Cheap FGFR3 Inhibition: You Do Not Need to Spend thousands on mainstream FGFR3 inhibitors

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Cheap FGFR3 Inhibition: You Do Not Need to Spend thousands on mainstream FGFR3 inhibitors


FGFR3 is very important for how our bones and cartilage grow. It helps control how our bones form, which means it can stop our bones from growing much.


Because of this people have been studying drugs that can stop FGFR3 from working. One example is Infigratinib, which is used to treat cancer (And to ascend you).


The problem is that these drugs are extremely expensive. They can cost between fifteen thousand dollars and twenty thousand dollars per month which's just too much money for most people to pay.


If you read about the science behind these drugs you will find something


An FGFR Inhibitor: PD173074



A long time ago before we had modern FGFR inhibitors scientists were already using a compound called PD173074.


PD173074 is a molecule that stops FGFR1 and FGFR3 from working. It does this by binding to a part of the FGFR3, which's important for how it works. In experiments PD173074 is very good at stopping FGFR3.


Many scientists have used PD173074 to study how FGFR3 works. They have used it to see how FGFR3 is involved in how our bones and cartilage grow.


In words scientists have been studying FGFR3 inhibition with PD173074 for a long time even before the expensive drugs like Infigratinib were made.


Why It Never Became a Drug



Even though PD173074 is very good at stopping FGFR3 in experiments it was never made into a medicine. There are a reasons for this:


- it does not work well in the body

- it is not specific enough

- pharmaceutical companies made newer and better inhibitors


That is why newer drugs like Infigratinib, Erdafitinib and Futibatinib were used instead of PD173074.


Important Disclaimer


PD173074 is only sold for use in research. It is meant to be used in experiments like growing cells in a lab.

It is not approved as a medicine. There are no studies to show if it is safe for people to use. Because of this we should only talk about PD173074 in the context of research not for use.

Conclusion:

If you’re too broke to afford mainstream FGFR3 Inhibitors you may have a look into this. If you have the finances for the real stuff, that’s probably better for you - but no medical advice of course.
 
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if you tell me a good source I will be a lab rat
 
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It is not approved as a medicine. There are no studies to show if it is safe for people to use. Because of this we should only talk about PD173074 in the context of research not for use.
So we do this blind? Not even case studies?
 
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Fgfr3 inhibition is a looksmin anyway it rapes your skin and hair
 
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No human studies but lots of animal studies. Works through pretty much the same mechanisms as the other ones tho
sure, but we cant base everything off of animal studies as our proof

Animal trials are done before trials on humans to see the effect on the average mammal, we cant thread on them
 
if you tell me a good source I will be a lab rat
I think there are lots of good sources even by google search since it’s oral, research use only and pretty cheap to produce.
 
sure, but we cant base everything off of animal studies as our proof

Animal trials are done before trials on humans to see the effect on the average mammal, we cant thread on them
The post isn’t for telling people to use it, just inform about it. I added a disclaimer that it’s not designed for human use and also said that this isn’t medical advice. Everyone can decide on their own if they take it or not.
 
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Cheap FGFR3 Inhibition: You Do Not Need to Spend thousands on mainstream FGFR3 inhibitors


FGFR3 is very important for how our bones and cartilage grow. It helps control how our bones form, which means it can stop our bones from growing much.


Because of this people have been studying drugs that can stop FGFR3 from working. One example is Infigratinib, which is used to treat cancer (And to ascend you).


The problem is that these drugs are extremely expensive. They can cost between fifteen thousand dollars and twenty thousand dollars per month which's just too much money for most people to pay.


If you read about the science behind these drugs you will find something


An FGFR Inhibitor: PD173074


A long time ago before we had modern FGFR inhibitors scientists were already using a compound called PD173074.


PD173074 is a molecule that stops FGFR1 and FGFR3 from working. It does this by binding to a part of the FGFR3, which's important for how it works. In experiments PD173074 is very good at stopping FGFR3.


Many scientists have used PD173074 to study how FGFR3 works. They have used it to see how FGFR3 is involved in how our bones and cartilage grow.


In words scientists have been studying FGFR3 inhibition with PD173074 for a long time even before the expensive drugs like Infigratinib were made.


Why It Never Became a Drug


Even though PD173074 is very good at stopping FGFR3 in experiments it was never made into a medicine. There are a reasons for this:


- it does not work well in the body

- it is not specific enough

- pharmaceutical companies made newer and better inhibitors


That is why newer drugs like Infigratinib, Erdafitinib and Futibatinib were used instead of PD173074.


Important Disclaimer


PD173074 is only sold for use in research. It is meant to be used in experiments like growing cells in a lab.

It is not approved as a medicine. There are no studies to show if it is safe for people to use. Because of this we should only talk about PD173074 in the context of research not for use.

Conclusion:

If you’re too broke to afford mainstream FGFR3 Inhibitors you may have a look into this. If you have the finances for the real stuff, that’s probably better for you - but no medical advice of course.
DNR
PD173074 also antagonizes HMGA2 and is too weak an fgfr3 inhibitor anyway even if found for dirt cheap ud need to take tens/hundreds of mgs a day depending on oral bioavailability+ infigratinib and erdafitinib arent expensive anyway, no one is buying pharma brand infig.
 
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DNR
PD173074 also antagonizes HMGA2 and is too weak an fgfr3 inhibitor anyway even if found for dirt cheap ud need to take tens/hundreds of mgs a day depending on oral bioavailability+ infigratinib and erdafitinib arent expensive anyway, no one is buying pharma brand infig.
infig and erdafitinib arent selective at all in which fgfr3 they inhibit. they hit all 4.
 
infig and erdafitinib arent selective at all in which fgfr3 they inhibit. they hit all 4.
infigratinib is selective, and pd no proof that it actually even penetrates the growth plates effectively. just theortical crap, imagine using an fgfr3 inhib just for it to antagonize hmga2, hmga2 is by far one of the most important factors in ssc stemness and self renewal and overall gp function. good luck gettin a millimeter of growth outta that crap.
 
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infigratinib is selective, and pd no proof that it actually even penetrates the growth plates effectively. just theortical crap, imagine using an fgfr3 inhib just for it to antagonize hmga2, hmga2 is by far one of the most important factors in ssc stemness and self renewal and overall gp function. good luck gettin a millimeter of growth outta that crap.
Not to mention partial blindness and an awful amount of dairreha:lul:
 
infigratinib is selective, and pd no proof that it actually even penetrates the growth plates effectively. just theortical crap, imagine using an fgfr3 inhib just for it to antagonize hmga2, hmga2 is by far one of the most important factors in ssc stemness and self renewal and overall gp function. good luck gettin a millimeter of growth outta that crap.
im not saying pd is good im just saying infig is also shit. inhibits all 3-4 fgfr’s which you need for proper growth. as far as i know you would be better off with nevapegritide
 
im not saying pd is good im just saying infig is also shit. inhibits all 3-4 fgfr’s which you need for proper growth. as far as i know you would be better off with nevapegritide
u dont need 1-4 fgfrs for " proper growth" u have no ground making such claim, if anything fgfr2 somewhat restricts craniofacial growth so its accidental inhibition by pan-fgfris is potentially benefecial, but again more sides compared to selective ones like tyra.
 
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u dont need 1-4 fgfrs for " proper growth" u have no ground making such claim, if anything fgfr2 somewhat restricts craniofacial growth so its accidental inhibition by pan-fgfris is potentially benefecial, but again more sides compared to selective ones like tyra.
fgfr 4, 1, 2 getting inhibited will fuck up ur endocrine system, organs, glucose homeostatis, insulin sensitivy overall fgfr3 inhibitors are ass unless ur taking tyra-300
 
u dont need 1-4 fgfrs for " proper growth" u have no ground making such claim, if anything fgfr2 somewhat restricts craniofacial growth so its accidental inhibition by pan-fgfris is potentially benefecial, but again more sides compared to selective ones like tyra.
loss of fgfr1 impaires signaling to cartilage so bones may grow too little or abnormally. look at kallman syndrome or people with loss of fgfr1.
look in bones you have progenitor cells that can turn into 1: osteoblasts
2: chondrocytes
FGFR1 keeps progenitors from being used up to fast. if its gone we „use up our bone making supply” too fast. thats why some studies with knock out fgfr1 find more bone mass. but long term its bad
 
No human studies but lots of animal studies. Works through pretty much the same mechanisms as the other ones tho
Reading this spiked my cortisol horrifically, no you little goblins we do not get wishy washy and equivocal with potentially life altering pharmaceutical biological modifications

BAD NEW GEN BAD BAD BAD BACK IN THE NO SPEAKING CORNER
 
loss of fgfr1 impaires signaling to cartilage so bones may grow too little or abnormally. look at kallman syndrome or people with loss of fgfr1.
look in bones you have progenitor cells that can turn into 1: osteoblasts
2: chondrocytes
FGFR1 keeps progenitors from being used up to fast. if its gone we „use up our bone making supply” too fast. thats why some studies with knock out fgfr1 find more bone mass. but long term its bad
pan fgfr inhibitors dont even come close to mimicking full genetic knockout, like i said before, ur a retard, as for progenitor cells that turn into osteoblasts or chondrocytes, those are marginal amounts compared to the resting zone stem cells which are the primary source of progenitors for the growth plate and are all commited to the chondrogenic fate.

keep going with the ai slop to debate me lol mirin
 
u dont need 1-4 fgfrs for " proper growth" u have no ground making such claim, if anything fgfr2 somewhat restricts craniofacial growth so its accidental inhibition by pan-fgfris is potentially benefecial, but again more sides compared to selective ones like tyra.
Have you read the literature
 
Have you read the literature
the question is did YOU? in addition to ur crap, fgfr1 and 3 inhibition not only derepresses growth plate activity but also enhances IVD expansion, clearly u didnt read the literature but i for sure did. if the standard pan-fgfr inhibitors are soo bad and fgfr1 inhibition is soo negative to growth why would healthy non ACH patients have increased linear growth velocity? i mean its inhibiting fgfr2 and 1 which are sooo negative for growth, right? fucking dork if anything the inhibition is benefical outside of obviously mediating side effects.
 
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pan fgfr inhibitors dont even come close to mimicking full genetic knockout, like i said before, ur a retard, as for progenitor cells that turn into osteoblasts or chondrocytes, those are marginal amounts compared to the resting zone stem cells which are the primary source of progenitors for the growth plate and are all commited to the chondrogenic fate.

keep going with the ai slop to debate me lol mirin
so you've correctly identified the resting zone stem cells as the primary progenitor source "committed to the chondrogenic fate" (irreplaceable), great, however slight problem with your logic

do you know what role FGFR1 signalling plays specifically in maintaining resting zone quiescence and preventing premature progenitor depletion, and what pan-FGFR inhibition does to that population? It makes your point null.
 
the question is did YOU? in addition to ur crap, fgfr1 and 3 inhibition not only derepresses growth plate activity but also enhances IVD expansion, clearly u didnt read the literature but i for sure did. if the standard pan-fgfr inhibitors are soo bad and fgfr1 inhibition is soo negative to growth why would healthy non ACH patients have increased linear growth velocity? i mean its inhibiting fgfr2 and 1 which are sooo negative for growth, right? fucking dork if anything the inhibition is benefical outside of obviously mediating side effects.

There's no need to seethe, do you have citations for the healthy non ACH patients with increased linear growth velocity? would love to read where you found that tidbit
 
so you've correctly identified the resting zone stem cells as the primary progenitor source "committed to the chondrogenic fate" (irreplaceable), great, however slight problem with your logic

do you know what role FGFR1 signalling plays specifically in maintaining resting zone quiescence and preventing premature progenitor depletion, and what pan-FGFR inhibition does to that population? It makes your point null.
any effect of fgfr1 on the rz is insignificant given that pan fgfr inhibitor intervention doesnt prematurely exhaust the rz, give me one solid study where fgfr1 was a signficant contributor to rz maintenance, yeah theres none. and btw even if it did affect the rz in any NEAR signficant way, fgfr3 inhibition mediated ihh derepression would fully compensate for it and net positive too.
 
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There's no need to seethe, do you have citations for the healthy non ACH patients with increased linear growth velocity? would love to read where you found that tidbit
i do but im not gonna go out of my way to find it and link it just so mr takateo acknowledges my point, find it urself fag
 
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any effect of fgfr1 on the rz is insignificant given that pan fgfr inhibitor intervention doesnt prematurely exhaust the rz, give me one solid study where fgfr1 was a signficant contributor to rz maintenance, yeah theres none. and btw even if it did affect the rz in any NEAR signficant way, fgfr3 inhibition mediated ihh derepression would fully compensate for it and net positive too.
okay, so give you one study? but you can't cite your sources? How confidently absent minded of you.
i do but im not gonna go out of my way to find it and link it just so mr takateo acknowledges my point, find it urself fag
you are so cute, it's not for the acknowledgement, it's because if you cant provide scientific evidence to back up a scientific point, your point becomes worthless!
that and I thought it'd be nicer for you to let me choose which study I get to breakdown to you first :(
 
okay, so give you one study? but you can't cite your sources? How confidently absent minded of you.

you are so cute, it's not for the acknowledgement, it's because if you cant provide scientific evidence to back up a scientific point, your point becomes worthless!
that and I thought it'd be nicer for you to let me choose which study I get to breakdown to you first :(
if ur makin a retarded claim like that u better give literature proof, im not makin a retarded claim myself hence not going out of my way to cite a study that is already there if you just fucking search " erdafitinib growth plate pubmed".
 
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pan fgfr inhibitors dont even come close to mimicking full genetic knockout, like i said before, ur a retard, as for progenitor cells that turn into osteoblasts or chondrocytes, those are marginal amounts compared to the resting zone stem cells which are the primary source of progenitors for the growth plate and are all commited to the chondrogenic fate.

keep going with the ai slop to debate me lol mirin
im not using ai. anyway infig / erda hits all 4 fgfrs which is fucking ass. i dobt get why wont you pay a little more and get tyra which is selective on fgfr3. again look at fgfr1 knockout in people. shorts limbs , sub5 etc.
using infig wont „knockout „ tgese fgfrs but while using it you cant go „nuclear” like you could when using tyra. yeah its like twice as expensive but still way better than a nonselective drug. if u cant afford tyra nevapeg is still WAYYY better than infig.
 
im not using ai. anyway infig / erda hits all 4 fgfrs which is fucking ass. i dobt get why wont you pay a little more and get tyra which is selective on fgfr3. again look at fgfr1 knockout in people. shorts limbs , sub5 etc.
using infig wont „knockout „ tgese fgfrs but while using it you cant go „nuclear” like you could when using tyra. yeah its like twice as expensive but still way better than a nonselective drug. if u cant afford tyra nevapeg is still WAYYY better than infig.
firstly infig is a pan fgfr 1-3 inhib primarily, its so weak in binding affinity for fgfr4 that it doesnt matter at all, but even if erda and infig are pan fgfr inhibitors it does NOT fucking mean they would reproduce the same effects as full genetic deletion of fgfr1 retard, u keep sticking to ur moronic logic that if an fgfr inhibitor inhibits fgfr1 that it would stall out growth like conditional knockout humans born with it, erdafitinib doesnt even come close to full inhibition of fgfr1, matter fact there cannot be any TRKI that truly fully inhibits a kinase, if erdafitinib inhibited fgfr1 even at 80% every patient would get severe hyperphosphatemia ( which doesnt happen, they have mild hyperphosphatemia meaning there is enough fgfr1 for most biological processes).

as for your point in using tyra or transcon cnp, they are NOT twice as expensive, maybe 5x as expensive that is if u could source them, tyra is sourceable but expensive enough to not look at twice due to around 50mg dosing daily if i remember correctly. and even if you did buy it, erdafitinib would still sweep the floor with it.
 
firstly infig is a pan fgfr 1-3 inhib primarily, its so weak in binding affinity for fgfr4 that it doesnt matter at all, but even if erda and infig are pan fgfr inhibitors it does NOT fucking mean they would reproduce the same effects as full genetic deletion of fgfr1 retard, u keep sticking to ur moronic logic that if an fgfr inhibitor inhibits fgfr1 that it would stall out growth like conditional knockout humans born with it, erdafitinib doesnt even come close to full inhibition of fgfr1, matter fact there cannot be any TRKI that truly fully inhibits a kinase, if erdafitinib inhibited fgfr1 even at 80% every patient would get severe hyperphosphatemia ( which doesnt happen, they have mild hyperphosphatemia meaning there is enough fgfr1 for most biological processes).

as for your point in using tyra or transcon cnp, they are NOT twice as expensive, maybe 5x as expensive that is if u could source them, tyra is sourceable but expensive enough to not look at twice due to around 50mg dosing daily if i remember correctly. and even if you did buy it, erdafitinib would still sweep the floor with it.
no erda wont „sweep the floor” while being a pan fgfr inhibitor when our goal is inhibiting only fgfr3😭. plus when your running something like erda or infig you cannot get maximum potential out of the drug (max inhibiton on fgfr3) without sides. as far as i remember infig > erda because erda went too hard on fgfr4 (correct me if im wrong) still both drugs hit fgfr1and2 at the same strenght as fgfr3 so again you cannot go nuclear without sides. and yes you need to make sure your fgfr1 isnt nuked too much
 
no erda wont „sweep the floor” while being a pan fgfr inhibitor when our goal is inhibiting only fgfr3😭. plus when your running something like erda or infig you cannot get maximum potential out of the drug (max inhibiton on fgfr3) without sides. as far as i remember infig > erda because erda went too hard on fgfr4 (correct me if im wrong) still both drugs hit fgfr1and2 at the same strenght as fgfr3 so again you cannot go nuclear without sides. and yes you need to make sure your fgfr1 isnt nuked too much
yes it will retard, i do not care about in vitro data, when comparing in vivo results erdafitinib is clearly one of the most potent if not the most potent fgfr3 inhibitor. i also never FUCKING SAID ONCE THAT ERDA HAS NO SIDES IT DOES BUT TAKE AS MUCH OF TYRA AS U WANT AND UR NOT GONNA ACHIEVE BETTER RESULTS THAN THE STANDARD CLINICALLY TESTED 4-8MG. fucking retard repeating the same points even though i debunked them several times ur a fucking ragebaiter. and btw for your fgfr4 point, erda binds it the least selectively out of the other 3 receptor subtypes.
 
yes it will retard, i do not care about in vitro data, when comparing in vivo results erdafitinib is clearly one of the most potent if not the most potent fgfr3 inhibitor. i also never FUCKING SAID ONCE THAT ERDA HAS NO SIDES IT DOES BUT TAKE AS MUCH OF TYRA AS U WANT AND UR NOT GONNA ACHIEVE BETTER RESULTS THAN THE STANDARD CLINICALLY TESTED 4-8MG. fucking retard repeating the same points even though i debunked them several times ur a fucking ragebaiter. and btw for your fgfr4 point, erda binds it the least selectively out of the other 3 receptor subtypes.
if u dont care about in vitro data then you shouldn’t be touching pharmaceuticals. for reference look at this
fgfr1. 2. 3. 4
Infig~0.9 nM~1.4 nM~1.0 nM~60 nM
erda~1.2 nM~2.5 nM~1.8 nM~5-6nM

the lower the mM the stronger the drug inhibits it. i get why you „only look at in vivo” yeah the study where they used erda on a prepubertal boy and he got insane growth is promising BUT doesnt mean it sweeps the floor with tyra or infig. he probably wouldve grown taller if they switched the drug.

look at this study on fgfr 1 and 2.


i probably could be running infigatinib myself if i end up running short on money because i may not be able to afford both ky and tyra. *not looking good currently looking at the sources i have* but still
tyra>infig>erda.
ALL THESE DRUGS ARE VERY STRONG COMPARED TO ANYTHING ELSE but still inferior to tyra.
 
if u dont care about in vitro data then you shouldn’t be touching pharmaceuticals. for reference look at this
fgfr1. 2. 3. 4
Infig~0.9 nM~1.4 nM~1.0 nM~60 nM
erda~1.2 nM~2.5 nM~1.8 nM~5-6nM

the lower the mM the stronger the drug inhibits it. i get why you „only look at in vivo” yeah the study where they used erda on a prepubertal boy and he got insane growth is promising BUT doesnt mean it sweeps the floor with tyra or infig. he probably wouldve grown taller if they switched the drug.

look at this study on fgfr 1 and 2.


i probably could be running infigatinib myself if i end up running short on money because i may not be able to afford both ky and tyra. *not looking good currently looking at the sources i have* but still
tyra>infig>erda.
ALL THESE DRUGS ARE VERY STRONG COMPARED TO ANYTHING ELSE but still inferior to tyra.
can i get tyra source sir
 
if u dont care about in vitro data then you shouldn’t be touching pharmaceuticals. for reference look at this
fgfr1. 2. 3. 4
Infig~0.9 nM~1.4 nM~1.0 nM~60 nM
erda~1.2 nM~2.5 nM~1.8 nM~5-6nM

the lower the mM the stronger the drug inhibits it. i get why you „only look at in vivo” yeah the study where they used erda on a prepubertal boy and he got insane growth is promising BUT doesnt mean it sweeps the floor with tyra or infig. he probably wouldve grown taller if they switched the drug.

look at this study on fgfr 1 and 2.


i probably could be running infigatinib myself if i end up running short on money because i may not be able to afford both ky and tyra. *not looking good currently looking at the sources i have* but still
tyra>infig>erda.
ALL THESE DRUGS ARE VERY STRONG COMPARED TO ANYTHING ELSE but still inferior to tyra.
you are simply mistaken. sure infigratinib sounds good on paper but i said i dont care about in vitro studies if there are in vivo studies aswell, in vitro isnt always accurate at predicting results in a living species, if u look at those binding affinities u mentioned, infigratinib looks promising right? wrong, its only effective for ACH and barely at that anyway whereas erdafitinib has multiple in vivo healthy teenager studies showing dramatic results, its not one study showing one kid growing dramatically, its multiple. you also gotta understand binding affinities only show one side of the story, results in vivo are determined by the half life, permeability of the drug into the hypoxic growth plate cartilage, etc.

as for your point on fgfr1 knockout, you are extremely retarded to think that erda or infig replicate a genetic knockout because they dont even close CLOSE. even using high cancer doses of erdafitinib probably only inhibit 60 or less % of fgfr1 activity and if it did inhibit more or the untouched receptors didnt upregulate their expression then people would be dying left and right from extreme hyperphosphatemia that no fucking phosphate binder can prevent. for a drug to only cause mild hyperphosphatemia ( like erda at 5-6mg range) it means its nowhere near even a heterozygous mutation level of reduction of fgfr1 activity ( if a documented heterozygous mutation for fgfr1 even exists)
 
you are simply mistaken. sure infigratinib sounds good on paper but i said i dont care about in vitro studies if there are in vivo studies aswell, in vitro isnt always accurate at predicting results in a living species, if u look at those binding affinities u mentioned, infigratinib looks promising right? wrong, its only effective for ACH and barely at that anyway whereas erdafitinib has multiple in vivo healthy teenager studies showing dramatic results, its not one study showing one kid growing dramatically, its multiple. you also gotta understand binding affinities only show one side of the story, results in vivo are determined by the half life, permeability of the drug into the hypoxic growth plate cartilage, etc.

as for your point on fgfr1 knockout, you are extremely retarded to think that erda or infig replicate a genetic knockout because they dont even close CLOSE. even using high cancer doses of erdafitinib probably only inhibit 60 or less % of fgfr1 activity and if it did inhibit more or the untouched receptors didnt upregulate their expression then people would be dying left and right from extreme hyperphosphatemia that no fucking phosphate binder can prevent. for a drug to only cause mild hyperphosphatemia ( like erda at 5-6mg range) it means its nowhere near even a heterozygous mutation level of reduction of fgfr1 activity ( if a documented heterozygous mutation for fgfr1 even exists)

infig in achondroplasia children. yes its tested on humans and shows promising results.

and the study i showed before isnt a genetic knockout its a reduction in fgfr1-2. no i dont think of it inhibiting it completely
can you show studies your basing your opinion (erda>infing) on? erda and infig are almost the same just infig doesnt inhibit fgfr4 that much. corrext me if im wrong idk what studies you are referring too
 

infig in achondroplasia children. yes its tested on humans and shows promising results.

and the study i showed before isnt a genetic knockout its a reduction in fgfr1-2. no i dont think of it inhibiting it completely
can you show studies your basing your opinion (erda>infing) on? erda and infig are almost the same just infig doesnt inhibit fgfr4 that much. corrext me if im wrong idk what studies you are referring too
Just take a Phosphat binder and ur good
 
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infig in achondroplasia children. yes its tested on humans and shows promising results.

and the study i showed before isnt a genetic knockout its a reduction in fgfr1-2. no i dont think of it inhibiting it completely
can you show studies your basing your opinion (erda>infing) on? erda and infig are almost the same just infig doesnt inhibit fgfr4 that much. corrext me if im wrong idk what studies you are referring too
are u on infig?
 
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Cheap FGFR3 Inhibition: You Do Not Need to Spend thousands on mainstream FGFR3 inhibitors


FGFR3 is very important for how our bones and cartilage grow. It helps control how our bones form, which means it can stop our bones from growing much.


Because of this people have been studying drugs that can stop FGFR3 from working. One example is Infigratinib, which is used to treat cancer (And to ascend you).


The problem is that these drugs are extremely expensive. They can cost between fifteen thousand dollars and twenty thousand dollars per month which's just too much money for most people to pay.


If you read about the science behind these drugs you will find something


An FGFR Inhibitor: PD173074


A long time ago before we had modern FGFR inhibitors scientists were already using a compound called PD173074.


PD173074 is a molecule that stops FGFR1 and FGFR3 from working. It does this by binding to a part of the FGFR3, which's important for how it works. In experiments PD173074 is very good at stopping FGFR3.


Many scientists have used PD173074 to study how FGFR3 works. They have used it to see how FGFR3 is involved in how our bones and cartilage grow.


In words scientists have been studying FGFR3 inhibition with PD173074 for a long time even before the expensive drugs like Infigratinib were made.


Why It Never Became a Drug


Even though PD173074 is very good at stopping FGFR3 in experiments it was never made into a medicine. There are a reasons for this:


- it does not work well in the body

- it is not specific enough

- pharmaceutical companies made newer and better inhibitors


That is why newer drugs like Infigratinib, Erdafitinib and Futibatinib were used instead of PD173074.


Important Disclaimer


PD173074 is only sold for use in research. It is meant to be used in experiments like growing cells in a lab.

It is not approved as a medicine. There are no studies to show if it is safe for people to use. Because of this we should only talk about PD173074 in the context of research not for use.

Conclusion:

If you’re too broke to afford mainstream FGFR3 Inhibitors you may have a look into this. If you have the finances for the real stuff, that’s probably better for you - but no medical advice of course.
Won’t listen to grey with 40 rep
 

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