of money and you have to dose it right if you do take it.

Naturally, when you have the growth stimulus in your epiphyseal growth plates, the thing that you’re going to see if you were to do epigenetic analysis is that fibroblast growth factor 23 is upregulated in proportion to how much is needed to fulfill the growth objectives. Your only job is to make sure that the epigenetic program is running and stays running for as long as possible until you get to your target height. to add extra fibroblast growth factor 23 to the mix risks throwing the equilibrium balance in my opinion .

 

[enchanted_elixir]

This is the first time I heard this drug, but what I would say is that, for height growth, is probably just going along with the growth hormone, protein, and aromatase inhibitors. now I am not going to say that fibroblast growth factor 23 is useless, it is useful because it helps contribute to making new cartilage which will turn into bone but I think it’s a waste of money and you have to dose it right if you do take it.

Naturally, when you have the growth stimulus in your epiphyseal growth plates, the thing that you’re going to see if you were to do epigenetic analysis is that fibroblast growth factor 23 is upregulated in proportion to how much is needed to fulfill the growth objectives. Your only job is to make sure that the epigenetic program is running and stays running for as long as possible until you get to your target height. to add extra fibroblast growth factor 23 to the mix risks throwing the equilibrium balance in my opinion .

I made edits

 

[Niebvll]

More tyra research is gonna be published last quartal of this year
You can get a better overview of the rirks here:

https://www.sciencedirect.com/science/article/pii/S2666379123003713

 

[duduboy]

This is the first time I heard this drug, but what I would say is that, for height growth, is probably just going along with the growth hormone, protein, and aromatase inhibitors. now I am not going to say that fibroblast growth factor 23 is useless, it is useful because it helps contribute to making new cartilage which will turn into bone but I think it’s a waste of money and you have to dose it right if you do take it.

Naturally, when you have the growth stimulus in your epiphyseal growth plates, the thing that you’re going to see if you were to do epigenetic analysis is that fibroblast growth factor 23 is upregulated in proportion to how much is needed to fulfill the growth objectives. Your only job is to make sure that the epigenetic program is running and stays running for as long as possible until you get to your target height. to add extra fibroblast growth factor 23 to the mix risks throwing the equilibrium balance in my opinion .

More tyra research is gonna be published last quartal of this year
You can get a better overview of the rirks here:

https://www.sciencedirect.com/science/article/pii/S2666379123003713

Beyond patients with FGFR3 driven skeletal dysplasias, would there be any legitimate rationale for using an FGFR3 inhibitor like erdafitinib or TYRA-300 in people without elevated or mutated FGFR3 signalin, for example, someone with normal growth plates just trying to gain extra height? Or does inhibiting a pathway that isnt actually overactive in that context provide no real benefit, and potentially just add unnecessary risk?

 

[mewzilla]

This is the first time I heard this drug, but what I would say is that, for height growth, is probably just going along with the growth hormone, protein, and aromatase inhibitors. now I am not going to say that fibroblast growth factor 23 is useless, it is useful because it helps contribute to making new cartilage which will turn into bone but I think it’s a waste of money and you have to dose it right if you do take it.

Naturally, when you have the growth stimulus in your epiphyseal growth plates, the thing that you’re going to see if you were to do epigenetic analysis is that fibroblast growth factor 23 is upregulated in proportion to how much is needed to fulfill the growth objectives. Your only job is to make sure that the epigenetic program is running and stays running for as long as possible until you get to your target height. to add extra fibroblast growth factor 23 to the mix risks throwing the equilibrium balance in my opinion .

so what im hearing is 0 estrogen, organ growth and whatever the fuck fgfr3 inhibs do (blindness and scoliosis i think...) osteoporosis and brain damage in exchange for POTENTIAL minimal height gains....hm...
seems like a good trade to me! time to order it all in one indiamart order for 20 bucks

 

[mewzilla]

Beyond patients with FGFR3 driven skeletal dysplasias, would there be any legitimate rationale for using an FGFR3 inhibitor like erdafitinib or TYRA-300 in people without elevated or mutated FGFR3 signalin, for example, someone with normal growth plates just trying to gain extra height? Or does inhibiting a pathway that isnt actually overactive in that context provide no real benefit, and potentially just add unnecessary risk?

People report height growth from it, but its always taken with other "height" compounds so you cant really say.


honestly i think its just another thing that tiktok grifters made popular
though i know virtually nothing about it so i could be speaking bullshit

 

[duduboy]

People report height growth from it, but its always taken with other "height" compounds so you cant really say.


honestly i think its just another thing that tiktok grifters made popular
though i know virtually nothing about it so i could be speaking bullshit

For real man, I saw some brazilian tiktok Guy (thats controversial asf) "debunking" It. Thats why I made those questions, since everyone here taking it or testing.

 

[Niebvll]

Beyond patients with FGFR3 driven skeletal dysplasias, would there be any legitimate rationale for using an FGFR3 inhibitor like erdafitinib or TYRA-300 in people without elevated or mutated FGFR3 signalin, for example, someone with normal growth plates just trying to gain extra height? Or does inhibiting a pathway that isnt actually overactive in that context provide no real benefit, and potentially just add unnecessary risk?

Yes.

 

[enchanted_elixir]

Beyond patients with FGFR3 driven skeletal dysplasias, would there be any legitimate rationale for using an FGFR3 inhibitor like erdafitinib or TYRA-300 in people without elevated or mutated FGFR3 signalin, for example, someone with normal growth plates just trying to gain extra height? Or does inhibiting a pathway that isnt actually overactive in that context provide no real benefit, and potentially just add unnecessary risk?

Not sure to be fair.

 

[Dolorous]

thanks for tagging me, i wish i could provide useful commentary but i'm still struggling on my own to figure things out

 

[Dolorous]

Not sure to be fair.

with the knowledge you have gained in the past 3ish years, would you still say that growth in the knee stops at around 19 and 25 for the spine?

 

[enchanted_elixir]

with the knowledge you have gained in the past 3ish years, would you still say that growth in the knee stops at around 19 and 25 for the spine?

Its really hard to give numbers here since it depends on genetics and environment like diet, xenoestrogen exposure, fluoride exposure (effects on thyroid hormones), epigenetics regarding degree on regulation of aromatase, toxin exposure, and more.

Would be irresponsible for me to give precise age numbers without more context, since its more specific.

Like some people have higher aromatase activity, and a lack of counteracting factors making their plates close sooner.