ThatDewd
Iron
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FGFR3 is shown to cause downstream inhibition of B-CATENIN by increasing SOX-9 which destroys B-CATENIN (https://pubmed.ncbi.nlm.nih.gov/22843502/). So theoretically, inhibition of it may give us more B-CATENIN, which is extremely influential on bone growth.
A particularly relevant 2026 study examined an FGFR3 loss-of-function zebrafish model and found that loss of FGFR3 caused B-CATENIN activity increase, altered osteoprogenitor behavior, disrupted osteoblast maturation, abnormal collagen organization, and major abnormalities in suture formation and maintenance (https://pmc.ncbi.nlm.nih.gov/articles/PMC13421612/). The authors specifically found that FGFR3 limits the number of osteoprogenitors at the osteogenic front and promotes osteoblast maturation at the suture edge, which is the pathway to suture closure.
And in mice, the older literature found that FGFR3 knockout mice did not have obvious calvarial defects, whereas certain FGFR3 gain-of-function mutations could cause partial coronal suture fusion. This demonstrates substantial species/model dependence (https://pmc.ncbi.nlm.nih.gov/articles/PMC1571561/).
Inhibiting FGFR3 may not just benefit your height, but your craniofacial development as well.
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FGFR1 is shown to promote craniofacial suture closure by driving osteogenic differentiation, whereas FGFR2 is shown to maintain the craniofacial suture by supporting proliferation of osteogenic progenitor cells (https://journals.biologists.com/dev...t-differentiation-and?redirectedFrom=fulltext). FGF signaling helps determine which FGFR-associated state predominates. When FGF signaling is high, FGFR1 expression increases and FGFR2 expression decreases; when FGF signaling is lower, FGFR2 is maintained while FGFR1 expression is reduced.
Having more FGFR2 than necessary also causes premature fusion (https://pmc.ncbi.nlm.nih.gov/articles/PMC5723914/). So it being reduced while still maintaining a higher FGR2 to FGFR1 ratio is also good. But there needs to be enough so the sutural cells can proliferate.
Therefore, broad inhibition of FGF/FGFR (Erdafitinib) signaling may possibly functionally shift the suture toward an FGFR2-associated, proliferative state by suppressing the FGFR1-associated differentiation program if the differential regulation observed in the developmental suture model applies during pharmacological FGFR inhibition. With Erdafitinib, the overall FGFR inhibition would lower FGFR2 as well, but it would be relatively higher than FGFR1, the ratio giving us a proliferative environment.
It is already established that Erdafitinib inhibits FGFR1 more than FGFR2, so this theory is supported (https://aacrjournals.org/mct/articl...overy-and-Pharmacological-Characterization-of).
My ANECDOTE of being on Erdafitinib for a few months is that it grew my midface forward, fixing my underbite. I couldn’t properly bite at all before, the mandible was too big relative to the maxilla by few millimeters. What makes my anecdote more solid is the fact that I didn't simply notice a aesthetic change, but a functional change that could only take place if the structure shifted. When I was on it I was spamming tons of raw milk and sugar to try and upregulate growth factors as much as posisble. I was on Erdafitinib solo, next time I hop back on I will be using exogenous growth factors and androgens.
Proliferation = making more cells
Differentiation = becoming a specialized cell
This is a mechanistically motivated hypothesis extrapolated across several experimental findings, rather than evidence that erdafitinib itself has this effect.Erdafitinib was developed as an anticancer drug, so its clinical evidence base is overwhelmingly in adults with advanced cancers rather than in developing skeletal tissue. There are very few studies involving adolescents, and the available adolescent evidence is limited to individual case reports (n=1).
A particularly relevant 2026 study examined an FGFR3 loss-of-function zebrafish model and found that loss of FGFR3 caused B-CATENIN activity increase, altered osteoprogenitor behavior, disrupted osteoblast maturation, abnormal collagen organization, and major abnormalities in suture formation and maintenance (https://pmc.ncbi.nlm.nih.gov/articles/PMC13421612/). The authors specifically found that FGFR3 limits the number of osteoprogenitors at the osteogenic front and promotes osteoblast maturation at the suture edge, which is the pathway to suture closure.
And in mice, the older literature found that FGFR3 knockout mice did not have obvious calvarial defects, whereas certain FGFR3 gain-of-function mutations could cause partial coronal suture fusion. This demonstrates substantial species/model dependence (https://pmc.ncbi.nlm.nih.gov/articles/PMC1571561/).
Inhibiting FGFR3 may not just benefit your height, but your craniofacial development as well.
------------------------------------------------------------------------------------------------
FGFR1 is shown to promote craniofacial suture closure by driving osteogenic differentiation, whereas FGFR2 is shown to maintain the craniofacial suture by supporting proliferation of osteogenic progenitor cells (https://journals.biologists.com/dev...t-differentiation-and?redirectedFrom=fulltext). FGF signaling helps determine which FGFR-associated state predominates. When FGF signaling is high, FGFR1 expression increases and FGFR2 expression decreases; when FGF signaling is lower, FGFR2 is maintained while FGFR1 expression is reduced.
Having more FGFR2 than necessary also causes premature fusion (https://pmc.ncbi.nlm.nih.gov/articles/PMC5723914/). So it being reduced while still maintaining a higher FGR2 to FGFR1 ratio is also good. But there needs to be enough so the sutural cells can proliferate.
Therefore, broad inhibition of FGF/FGFR (Erdafitinib) signaling may possibly functionally shift the suture toward an FGFR2-associated, proliferative state by suppressing the FGFR1-associated differentiation program if the differential regulation observed in the developmental suture model applies during pharmacological FGFR inhibition. With Erdafitinib, the overall FGFR inhibition would lower FGFR2 as well, but it would be relatively higher than FGFR1, the ratio giving us a proliferative environment.
It is already established that Erdafitinib inhibits FGFR1 more than FGFR2, so this theory is supported (https://aacrjournals.org/mct/articl...overy-and-Pharmacological-Characterization-of).
My ANECDOTE of being on Erdafitinib for a few months is that it grew my midface forward, fixing my underbite. I couldn’t properly bite at all before, the mandible was too big relative to the maxilla by few millimeters. What makes my anecdote more solid is the fact that I didn't simply notice a aesthetic change, but a functional change that could only take place if the structure shifted. When I was on it I was spamming tons of raw milk and sugar to try and upregulate growth factors as much as posisble. I was on Erdafitinib solo, next time I hop back on I will be using exogenous growth factors and androgens.
Proliferation = making more cells
Differentiation = becoming a specialized cell
This is a mechanistically motivated hypothesis extrapolated across several experimental findings, rather than evidence that erdafitinib itself has this effect.Erdafitinib was developed as an anticancer drug, so its clinical evidence base is overwhelmingly in adults with advanced cancers rather than in developing skeletal tissue. There are very few studies involving adolescents, and the available adolescent evidence is limited to individual case reports (n=1).
