50footstatues
Iron
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In this thread I will try and explain FGFR3 inhibitors, what they are and why they are theoretically good for height gain. AND THEN which one is best... (water ik but we start somewhere)
inspired by @lewanay so dont be suprised if format is familiar
key words and terms:
FGFR3: (fibroblast growth factor receptor 3) is an rtk (receptor tyrosine kinase) that fucks over bone growth. Activating mutations in fgfr3 cause achondroplasia (dwarfism) by inhibiting chondrocyte proliferation and differentiation in the growth plates (ruins endochondral ossification).
Erdafitinhib: we all know erda, but its a pan-fgfr inhibitor that targets fgfr1-4, used primarily for treating cancer with fgfr alterations.
TYRA-300: A highly fgfr3-selective inhibitor in phase 2 trials with 63-fold selectivity over fgfr1 and 19-fold over fgfr2. it was made to avoid toxicities that come along with with fgfr1/2 inhibition while maintaining its efficiency.
LOXO-435: also an fgfr3-selective inhibitor thats in phase 1 trials for advanced solid tumors with fgfr3 alterations. its one of only two selective fgfr3 inhibitors currently in proper clinical development.
so what is fgfr3 signalling even for?
fgfr3 is essentially the big stopper of bone growth. In the growth plates, fgfr3 activation stops chondrocyte proliferation and speeds up their differentiation toward hypertrophy. This signaling pathway reduces the duration of the proliferative phase and limits your overall height potential. In normal physiology, fgfr3 helps regulate bone growth to stop excessive elongation, but when theres too much activation (as in achondroplasia), it ruins your growth.
FGFR3 and other growth pathways
fgfr3 doesn't work alone, it goes against the growth promoting effects of the igf-1/gh axis and instead interacts with the Indian hedgehog (real protein ik)/pthrp feedback loop. When fgfr3 signaling is excessive, it suppresses chondrocyte proliferation and accelerates growth plate senescence. By inhibiting fgfr3, we can allow chondrocytes to grow and spread more extensively and remain in the growth plate longer, helping our final height potential.
the catch
:
completely inbititing fgfr3 could in theory lead to uncontrolled chondrocyte proliferation, maybe resulting in skeletal dysplasia or weird bone formation. Also, since fgfr3 signaling helps regulate the transition from proliferation to hypertrophy, doing this wrong could disrupt the normal sequence of growth plate development. which is BAD
BUT we can mitigate it:
you could use intermittent dosing schedules to allow normal signaling periods
use biomarkers to monitor growth plate activity and adjust dosing
OR you could just use selective fgfr3 inhibitors like tyra rather than erda (looking at you wizard)
now... which one is best for height? (theoretically)
when it comes to height, not all FGFR3 inhibitors are created equal, the main thing is finding one that inhibits fgfr3 signaling well without causing bad sides.
The most important consideration is selectivity - you want an inhibitor that specifically targets FGFR3 without significantly affecting FGFR1, FGFR2, and FGFR4. This is crucial because fgfr1 inhibition can cause hyperphosphatemia and soft tissue calcification, fgfr2 inhibition may lead to retinal issues and nail changes aaand fgfr4 inhibition can affect bile acid metabolism and liver function.
for erda:
Pros: fda approved, easily sourced, proven fgfr inhibition
Cons: pan-fgfr inhibitor (targets fgfr1-4), more side effects, not really designed for height growth
What id say: not really ideal for height purposes due to sides
for tyra:
Pros: good fgfr3 inhibitor (63-fold over fgfr1, 19-fold over fgfr2), good clinical with 55% overall RR in trials, maybe avoids issues of pan-fgfr inhibitors
Cons: still investigational, not so easy to source
What id say: probably most promising for height
and for loxo:
Pros: fgfr3 inhibitor, decent option if tyra unavailable
Cons: very limited clinical data, too early development stage
What id say: decent backup option but less developed than tyra
ancillaries if you're not ignoring the sides:
gh secretagogues - work well with fgfr3 inhibition by helping chondrocyte proliferation
vitamin D3 and K2 - calcium absorb
calcium and magnesium - give raw materials for bone
MAYBE Ipriflavone - can support chondrocyte proliferation and differentiation
conclusion:
yeah so basically in theory fgfr3 inhibition could make u taller and tyra is best
first big thread so lmk if i fucked anything up open to all critisism
id @ but idk like anyone
inspired by @lewanay so dont be suprised if format is familiar
key words and terms:
FGFR3: (fibroblast growth factor receptor 3) is an rtk (receptor tyrosine kinase) that fucks over bone growth. Activating mutations in fgfr3 cause achondroplasia (dwarfism) by inhibiting chondrocyte proliferation and differentiation in the growth plates (ruins endochondral ossification).
Erdafitinhib: we all know erda, but its a pan-fgfr inhibitor that targets fgfr1-4, used primarily for treating cancer with fgfr alterations.
TYRA-300: A highly fgfr3-selective inhibitor in phase 2 trials with 63-fold selectivity over fgfr1 and 19-fold over fgfr2. it was made to avoid toxicities that come along with with fgfr1/2 inhibition while maintaining its efficiency.
LOXO-435: also an fgfr3-selective inhibitor thats in phase 1 trials for advanced solid tumors with fgfr3 alterations. its one of only two selective fgfr3 inhibitors currently in proper clinical development.
so what is fgfr3 signalling even for?
fgfr3 is essentially the big stopper of bone growth. In the growth plates, fgfr3 activation stops chondrocyte proliferation and speeds up their differentiation toward hypertrophy. This signaling pathway reduces the duration of the proliferative phase and limits your overall height potential. In normal physiology, fgfr3 helps regulate bone growth to stop excessive elongation, but when theres too much activation (as in achondroplasia), it ruins your growth.
FGFR3 and other growth pathways
fgfr3 doesn't work alone, it goes against the growth promoting effects of the igf-1/gh axis and instead interacts with the Indian hedgehog (real protein ik)/pthrp feedback loop. When fgfr3 signaling is excessive, it suppresses chondrocyte proliferation and accelerates growth plate senescence. By inhibiting fgfr3, we can allow chondrocytes to grow and spread more extensively and remain in the growth plate longer, helping our final height potential.
the catch
:completely inbititing fgfr3 could in theory lead to uncontrolled chondrocyte proliferation, maybe resulting in skeletal dysplasia or weird bone formation. Also, since fgfr3 signaling helps regulate the transition from proliferation to hypertrophy, doing this wrong could disrupt the normal sequence of growth plate development. which is BAD
BUT we can mitigate it:
you could use intermittent dosing schedules to allow normal signaling periods
use biomarkers to monitor growth plate activity and adjust dosing
OR you could just use selective fgfr3 inhibitors like tyra rather than erda (looking at you wizard)
now... which one is best for height? (theoretically)
when it comes to height, not all FGFR3 inhibitors are created equal, the main thing is finding one that inhibits fgfr3 signaling well without causing bad sides.
The most important consideration is selectivity - you want an inhibitor that specifically targets FGFR3 without significantly affecting FGFR1, FGFR2, and FGFR4. This is crucial because fgfr1 inhibition can cause hyperphosphatemia and soft tissue calcification, fgfr2 inhibition may lead to retinal issues and nail changes aaand fgfr4 inhibition can affect bile acid metabolism and liver function.
for erda:
Pros: fda approved, easily sourced, proven fgfr inhibition
Cons: pan-fgfr inhibitor (targets fgfr1-4), more side effects, not really designed for height growth
What id say: not really ideal for height purposes due to sides
for tyra:
Pros: good fgfr3 inhibitor (63-fold over fgfr1, 19-fold over fgfr2), good clinical with 55% overall RR in trials, maybe avoids issues of pan-fgfr inhibitors
Cons: still investigational, not so easy to source
What id say: probably most promising for height
and for loxo:
Pros: fgfr3 inhibitor, decent option if tyra unavailable
Cons: very limited clinical data, too early development stage
What id say: decent backup option but less developed than tyra
ancillaries if you're not ignoring the sides:
gh secretagogues - work well with fgfr3 inhibition by helping chondrocyte proliferation
vitamin D3 and K2 - calcium absorb
calcium and magnesium - give raw materials for bone
MAYBE Ipriflavone - can support chondrocyte proliferation and differentiation
conclusion:
yeah so basically in theory fgfr3 inhibition could make u taller and tyra is best
first big thread so lmk if i fucked anything up open to all critisism
id @ but idk like anyone
