Erdafitinib vendor

[deadlytoastcat]

Anyone have a erdafitinib vendor because i see other vendors selling it for cheaper than indiamart?

 

[copecel4]

Anyone have a erdafitinib vendor because i see other vendors selling it for cheaper than indiamart?

erda is trash anyway

 

[exsttttt]

erda is trash anyway

quite literally the opposite

 

[copecel4]

quite literally the opposite

u have no idea what ur talking about, i can debunk ur ass rn but its not really worth the time. do some research instead of blindly taking medical advice from some tiktok retard jfl

 

[exsttttt]

u have no idea what ur talking about, i can debunk ur ass rn but its not really worth the time. do some research instead of blindly taking medical advice from some tiktok retard jfl

go ahead and debunk my ass fag and ive done more research than you would ever do in 10 years

 

[copecel4]

go ahead and debunk my ass fag and ive done more research than you would ever do in 10 years

You've obviously never read a single study in ur life u egomaxxed sub80 iq faggot

fgfr3 is very complex and all the tt retards u be getting ur information from dont mention the potential for growth stunting when inhibited.
Fgfr3 works mainly through downstream activation of ERK which the fgfr3 receptor maintains a postive feedback loop with itself by inhibiting the feedback from the cell to inhibit surface receptor signaling, through this mechanism it increases ERK but does this in a very prolonged way which leads to a response from the cell to increase p21 which inhibits the mitosis the ERK pathway would usually promote, fgfr3 also uses stat1 signaling which is proven in fgfr3 gain of function mutation but has mixed results in wild type fgfr3 signaling

now take a look at this

according to this interesting piece of evidence, fgfr3 is actually positive for the resting zone of the growth plates

also keep in mind that fgfr3 has opposite effect on resting zone chondrocytes compared to proliferation zone

Now let's take a look at something else that's interesting, many studies show different results when inhibiting fgfr3

mouse without fgfr3 actually looked shorter

in this study the bonos did get significantly larger than control, but that was likely a result of increased growth velocity and not final height (also mice dont really have a final height because their growth plates dont close)

this study also show an increase in VELOCITY after using the fgfr3 inhibitor TYRA300

in humans this was also shown by the pan fgfr inhibitor ERDAFTINIB.
whats interesting id that if u look at the xrays, u can see that after he got the growth spurt he stopped taking the fgfr inhibitor (erda) and actually his plates fusef almost completely after.
This suggests that the increased growth velocity also lead to depletion of the resting zone of the growth plates.

we can look further into this through the rodent study on another pan fgfr inhibitor known as AZD4547

the bones were actually shorter than DSMO vehicle jfl

also fgfr1 leads to severe skeletal hypoplasia.

There is a condition in humans called CATSHL syndrome and it is a loss of function of the fgfr3 gene, this leads to tall stature which directly proves fgfr3 inhibition can increase growth, although this condition also can cause bones to curve as they grow

inhibiting fgfr3 could possibly increase final height, but unfortunately people often can’t source or afford selective fgfr3 inhibitors, they use pan fgfr inhibitors like erdafitinib which could actually lead to shorter final adult height. Fgfr3 can become positive for height but signaling must be modified in order to make it growth promoting.

 

[exsttttt]

You've obviously never read a single study in ur life u egomaxxed sub80 iq faggot

fgfr3 is very complex and all the tt retards u be getting ur information from dont mention the potential for growth stunting when inhibited.
Fgfr3 works mainly through downstream activation of ERK which the fgfr3 receptor maintains a postive feedback loop with itself by inhibiting the feedback from the cell to inhibit surface receptor signaling, through this mechanism it increases ERK but does this in a very prolonged way which leads to a response from the cell to increase p21 which inhibits the mitosis the ERK pathway would usually promote, fgfr3 also uses stat1 signaling which is proven in fgfr3 gain of function mutation but has mixed results in wild type fgfr3 signaling
View attachment 4901105View attachment 4901108

now take a look at this
View attachment 4901112according to this interesting piece of evidence, fgfr3 is actually positive for the resting zone of the growth plates

also keep in mind that fgfr3 has opposite effect on resting zone chondrocytes compared to proliferation zone
View attachment 4901139

Now let's take a look at something else that's interesting, many studies show different results when inhibiting fgfr3
View attachment 4901154
mouse without fgfr3 actually looked shorter
View attachment 4901171 in this study the bonos did get significantly larger than control, but that was likely a result of increased growth velocity and not final height (also mice dont really have a final height because their growth plates dont close)

View attachment 4901201 this study also show an increase in VELOCITY after using the fgfr3 inhibitor TYRA300

View attachment 4901208 in humans this was also shown by the pan fgfr inhibitor ERDAFTINIB.
whats interesting id that if u look at the xrays, u can see that after he got the growth spurt he stopped taking the fgfr inhibitor (erda) and actually his plates fusef almost completely after.
This suggests that the increased growth velocity also lead to depletion of the resting zone of the growth plates.

we can look further into this through the rodent study on another pan fgfr inhibitor known as AZD4547
View attachment 4901318
the bones were actually shorter than DSMO vehicle jfl

View attachment 4901322
also fgfr1 leads to severe skeletal hypoplasia.

There is a condition in humans called CATSHL syndrome and it is a loss of function of the fgfr3 gene, this leads to tall stature which directly proves fgfr3 inhibition can increase growth, although this condition also can cause bones to curve as they grow
View attachment 4901336View attachment 4901338

inhibiting fgfr3 could possibly increase final height, but unfortunately people often can’t source or afford selective fgfr3 inhibitors, they use pan fgfr inhibitors like erdafitinib which could actually lead to shorter final adult height. Fgfr3 can become positive for height but signaling must be modified in order to make it growth promoting.

boohoo nigga imma rape u rq so u drop that fucking ego thinking u can get away w callin me an egomaxxed sub 80iq fag.

first two graphs u shared dont prove shit, one proves stat1 is one of the primary mediators of fgfr3 driven growth inhibition, the other says it aint so much signficant, but the general consensus proven by a signficant amount of studies is that its one of the primary drivers but not the most signficant.

for your second point on the rz, a big useless rz wont do shit but sit there, the rz is supposed to be used, the reason ach have a bigger rz is because the stem cells arent being forced to transition into the pz and then hz, fgfr3 inhibition doesnt have a negative impact plainly, just derepresses the assymmetrical divisions needed to flow into the pz.


third point, its fgfr3 neo/neo not null and i wont explain it to u as u should already know based on the graph faggot.

the sixth graph you sent proves you exactly wrong, fgfr3 homozygous mutations or full knockouts induce growth, indicating the false conclusion you made up on neo/neo without even knowing what the fuck it means you fucking moron.

the 7th graph on tyra shows an increase in velocity but that doesnt mean it wont increase final adult height, it just means they werent looking for conclusions on its impact on final adult height as it is pretty clear in countless other mouse studies and human cases with catshl or erdafitinib treatement for CNS cases.

the 8th graph that shows erdafitinib treatement and xrays according to timeline doesnt prove shit, if anything it indicates that the erdafitinib could have been delaying fusion, it does NOT mean rz was exhausted it would only have been proven so if they didnt discontinue erdafitinib treatement AND didnt start testosterone treatement. as usual, brainless data that you havent even read for more than 1min and didnt even understand what anything means.

AZD4547 is a signficantly off target multi kinase inhib drug, nowhere near selective to only the fgfr family of kinases.

and pan fgfr inhibs come nowhere near inhibiting fgfr1 at 100%, no molecule on earth no matter its selectivity or potency can inhibit a kinase the same as a genetic knockout.

as for CATSHL syndrom, its actually a homozygous mutation inhibiting only an allele of the two, so about 50% function of wt.


"Fgfr3 can become positive for height but signaling must be modified in order to make it growth promoting." nope, it never can be, how are you planning on a consecutive erk activation to become a pulsatile activation? no matter what you do, inhibit stat1, or anything else that fgfr3 uses for its growth inhibitory effects, you still cannot reproduce just inhibiting the receptor, mek/erk pathway would induce dwarfism if inhibited so you cannot touch it broadly as it is mitogenic in pulsatile activation ( such as igf1 driven erk signaling).


whos the egomaxxed fag now huh?

 

[groidslayer69]

boohoo nigga imma rape u rq so u drop that fucking ego thinking u can get away w callin me an egomaxxed sub 80iq fag.

first two graphs u shared dont prove shit, one proves stat1 is one of the primary mediators of fgfr3 driven growth inhibition, the other says it aint so much signficant, but the general consensus proven by a signficant amount of studies is that its one of the primary drivers but not the most signficant.

for your second point on the rz, a big useless rz wont do shit but sit there, the rz is supposed to be used, the reason ach have a bigger rz is because the stem cells arent being forced to transition into the pz and then hz, fgfr3 inhibition doesnt have a negative impact plainly, just derepresses the assymmetrical divisions needed to flow into the pz.


third point, its fgfr3 neo/neo not null and i wont explain it to u as u should already know based on the graph faggot.

the sixth graph you sent proves you exactly wrong, fgfr3 homozygous mutations or full knockouts induce growth, indicating the false conclusion you made up on neo/neo without even knowing what the fuck it means you fucking moron.

the 7th graph on tyra shows an increase in velocity but that doesnt mean it wont increase final adult height, it just means they werent looking for conclusions on its impact on final adult height as it is pretty clear in countless other mouse studies and human cases with catshl or erdafitinib treatement for CNS cases.

the 8th graph that shows erdafitinib treatement and xrays according to timeline doesnt prove shit, if anything it indicates that the erdafitinib could have been delaying fusion, it does NOT mean rz was exhausted it would only have been proven so if they didnt discontinue erdafitinib treatement AND didnt start testosterone treatement. as usual, brainless data that you havent even read for more than 1min and didnt even understand what anything means.

AZD4547 is a signficantly off target multi kinase inhib drug, nowhere near selective to only the fgfr family of kinases.

and pan fgfr inhibs come nowhere near inhibiting fgfr1 at 100%, no molecule on earth no matter its selectivity or potency can inhibit a kinase the same as a genetic knockout.

as for CATSHL syndrom, its actually a homozygous mutation inhibiting only an allele of the two, so about 50% function of wt.


"Fgfr3 can become positive for height but signaling must be modified in order to make it growth promoting." nope, it never can be, how are you planning on a consecutive erk activation to become a pulsatile activation? no matter what you do, inhibit stat1, or anything else that fgfr3 uses for its growth inhibitory effects, you still cannot reproduce just inhibiting the receptor, mek/erk pathway would induce dwarfism if inhibited so you cannot touch it broadly as it is mitogenic in pulsatile activation ( such as igf1 driven erk signaling).


whos the egomaxxed fag now huh?

holry diff