Noriju
wonderfully mysterious
- Joined
- Mar 8, 2026
- Posts
- 706
- Reputation
- 559
Paper: https://www.sciencedirect.com/science/article/pii/S2405844024069184#fig1
Will make this short, nothing fancy
Still rep because this is the greatest hopefuel you'll ever read.
These researchers have studied a causal relationship between the use of igf-1 and erdafinitibs inhibitory effects.
See this excerpt
Erdafinitib inhibits PI3K/AKT and MAPK/ERK signaling pathways.
During erdafinitib inhibition, IGF-1 can activate the PI3K/AKT pathway but not the MAPK/ERK pathway.
The researchers speculate this might be the cause for profound longitudinal growth seen in case studies of extreme growth spurts in cancer kids using erdafinitib.
This clearly suggests that the inhibition of MAPK/ERK and promotion of PI3K/AKT simultaneously causes rapid height gain / growth
Take a look at these figures.
Patient 1 started GH at 8yr to treat GHD (Growth hormone deficiency) And is treated with erdafinitib to treat a brain tumor. (mesencephalic glioma)
So basically kid no. 1 only gets thick bones in his hand as a result.
pretty cheap for good height gains. (still sub 180 tho
)
Another one:
Patient started 7mg/day erdafinitib at 15 yr and 4 months, Experienced many treatment pauses because of hyperphosphatemia and was using high doses of phosphate binding medicine to combat this.
5 months after treatment with erdafinitib starts, the dose is lowered to 5mg/day due to relocation and to lower treatment pauses.
Patient was on erdafinitib to treat cancer and has an "activating FGFR1 variant" (gene mutation that causes overexpression of FGFR1 gene)
Kid goes from 10 cm/yr AGV, to 19 cm/yr AGV. Pretty insane.
However the consequences are concerning.
Fig. 2. Abnormal rapid skeletal growth in a patient treated with erdafitinib, a pan-FGFR inhibitor.
A. X-ray of the cervical and thoracic spine before treatment (a, b, and c) and 9 months after treatment (d, e, f, g, h, and i) with erdafitinib showing the development of cervical lordosis and thoracic scoliosis.
B. MRI images (sagittal, T1 post- Contrast Fat saturation (FS) pulse sequences) of the cervical, thoracic, and lumbar spine demonstrating the development and progression of spinal deformities after commencing erdafitinib: a. Baseline; b. at 2 months; c. at 5 months; d. at 9 months; e. at 12 months which was 3 months after cessation of erdafitinib and after cervical deformity surgical correction.
In short: He needed surgery because his spine had crumpled into a C shape around the neck area.
You can see the spinal development if you look from left to right.
Bone analysis revealed that his bone density was equal to that of osteoporosis.
"0.6322 gm/sq.cm, which is −3.8 standard deviation below the mean value for the age-matched population and more than 2.5 standard deviations below the value for males at peak bone mass."
All hormonal markers (hgh, test, IGF-1 ETC..) Stayed within normal range during treatment. i.e. you don't need to blast gh when on ts.
It's pretty clear that erda is a potent and strong drug to increase height velocity. But the sideeffect profile is just as dire. Stick to a low dose and don't use it for longer than 6 months unless you want to look like a camel-necked freak...
I've got no more time saars. read the rest if you want to - it's a really interesting study.
Start from here: https://www.sciencedirect.com/science/article/pii/S2405844024069184#fig1:~:text=Bone age assessments had not been performed prior to or during erdafitinib therapy. At cessation of therapy, bone
Will make this short, nothing fancy
Still rep because this is the greatest hopefuel you'll ever read.
These researchers have studied a causal relationship between the use of igf-1 and erdafinitibs inhibitory effects.
See this excerpt
Erdafinitib inhibits PI3K/AKT and MAPK/ERK signaling pathways.
During erdafinitib inhibition, IGF-1 can activate the PI3K/AKT pathway but not the MAPK/ERK pathway.
The researchers speculate this might be the cause for profound longitudinal growth seen in case studies of extreme growth spurts in cancer kids using erdafinitib.
This clearly suggests that the inhibition of MAPK/ERK and promotion of PI3K/AKT simultaneously causes rapid height gain / growth
Take a look at these figures.
Patient 1 started GH at 8yr to treat GHD (Growth hormone deficiency) And is treated with erdafinitib to treat a brain tumor. (mesencephalic glioma)
So basically kid no. 1 only gets thick bones in his hand as a result.
pretty cheap for good height gains. (still sub 180 tho
Another one:
Patient started 7mg/day erdafinitib at 15 yr and 4 months, Experienced many treatment pauses because of hyperphosphatemia and was using high doses of phosphate binding medicine to combat this.
5 months after treatment with erdafinitib starts, the dose is lowered to 5mg/day due to relocation and to lower treatment pauses.
Patient was on erdafinitib to treat cancer and has an "activating FGFR1 variant" (gene mutation that causes overexpression of FGFR1 gene)
Kid goes from 10 cm/yr AGV, to 19 cm/yr AGV. Pretty insane.
However the consequences are concerning.
Fig. 2. Abnormal rapid skeletal growth in a patient treated with erdafitinib, a pan-FGFR inhibitor.
A. X-ray of the cervical and thoracic spine before treatment (a, b, and c) and 9 months after treatment (d, e, f, g, h, and i) with erdafitinib showing the development of cervical lordosis and thoracic scoliosis.
B. MRI images (sagittal, T1 post- Contrast Fat saturation (FS) pulse sequences) of the cervical, thoracic, and lumbar spine demonstrating the development and progression of spinal deformities after commencing erdafitinib: a. Baseline; b. at 2 months; c. at 5 months; d. at 9 months; e. at 12 months which was 3 months after cessation of erdafitinib and after cervical deformity surgical correction.
In short: He needed surgery because his spine had crumpled into a C shape around the neck area.
You can see the spinal development if you look from left to right.
Bone analysis revealed that his bone density was equal to that of osteoporosis.
"0.6322 gm/sq.cm, which is −3.8 standard deviation below the mean value for the age-matched population and more than 2.5 standard deviations below the value for males at peak bone mass."
All hormonal markers (hgh, test, IGF-1 ETC..) Stayed within normal range during treatment. i.e. you don't need to blast gh when on ts.
It's pretty clear that erda is a potent and strong drug to increase height velocity. But the sideeffect profile is just as dire. Stick to a low dose and don't use it for longer than 6 months unless you want to look like a camel-necked freak...
I've got no more time saars. read the rest if you want to - it's a really interesting study.
Start from here: https://www.sciencedirect.com/science/article/pii/S2405844024069184#fig1:~:text=Bone age assessments had not been performed prior to or during erdafitinib therapy. At cessation of therapy, bone
Last edited:


nein, bin aus midtjylland horsens.