Erda

[the big A]

How long do you have to take this cancer med for to get the benefits

 

[FemurSmasher]

How long do you have to take this cancer med for to get the benefits

u dont lol

 

[the big A]

u dont lol

cap bitchass niga

 

[SabiWabi]

erda is cope

 

[the big A]

erda is cope

How so studies show otherwise

 

[SabiWabi]

How so studies show otherwise

did u see documented studies

 

[truecel_KHHV]

How long do you have to take this cancer med for to get the benefits

Erda is gay


It makes u gay

 

[the big A]

did u see documented studies

I’ve only seen one study lowkey comparing it to other roids and people using Erda had the most growth

 

[the big A]

Erda is gay


It makes u gay

Bar

 

[SabiWabi]

I’ve only seen one study lowkey comparing it to other roids and people using Erda had the most growth

ngl its hard to tell if its natural growth or not, none of the studies show if it is or isnt

 

[the big A]

ngl its hard to tell if its natural growth or not, none of the studies show if it is or isnt

true I guess we never know really

 

[Niebvll]

a few months

 

[Niebvll]

ngl its hard to tell if its natural growth or not, none of the studies show if it is or isnt

It OBVIOUSLY ISNT you fucktard
you havent read a single study on this
they even put graphics there so you wouldnt have had to read it and just look at the images
you probably never even opened one even

 

[SabiWabi]

It OBVIOUSLY ISNT you fucktard
you havent read a single study on this
they even put graphics there so you wouldnt have had to read it and just look at the images
you probably never even opened one even

nga do u know how a study works, so many confounding variables that can effect the experiment, impossible to eliminate each of them, so it cannot be a conclusive study, otherwise show me just one valid study

 

[Niebvll]

nga do u know how a study works, so many confounding variables that can effect the experiment, impossible to eliminate each of them, so it cannot be a conclusive study, otherwise show me just one valid study

No it isnt
What a stupid post this is

 

[SabiWabi]

No it isnt
What a stupid post this is

then give a study

 

[Niebvll]

then give a study

Why would I bother?
Look at ANY trial
THOR or even case studies

 

[SabiWabi]

Why would I bother?
Look at ANY trial
THOR or even case studies

i already checked all all of them have confounding variables that signal its natural growth

 

[Niebvll]

i already checked all all of them have confounding variables that signal its natural growth

They dont
You obviously didnt check them
THOR was a randomized trial, if it had been natural growth we would have seen a proportional distribution among placebo and treated cohorts of this extra growth
We didnt
It even more logical that the FGFR3 Inhibition is the reason for the growth, when looking at FGFR3s general purpose in chondrocyte differentiation

 

[SabiWabi]

They dont
You obviously didnt check them
THOR was a randomized trial, if it had been natural growth we would have seen a proportional distribution among placebo and treated cohorts of this extra growth
We didnt
It even more logical that the FGFR3 Inhibition is the reason for the growth, when looking at FGFR3s general purpose in chondrocyte differentiation

i just checked the article again, in the study it shows that it accelerates growth and the FGFR3 is a signal to slow down bone lengthening and ERDA is basically acting like an inhibitor to the growth plates and it causes cartilage to expand rapidly in the growth plates. theres also a lot of side effects in the article like skeletal damage and bone pain also if it wasnt natural growth then either the ERDA should allow people to grow past the closure of growth plates, or it should not have a limit for height if the growth plates are open if u think about it logically

 

[Niebvll]

i just checked the article again, in the study it shows that it accelerates growth

It accelerates growth velocity but not the way HGH for example does, while HGH does not increase FAH (except in rare cases) because it only increases cell cycles, the FGFR3 inhibition leads to extra chondrocyte proliferation and differentiation, resulting in a) faster growth and b)permanent FAH increases due to cells being added to the gp that would not have existed without treatment

and the FGFR3 is a signal to slow down bone lengthening and ERDA is basically acting like an inhibitor to the growth plates

No?
Theres no "inhibition of growth plates"Y
Youre just dumbing shit down completely
FGFR3 isnt a signal to slow done bone lengthening but the phosphorylation of it suppresses other pathways and in return their suppression leads to an inhibition of chondrocyte limitation
So FGFR3 is a signal for a signal that ENDS chondrocyte activity
the "slow down" effect is just a logical consequence of less chondrocytes proliferating => less cells to differentiate into hypertrophy => less bone added per time unit

theres also a lot of side effects in the article like skeletal damage and bone pain

When was this about side effects?
I believe everyone who takes literal CANCER drugs should be aware of the side effects they can have, pain being among the less important ones in my opinion

also if it wasnt natural growth then either the ERDA should allow people to grow past the closure of growth plates

No?
Why does the premise of possible unnatural growth lead to the conclusion of impossible ways of growth? And why would the former actually have the latter as necessity to be true?

or it should not have a limit for height if the growth plates are open if u think about it logically

It shifts the limit by a lot, there are other pathways that matter for growth plate maturation / fusion so Erdafitinib itself cant completely stop this. In principle this is correct and happening.

For the rest, youre literally just classifying any cell induced growth as natural
NO SHIT
theres literally no other way to grow than through your growth plates

If you left those patients on no meds (which would have been their "natural" progress) they wouldnt have grown like on Erdafitinib, which is proven in the placebo cohort

Point stands Erdafitinib causes unnatural growth.

 

[SabiWabi]

It accelerates growth velocity but not the way HGH for example does, while HGH does not increase FAH (except in rare cases) because it only increases cell cycles, the FGFR3 inhibition leads to extra chondrocyte proliferation and differentiation, resulting in a) faster growth and b)permanent FAH increases due to cells being added to the gp that would not have existed without treatment

No?
Theres no "inhibition of growth plates"Y
Youre just dumbing shit down completely
FGFR3 isnt a signal to slow done bone lengthening but the phosphorylation of it suppresses other pathways and in return their suppression leads to an inhibition of chondrocyte limitation
So FGFR3 is a signal for a signal that ENDS chondrocyte activity
the "slow down" effect is just a logical consequence of less chondrocytes proliferating => less cells to differentiate into hypertrophy => less bone added per time unit

When was this about side effects?
I believe everyone who takes literal CANCER drugs should be aware of the side effects they can have, pain being among the less important ones in my opinion

No?
Why does the premise of possible unnatural growth lead to the conclusion of impossible ways of growth? And why would the former actually have the latter as necessity to be true?

It shifts the limit by a lot, there are other pathways that matter for growth plate maturation / fusion so Erdafitinib itself cant completely stop this. In principle this is correct and happening.

For the rest, youre literally just classifying any cell induced growth as natural
NO SHIT
theres literally no other way to grow than through your growth plates

If you left those patients on no meds (which would have been their "natural" progress) they wouldnt have grown like on Erdafitinib, which is proven in the placebo cohort

Point stands Erdafitinib causes unnatural growth.

Chondrocytes in the growth plate have a finite replicative capacity also known as proliferative senescence. Just because you push the chondrocytes, doesn't mean the divisions are infinite. Also if you accelerate the rate at which resting-zone chondrocytes differentiate and proliferate without altering the molecular clock that governs growth plate senescence you could risk the stem pool depleting faster Lastly this can lead to premature growth plate exhaustion and earlier fusion. Faster short-term height velocity does not guarantee a taller final adult height if the temporal window of growth is truncated which in this case it is.

In biology, a receptor that triggers downstream signaling cascades (like STAT1 and MAPK/ERK) to down regulate chondrocyte proliferation and matrix synthesis is, by definition, a negative regulator of bone elongation. Calling it a "signal to slow down or limit growth" is standard, accurate shorthand for describing a negative feedback pathway. Arguing over whether it's a "direct signal" or an "inhibitory signal of an activator pathway" is shifting the focus away from the actual physiological outcome.

Minimizing side effects when discussing pediatric skeletal growth is clinically invalid. ERDA is a potent pan-FGFR inhibitor with severe, systemic side effects that include hyperphosphatemia, soft tissue calcification, and subchondral bone damage. JFL at this dismissive argument, it's obvious that FGFR signaling isn't exclusive to the growth plate; it plays crucial roles in renal phosphate handling, vascular homeostasis, and tissue repair. Also, If a drug causes severe hyperphosphatemia or premature articular/skeletal degradation, the mechanical integrity of the bone is compromised. You cannot separate height gain from the structural quality of the bone being formed.

To ur last point, "Unnatural" is a philosophical label, not a biochemical one. The bone formed under FGFR3 inhibition is created via standard endochondrol ossification—the exact same cellular process the body always uses (resting chondrocytes → proliferative zone → hypertrophic zone → osteoblast invasion). By their definition, giving recombinant Human Growth Hormone (rHGH) to a deficient child, or giving thyroxine to a hypothyroid child, would also be "unnatural growth" because the placebo cohort wouldn't achieve it. Pharmacological intervention modifies pathway signaling intensity, but the underlying cellular cascade remains the body's intrinsic physiological mechanism.

Therefore, ERDA does not give unnatural growth like that of you are describing, it only accelerates the natural growth you receive from your genetic potential, plus the side effects of ERDA far outweigh the benefits which are not even benefits

 

[Niebvll]

Chondrocytes in the growth plate have a finite replicative capacity also known as proliferative senescence. Just because you push the chondrocytes, doesn't mean the divisions are infinite.

Are you even reading what I say?
This is why HGH doesnt increase FAH.
Erdafitinib and any FGFR3-inhibitor does because FGFR3s signalling pathway leading chondrocytes into their state of senescence (through telomere shortening) is reversible and thus delayable
Thats the whole fucking point of taking it
Erdafitinib does not speed up the cell cyclus, as I said it instead leads to extra proliferation.

Also if you accelerate the rate at which resting-zone chondrocytes differentiate and proliferate without altering the molecular clock that governs growth plate senescence you could risk the stem pool depleting faster

Yeah bro gpt slop
you dont even know what youre saying
MOLECULAR CLOCK LOL
Depletion is completely theoretical
If you pin 2000IU HGH ed you will deplete your restiong zone too
noone doing that
not even complete fgfr3 inhibition would lead to this (null-fgfr3 mice prove this)

Lastly this can lead to premature growth plate exhaustion and earlier fusion. Faster short-term height velocity does not guarantee a taller final adult height if the temporal window of growth is truncated which in this case it is.

No it cant
Its also not short term height velocity... as I explained the velocity is actually more long term. As the extra chondrocytes add up, the total proliferation rate per time unit increases even more (cycle), eventually you get more and more hypertrophic cells
Your whole point is just OBVIOUS ai slop with not even a theoretical base

In biology, a receptor that triggers downstream signaling cascades (like STAT1 and MAPK/ERK) to down regulate chondrocyte proliferation and matrix synthesis is, by definition, a negative regulator of bone elongation. Calling it a "signal to slow down or limit growth" is standard, accurate shorthand for describing a negative feedback pathway. Arguing over whether it's a "direct signal" or an "inhibitory signal of an activator pathway" is shifting the focus away from the actual physiological outcome.

Holy fucking AISLOP
If it has a whole signalling pathway, its not a direct signal. Period.

Minimizing side effects when discussing pediatric skeletal growth is clinically invalid. ERDA is a potent pan-FGFR inhibitor with severe, systemic side effects that include hyperphosphatemia, soft tissue calcification, and subchondral bone damage

Easily handleled or never seen side effects

. JFL at this dismissive argument, it's obvious that FGFR signaling isn't exclusive to the growth plate; it plays crucial roles in renal phosphate handling, vascular homeostasis, and tissue repair. Also, If a drug causes severe hyperphosphatemia or premature articular/skeletal degradation, the mechanical integrity of the bone is compromised. You cannot separate height gain from the structural quality of the bone being formed.

To ur last point, "Unnatural" is a philosophical label, not a biochemical one. The bone formed under FGFR3 inhibition is created via standard endochondrol ossification—the exact same cellular process the body always uses (resting chondrocytes → proliferative zone → hypertrophic zone → osteoblast invasion). By their definition, giving recombinant Human Growth Hormone (rHGH) to a deficient child, or giving thyroxine to a hypothyroid child, would also be "unnatural growth" because the placebo cohort wouldn't achieve it. Pharmacological intervention modifies pathway signaling intensity, but the underlying cellular cascade remains the body's intrinsic physiological mechanism.

Therefore, ERDA does not give unnatural growth like that of you are describing, it only accelerates the natural growth you receive from your genetic potential, plus the side effects of ERDA far outweigh the benefits which are not even benefits

DNR your stupid bullshit Im tired of this

It went from you being unknowledgable and being corrected to you shifting the topic focus from one thing to another after I showed youre wrong
Noone mentioned sides
Youre fucking retarded and putting in JFL emojis here and there wont change it
To the last sentence, genetic potential is a myth even the way you most likely think of it. Ive only ever met a single user with an actually strong definition of it

 

[Niebvll]

@Paul.jnxy was ein retard

 

[gothie]

How long do you have to take this cancer med for to get the benefits

Idk

 

[SabiWabi]

Are you even reading what I say?
This is why HGH doesnt increase FAH.
Erdafitinib and any FGFR3-inhibitor does because FGFR3s signalling pathway leading chondrocytes into their state of senescence (through telomere shortening) is reversible and thus delayable
Thats the whole fucking point of taking it
Erdafitinib does not speed up the cell cyclus, as I said it instead leads to extra proliferation.

Yeah bro gpt slop
you dont even know what youre saying
MOLECULAR CLOCK LOL
Depletion is completely theoretical
If you pin 2000IU HGH ed you will deplete your restiong zone too
noone doing that
not even complete fgfr3 inhibition would lead to this (null-fgfr3 mice prove this)

No it cant
Its also not short term height velocity... as I explained the velocity is actually more long term. As the extra chondrocytes add up, the total proliferation rate per time unit increases even more (cycle), eventually you get more and more hypertrophic cells
Your whole point is just OBVIOUS ai slop with not even a theoretical base


Holy fucking AISLOP
If it has a whole signalling pathway, its not a direct signal. Period.

Easily handleled or never seen side effects

DNR your stupid bullshit Im tired of this

It went from you being unknowledgable and being corrected to you shifting the topic focus from one thing to another after I showed youre wrong
Noone mentioned sides
Youre fucking retarded and putting in JFL emojis here and there wont change it
To the last sentence, genetic potential is a myth even the way you most likely think of it. Ive only ever met a single user with an actually strong definition of it

JFL AT THIS LOL ERDA is a potent FGFR3 inhibitor, using it off-label to manipulate human height presents critical clinical and physiological flaws that contradict the idea that it simply "accelerates natural growth."
ERDA is a pan-FGFR inhibitor (targeting FGFR1, FGFR2, FGFR3, and FGFR4), not a selective FGFR3 inhibitor. Because FGFR signaling is fundamental to renal phosphate handling, vascular stability, and tissue repair, systemic inhibition carries severe risks
For example severe hyperphosphatemia which blocks FGFR1/FGF23 signaling in the kidneys which disrupts phosphate balance and leads to tissue calcification and renal complications FGFR signaling maintains joint integrity. Inhibiting it globally risks subchondral bone degradation and joint damage, compromising the structural quality of the skeleton. Clinical trials for ERDA report significant risks of central serous retinopathy, retinal pigment epithelium detachment, and severe mucosal/nail toxicities. Dismissing these as "easily handled" ignores established clinical oncology data regarding pan-FGFR inhibition. Resting-zone chondrocytes possess a finite replicative capacity governed by complex genetic and epigenomic molecular clocks. Driven proliferation via signal suppression does not grant infinite divisions. Forcing rapid or prolonged entry of resting chondrocytes into the proliferative zone risks prematurely exhausting the stem cell niche. Even if short-term height velocity increases, depleting the resting pool early truncates the total temporal window of growth, potentially resulting in early growth plate fusion and a compromised final adult height. Extrapolating findings from knockout (null-FGFR3) mouse models directly to human pediatric physiology oversimplifies human skeletal maturation, which operates on vastly different timeframes and hormonal feedback loops. Downstream cascades like STAT1 and MAPK/ERK act as critical biological brakes to prevent dysregulated bone elongation and ensure structural integrity. Completely suppressing these pathways overrides the body's natural homeostatic checks. Accelerated endochondral ossification under strong pharmacological inhibition does not guarantee normal bone mineral density or architectural strength. The mechanical integrity of the newly formed trabecular and cortical bone can be significantly compromised. ERDA is an oncology medication designed for targeted cancer therapies with significant systemic toxicity. Framed physiologically, attempting to bypass negative feedback regulators like FGFR3 using a broad pan-FGFR inhibitor risks severe systemic side effects, premature depletion of the growth plate stem cell pool, and compromised structural bone integrity. JFL AT THIS COPE LOL ERDA IS LESS EFFECTIVE THAN DRINKING RAW MILK + RAW HONEY + RAW MEAT + RAW HEIGHT + RAW DAIRY + RAW HGH LOL