Why are people using erda early on in puberty???

[Jeezyyyyy]

Since erda inhibits the entire fgfr family wouldn't that means that once you hop off your growth plate closure will accelerate since ur body has been receiving heavy signals to prolong the time of it being open. so theoretically once ur body stops receiving these signals, ur body will rapidly start receiving new signals to speed up growth plate closure since its catching up on the closure that the plates should have had.

it makes sense that ur body would have a rebound reaction to the drug, but there isn't any human data to support it. (it's important to note that erda has a long half life so it would take about a week for ur body to completely flush out the drug, this would mean that the theoretical rapid growth plate closure wouldn't just happen after you take the last tablet).

so this raises the question; why take erdafitnib when growth plates are still wide open and early into adolescence/puberty?

 

[egyptianslayr]

they have no patience

 

[Jeezyyyyy]

they have no patience

theres no point tho, they're js stunting their growth + height isn't as important as it's going to be later in life, no point in being ahead of the curve while ur young js to fall back behind later when it really matters

 

[Shirobon]

Since erda inhibits the entire fgfr family wouldn't that means that once you hop off your growth plate closure will accelerate since ur body has been receiving heavy signals to prolong the time of it being open. so theoretically once ur body stops receiving these signals, ur body will rapidly start receiving new signals to speed up growth plate closure since its catching up on the closure that the plates should have had.

it makes sense that ur body would have a rebound reaction to the drug, but there isn't any human data to support it. (it's important to note that erda has a long half life so it would take about a week for ur body to completely flush out the drug, this would mean that the theoretical rapid growth plate closure wouldn't just happen after you take the last tablet).

so this raises the question; why take erdafitnib when growth plates are still wide open and early into adolescence/puberty?

erda is a pan inhibitor yes

but what ur describing no

 

[Jeezyyyyy]

erda is a pan inhibitor yes

but what ur describing no

can you elaborate on why that wouldn't be true (i'm not saying ur wrong js curious)

 

[Shirobon]

can you elaborate on why that wouldn't be true (i'm not saying ur wrong js curious)

The fgfr family handles most things related to signalling closure put simply

mutations in fgfr1-2 where there activity is upregulated caused things like craniosynostosis(premature suture ossification/closure)
in infants, and most importantly fgfr3 mutations can be a cause of dwarfism

realistically inhibition of 1-3 dont rlly have that much concerns

erda especially since it's lowest ic50 is in fgfr4 & 3

fgfr4 is more related to overall cell survival etc

wont be good for muscle growth but thats about it


starting early is dumb especially if they havent even started growing

but its rlly not that huge of a deal

could be wrong doe

 

[Sakl]

theres no point tho, they're js stunting their growth + height isn't as important as it's going to be later in life, no point in being ahead of the curve while ur young js to fall back behind later when it really matters

Just hype, and your theory us correct it does stunt growth after, and if you prolong the usage then how are still not dust?

They do not do research, no kid could ever think about that.

hgh or gh (go home)

 

[Jeezyyyyy]

The fgfr family handles most things related to signalling closure put simply

mutations in fgfr1-2 where there activity is upregulated caused things like craniosynostosis(premature suture ossification/closure)
in infants, and most importantly fgfr3 mutations can be a cause of dwarfism

realistically inhibition of 1-3 dont rlly have that much concerns

erda especially since it's lowest ic50 is in fgfr4 & 3

fgfr4 is more related to overall cell survival etc

wont be good for muscle growth but thats about it


starting early is dumb especially if they havent even started growing

but its rlly not that huge of a deal

could be wrong doe

yea i see what ur saying, but i guess we'll never know until someone does a study on it (which prob wont ever happen cuz the nih doesn't want us using cancer meds to grow jfl)

 

[Jeezyyyyy]

Just hype, and your theory us correct it does stunt growth after, and if you prolong the usage then how are still not dust?

They do not do research, no kid could ever think about that.

hgh or gh (go home)

jfl "hgh or gh" but yea i think u might be right abt kids not doing they're research, these kids see someone do it online and think its magic in a pill so they go do it and experience the sides then they hop off cuz they're high inhib, and stunt their growth for no reason at all

 

[Shirobon]

yea i see what ur saying, but i guess we'll never know until someone does a study on it (which prob wont ever happen cuz the nih doesn't want us using cancer meds to grow jfl)

there are studies for using it to treat achondroplasia if im not mistaken

 

[Sakl]

jfl "hgh or gh" but yea i think u might be right abt kids not doing they're research, these kids see someone do it online and think its magic in a pill so they go do it and experience the sides then they hop off cuz they're high inhib, and stunt their growth for no reason at all

Hgh is used by literal sons of korean CEO’s btw

It does age your bones insanely

 

[Jeezyyyyy]

there are studies for using it to treat achondroplasia if im not mistaken

no there was a study on a mouse using INFAGRITNIB that increased bone growth and fixed growth plate abnormalities in the mouse that had achondroplasia

 

[Shirobon]

no there was a study on a mouse using INFAGRITNIB that increased bone growth and fixed growth plate abnormalities in the mouse that had achondroplasia

ur right mb it was a case report the one i was referencing

Redirecting

 

[Shirobon]

no there was a study on a mouse using INFAGRITNIB that increased bone growth and fixed growth plate abnormalities in the mouse that had achondroplasia

Despite a remarkable tumor response, with an approximately 80 percent reduction in tumor volume and contrast enhancement on magnetic resonance imaging or MRI (Supplemental Fig. 1) erdafitinib had to be discontinued due to the patient's unusual rapid growth over the 9 months of therapy, severe kyphoscoliosis, and spinal cord compression with cervical myelopathy. The patient grew a total of 14.3 cm, or at an annualized growth of 19.06 cm (normal growth is ∼10 cm per year for a 15-year-old male). Growth prior to erdafitinib therapy was at the 16th to 25th percentile for height and shifted to the 70th percentile during therapy (Fig. 1). The rapid growth led to skeletal deformities which were visible on X-rays, when compared to normal cervical and thoracic spine before erdafitinib treatment (Fig. 2A–a to c). Cervical lordosis and thoracic scoliosis were evident after 9 months of erdafitinib treatment (Fig. 2A, d-i). MRI imaging of the cervical, thoracic and lumbar spine showed the development of deformities after commencing systemic erdafitinib therapy (Fig. 2B–a-d). Of note, he also developed hip flexor contractures not visualized on the imaging, resulting in an underestimation of his height measurements. The cranial vault (membranous bone), unlike cartilaginous skeletal bones, appeared to be unaffected. He returned to our medical center for surgical correction of his symptomatic kyphoscoliosis after cessation of therapy (Fig. 2B–e).