Heightmaxxing with Erdafinitib - summary of a study.

Noriju

Noriju

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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)
1784459209239

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:ROFLMAO::ROFLMAO:)

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)
1 s20 S2405844024069184 gr1

Kid goes from 10 cm/yr AGV, to 19 cm/yr AGV. Pretty insane.
However the consequences are concerning.



1 s20 S2405844024069184 gr2 lrg

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:
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The first photo (with 2 patients) is from a different paper than the first link given.
This is the link for that one.

After that we follow paper #1

Wrote this shit in a jiffy so i just had to clairfy
 
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)
View attachment 5385363
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:ROFLMAO::ROFLMAO:)

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)
View attachment 5385366
Kid goes from 10 cm/yr AGV, to 19 cm/yr AGV. Pretty insane.
However the consequences are concerning.



View attachment 5385398
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
i feel like erda is pretty overrated, the sides are often not worth it
 
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Forgot to mention that the synergy between igf-1 and erdafinitib is to be used carefully - as shown in these 3 cases, both patients who experienced rapid height growth also got skeletal deformations. Food for thought.

Although for oldcells 16-21 with a low AGV it should not be of much concern
 
i feel like erda is pretty overrated, the sides are often not worth it
Actually it’s not that bad.
Some changes were reversible as seen in the x-rays of the 1. Photo.
And if you stick to a low dose (3mg) and don’t exceed 6months of treatment.
I believe the side effect profile on skeletal development shouldn’t be too bad.
Keep in mind that both patients were in their peak of natural growth velocity.
rapid skeletal advancements wouldn’t happen for a guy like me (19yrs) but still growing
 
Last edited:
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Reactions: nwed
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)
View attachment 5385363
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:ROFLMAO::ROFLMAO:)

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)
View attachment 5385366
Kid goes from 10 cm/yr AGV, to 19 cm/yr AGV. Pretty insane.
However the consequences are concerning.



View attachment 5385398
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
So,basically height maxxing with alot of chances of good results
 
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Reactions: Noriju
So,basically height maxxing with alot of chances of good results
the theory checks out so well.
It really should work like miracles.
But who knows what reality will show.
I’m getting some xrays soon.
If they’re open im hopping on twinnem.
Low dose 6months
 
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i feel like erda is pretty overrated, the sides are often not worth it
“the most common toxicities associated with erdafitinib and other FGFR inhibitors include hyperphosphatemia, skin, and nail toxicities, as well as hand and foot syndrome (redness, swelling, peeling, or tenderness on the hands or feet) [10].”

“A novel mutation in FGFR3 causes camptodactyly, tall stature, and hearing loss (CATSHL) syndrome. Am J Hum Genet. 2006;79(5):935–41.”

Side effect profile seems quite mild as the eye and hearing problems are rarely reported in use with erdafinitib.
Skeletal disfiguration/deformities can be mitigated by not taking the shit at your peak AGV age.
 
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Doesnt prove anything related to an improved mechanism when combining Erda and GH
 
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Doesnt prove anything related to an improved mechanism when combining Erda and GH
ofcourse not.
It’s about erda and igf-1
I don’t know about any gh with this, but the connection between erda and igf-1 the researchers found is genuine
 
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Do you know what HGH gets converted to in the liver

:feelsuhh:
Ok so well then it means hgh and erda works synergystically downstream.
I don’t get your point here?
 
Ok so well then it means hgh and erda works synergystically downstream.
I don’t get your point here?
My point is that it does not mean that
1. They literally bathed the cells in vitro in igf1, you couldnt recreate this exposure with just injecting GH
2. n=1, are we deadass?
3. Its not synergystically at all, the IGF1 actually goes against the effects of Erdafitinib that would lead to apoptosis
Its a cool thought and shouldnt be overlooked but saying that this is definitive evidence for anything is highly exaggerated
 
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My point is that it does not mean that
1. They literally bathed the cells in vitro in igf1, you couldnt recreate this exposure with just injecting GH
2. n=1, are we deadass?
3. Its not synergystically at all, the IGF1 actually goes against the effects of Erdafitinib that would lead to apoptosis
Its a cool thought and shouldnt be overlooked but saying that this is definitive evidence for anything is highly exaggerated
Du bist so klug lieber mann
 
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Bist du deutsch?
ne
Ich bin dänisch aber mein deutsch lehrerin geb mir 10 (1 von die beste) in deutsch🥺🥺🥺
Doch mein grammatik ist scheisse..
 
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ne
Ich bin dänisch aber mein deutsch lehrerin geb mir 10 (1 von die beste) in deutsch🥺🥺🥺
Doch mein grammatik ist scheisse..
Ok krass
Wohnst du nah an der Grenze
Komme aus Kiel:Comfi:
 
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Ok krass
Wohnst du nah an der Grenze
Komme aus Kiel:Comfi:
😂nein, bin aus midtjylland horsens.
Ich fahre nach Tarp später so ich kann mit interrail um Europa fahren.
 
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My point is that it does not mean that
1. They literally bathed the cells in vitro in igf1, you couldnt recreate this exposure with just injecting GH
2. n=1, are we deadass?
3. Its not synergystically at all, the IGF1 actually goes against the effects of Erdafitinib that would lead to apoptosis
Its a cool thought and shouldnt be overlooked but saying that this is definitive evidence for anything is highly exaggerated
man fuck this bullshit i dont jack shit about any of this shit man

You say erdafinitib caused apoptosis.
And that Igf-1 prevents this?
Correct?
Apoptosis in general is just cell death.
Perhaps it’s because it plays a bigger role in the epiphysis? Am i missing some crucial knowledge here?

As far as i know, igf-1 preventing random apoptosis around the body wouldn’t effect the growth axis…
 
man fuck this bullshit i dont jack shit about any of this shit man

You say erdafinitib caused apoptosis.
And that Igf-1 prevents this?
Correct?

Apoptosis in general is just cell death.
Its programmed cell suicide not just random cell death
Perhaps it’s because it plays a bigger role in the epiphysis? Am i missing some crucial knowledge here?

As far as i know, igf-1 preventing random apoptosis around the body wouldn’t effect the growth axis…
Again, not random
Have you even taken a look at your own study? This was clearly talked about there
Erdafitinib kills off the fibroblasts due to inhibiting their survival pathways, thats why igf1 was used as co-treatment
 
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Erdafitinib kills off the fibroblasts due to inhibiting their survival pathways, thats why igf1 was used as co-treatment
So HGH should be used with Erdafitinib? I don't get it.
 
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So HGH should be used with Erdafitinib? I don't get it.
You can do that but it wont recreate the exposure in the in vitro study
Probably does have a similar effect though on a higher dosage
 
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So running low dose erda (like 3-4mg) for under 6 months really shouldnt be a problem? Why isn’t everybody on this
 
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Calling that "low dose" is impressive
Just a normal therapeutic dose

Maybe because its a cancerdrug
Wasnt normal therapeutic doses 8mg?

And also, what does that say? Thats it’s a "cancer drug" What would be so bad about taking it?
 
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)
View attachment 5385363
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:ROFLMAO::ROFLMAO:)

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)
View attachment 5385366
Kid goes from 10 cm/yr AGV, to 19 cm/yr AGV. Pretty insane.
However the consequences are concerning.



View attachment 5385398
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
2-4mg max
 
4 to 8


clearly not enough research buddy:trepidation:
Yeah i know i havent really done too much research on it, but thats why I am asking. What could be the worst? Ive seen people talk about blindness but that only happenned to 1 guy om a High dose for a long time. Other than I have only seen stuff like nail damage
 
Yeah i know i havent really done too much research on it, but thats why I am asking. What could be the worst?
cba listing it all nigger
Ive seen people talk about blindness but that only happenned to 1 guy om a High dose for a long time. Other than I have only seen stuff like nail damage
DNR
 
First of all: This is a very weak study

Second of of all: These kids have CNS tumors, prior brain surgery/radiation/chemotherapy, major hypothalamic pituitary disruption, GH deficiency, very very little sex hormones, probably high fgfr3 and impaired puberty signaling

Third of all: None of these kids showed any signs of infrease in final adult height, only increased catch up growth, even with all that
 
First of all: This is a very weak study

Second of of all: These kids have CNS tumors, prior brain surgery/radiation/chemotherapy, major hypothalamic pituitary disruption, GH deficiency, very very little sex hormones, probably high fgfr3 and impaired puberty signaling

Third of all: None of these kids showed any signs of infrease in final adult height, only increased catch up growth, even with all that
clearly not.
You can see how their growth trajectory changes completely.
Leaps and bounds.
It’s literally putting them in a different percentile.
How is going from 150 FAH to 175 FAH not an increase?
 

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