Hypothetical Stack for Maximum Epiphyseal Bone Growth

Im not gonna talk about what is obvious, everyone knows why the top compounds would be used.


rHGH at 15+ IU ED (as much as you can afford basically)


Letrozole 2.5mg ED (or any other AI at a dosage to nuke E2, but letro mogs)


Test + Tren (self explanatory)


Abaloparatide 80mcg ED (again, self explanatory)


Now the unusual stuff I am thinking about, I just put all of these together in a day so correct me if I make any retarded claims.


Infigratinib low dose :Daily treatment at 2 mg/kg significantly increased bone growth, and substantially lower doses of 0.2 and 0.5 mg/kg were sufficient to produce significant improvement of clinical hallmarks of achondroplasia including growth of the axial and appendicular skeleton.


Phase 3 human data also exists: Absolute AHV at week 52 favored infigratinib (5.96 vs 4.22 cm/year), the highest LS mean absolute AHV reported in a randomized achondroplasia trial


Tubastatin A :Wildtype and mutant activated forms of FGFR3 increase expression of HDAC6, and FGFR3 accumulation is compromised in cells lacking HDAC6 or following treatment with small molecule HDAC6 inhibitors. Both HDAC6 deletion and treatment with tubacin reduced FGFR3 accumulation in the growth plate and improved endochondral bone growth. Tubastatin A was likewise effective at reducing the accumulation of both wildtype and mutant FGFR3, and both tubacin and tubastatin A independently increased Sox9 expression in chondrocytes


LIPUS (Low Intensity Pulsed Ultrasound) In a randomized controlled animal trial in healthy immature rabbits, statistically significant differences in microscopic bone growth were observed between the LIPUS-stimulated legs and contralateral control legs (35%, p = 0.04), with no evidence of physeal bar formation


And now the most hypothetical part of this whole thing, trying to trigger growth on closed growth plates:


Surgical Microfracturing: No direct studies exist but in theory it seems possible? Atleast more possible than something like stem cells/yamanaka factors etc. Like I don't even know if it works but you wouldn't be able to do this anyways. I put this in because of this study: epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted, and once fusion occurs chondrocytes are replaced by bone elements in an abrupt event

 

[susisesi]

I used gpt to organize the studies and links btw idk if it messed it up the links dont work on my pc but does on my phone for some reason

 

[sherry12]

Im not gonna talk about what is obvious, everyone knows why the top compounds would be used.


rHGH at 15+ IU ED (as much as you can afford basically)


Letrozole 2.5mg ED (or any other AI at a dosage to nuke E2, but letro mogs)


Test + Tren (self explanatory)


Abaloparatide 80mcg ED (again, self explanatory)


Now the unusual stuff I am thinking about, I just put all of these together in a day so correct me if I make any retarded claims.


Infigratinib low dose :Daily treatment at 2 mg/kg significantly increased bone growth, and substantially lower doses of 0.2 and 0.5 mg/kg were sufficient to produce significant improvement of clinical hallmarks of achondroplasia including growth of the axial and appendicular skeleton.


Phase 3 human data also exists: Absolute AHV at week 52 favored infigratinib (5.96 vs 4.22 cm/year), the highest LS mean absolute AHV reported in a randomized achondroplasia trial


Tubastatin A :Wildtype and mutant activated forms of FGFR3 increase expression of HDAC6, and FGFR3 accumulation is compromised in cells lacking HDAC6 or following treatment with small molecule HDAC6 inhibitors. Both HDAC6 deletion and treatment with tubacin reduced FGFR3 accumulation in the growth plate and improved endochondral bone growth. Tubastatin A was likewise effective at reducing the accumulation of both wildtype and mutant FGFR3, and both tubacin and tubastatin A independently increased Sox9 expression in chondrocytes


LIPUS (Low Intensity Pulsed Ultrasound) In a randomized controlled animal trial in healthy immature rabbits, statistically significant differences in microscopic bone growth were observed between the LIPUS-stimulated legs and contralateral control legs (35%, p = 0.04), with no evidence of physeal bar formation


And now the most hypothetical part of this whole thing, trying to trigger growth on closed growth plates:


Surgical Microfracturing: No direct studies exist but in theory it seems possible? Atleast more possible than something like stem cells/yamanaka factors etc. Like I don't even know if it works but you wouldn't be able to do this anyways. I put this in because of this study: epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted, and once fusion occurs chondrocytes are replaced by bone elements in an abrupt event

Im sure if u started this young enough u could be 6+ inches taller then without good luck

 

[susisesi]

Im sure if u started this young enough u could be 6+ inches taller then without good luck

closed plates alr

just researching it because it interrests me, and maybe ill get cranifacial or frame gains.

With that said if I could be a labrat for microfratures / stem cels / Morphogen gradient reconstruction / Controlled distraction hardware. I would deffienetly volunteer.

Saying allat while being 6’2 but I am just salty that I didn’t get to do any heightmaxxing at all. Closed playes at 14-15

 

[Zagro]

Remove infig it stunts growth and remove tubastatin it’s pretty redundant on high dose gh

Surgical microfracturing sounds like Orc’s boen scratching method

 

[ilovedominos26]

Do I need to dose letrozole ed? Or could I do like 2.5 mg twice a week? Also is estrogen rebound a myth? Woulfnt estrogen just return to normal after hopping off?

 

[cometohaunted]

Im not gonna talk about what is obvious, everyone knows why the top compounds would be used.


rHGH at 15+ IU ED (as much as you can afford basically)


Letrozole 2.5mg ED (or any other AI at a dosage to nuke E2, but letro mogs)


Test + Tren (self explanatory)


Abaloparatide 80mcg ED (again, self explanatory)


Now the unusual stuff I am thinking about, I just put all of these together in a day so correct me if I make any retarded claims.


Infigratinib low dose :Daily treatment at 2 mg/kg significantly increased bone growth, and substantially lower doses of 0.2 and 0.5 mg/kg were sufficient to produce significant improvement of clinical hallmarks of achondroplasia including growth of the axial and appendicular skeleton.


Phase 3 human data also exists: Absolute AHV at week 52 favored infigratinib (5.96 vs 4.22 cm/year), the highest LS mean absolute AHV reported in a randomized achondroplasia trial


Tubastatin A :Wildtype and mutant activated forms of FGFR3 increase expression of HDAC6, and FGFR3 accumulation is compromised in cells lacking HDAC6 or following treatment with small molecule HDAC6 inhibitors. Both HDAC6 deletion and treatment with tubacin reduced FGFR3 accumulation in the growth plate and improved endochondral bone growth. Tubastatin A was likewise effective at reducing the accumulation of both wildtype and mutant FGFR3, and both tubacin and tubastatin A independently increased Sox9 expression in chondrocytes


LIPUS (Low Intensity Pulsed Ultrasound) In a randomized controlled animal trial in healthy immature rabbits, statistically significant differences in microscopic bone growth were observed between the LIPUS-stimulated legs and contralateral control legs (35%, p = 0.04), with no evidence of physeal bar formation


And now the most hypothetical part of this whole thing, trying to trigger growth on closed growth plates:


Surgical Microfracturing: No direct studies exist but in theory it seems possible? Atleast more possible than something like stem cells/yamanaka factors etc. Like I don't even know if it works but you wouldn't be able to do this anyways. I put this in because of this study: epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted, and once fusion occurs chondrocytes are replaced by bone elements in an abrupt event

All of heightmaxxing is just hypothetical it's honestly barely worth thinking about Mirin the effort tho

 

[cyrixxy]

Remove infig it stunts growth and remove tubastatin it’s pretty redundant on high dose gh

Surgical microfracturing sounds like Orc’s boen scratching method

how does infi stunt growth

 

[Zagro]

how does infi stunt growth

It inhibits FGFR1 and FGFR2 and although FGFR1 is a negative factor for growth inhibiting FGFR2 is insanely bad for you

Also the consequences of inhibiting 1 and 2 are:

“The mean bone density value for the lumbar spine measured 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.”

 

[cyrixxy]

It inhibits FGFR1 and FGFR2 and although FGFR1 is a negative factor for growth inhibiting FGFR2 is insanely bad for you

Also the consequences of inhibiting 1 and 2 are:

“The mean bone density value for the lumbar spine measured 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.”

View attachment 4809396

so even lower doses of 0.25-20mg/kg are harmful? Is this the same with others like erda/vosotride im guessing. and trya 300 is good because it inhibits specifically just fgfr3 or am i wrong?(yes we are all to poor to afford it anyways) I was talking to someone on 25mg of infi per day and he told me he grew 3cm in the first month, with him being currently on for 1 1/2 months (how true that is idk but he was a chill guy tbf), but would this hypothetically stunt his growth and close his plates earlier with earlier bone maturation

 

[birthdefect]

so even lower doses of 0.25-20mg/kg are harmful? Is this the same with others like erda/vosotride im guessing. and trya 300 is good because it inhibits specifically just fgfr3 or am i wrong?(yes we are all to poor to afford it anyways) I was talking to someone on 25mg of infi per day and he told me he grew 3cm in the first month, with him being currently on for 1 1/2 months (how true that is idk but he was a chill guy tbf), but would this hypothetically stunt his growth and close his plates earlier with earlier bone maturation

not voso, voso mogs

 

[cyrixxy]

not voso, voso mogs

how come (too expensive anyways) but

 

[Zagro]

so even lower doses of 0.25-20mg/kg are harmful? Is this the same with others like erda/vosotride im guessing. and trya 300 is good because it inhibits specifically just fgfr3 or am i wrong?(yes we are all to poor to afford it anyways) I was talking to someone on 25mg of infi per day and he told me he grew 3cm in the first month, with him being currently on for 1 1/2 months (how true that is idk but he was a chill guy tbf), but would this hypothetically stunt his growth and close his plates earlier with earlier bone maturation

Voso and tyra (yes it’s good because of FGFR3 selectivity) are the only fathomable decent options and erda is even more horrible

These case reports and studies are in low-doses

He’s fucking lying and larping lmao don’t trust everyone that tells you “bro i took “x” compound for “x” amount of time and grew insanely”

It will cause less adult height, insanely bad BMD so potentially osteoporosis, multiple HORRIBLE side-effects and spinal deformities which are seen in humans and mice with literally above 50% potential of happening for maybe faster growth velocity and less final height

There are much better “niche” compounds you could take if you wanna feel like special or some shit cause idk what the fuck y’all want other than gh, ai and androgens

 

[cyrixxy]

Voso and tyra (yes it’s good because of FGFR3 selectivity) are the only fathomable decent options and erda is even more horrible

These case reports and studies are in low-doses

He’s fucking lying and larping lmao don’t trust everyone that tells you “bro i took “x” compound for “x” amount of time and grew insanely”

It will cause less adult height, insanely bad BMD so potentially osteoporosis, multiple HORRIBLE side-effects and spinal deformities which are seen in humans and mice with literally above 50% potential of happening for maybe faster growth velocity and less final height

There are much better “niche” compounds you could take if you wanna feel like special or some shit cause idk what the fuck y’all want other than gh, ai and androgens

like pth analogues or what else (im completely clueless on this field), im planning to go on 8-10iu with ai ( no test ) but if ofter things have a chance of helping likeeeee

 

[Zagro]

like pth analogues or what else (im completely clueless on this field), im planning to go on 8-10iu with ai ( no test ) but if ofter things have a chance of helping likeeeee

Honestly just increase your rhGH dose if you have the money left instead of these “niche” comps. You’ll get both the effects of FGFR3 inhibition and HDAC6 inhibition at a decent rate but of course not full blown inhibition as the selective drugs achieve

 

[cyrixxy]

Honestly just increase your rhGH dose if you have the money left instead of these “niche” comps. You’ll get both the effects of FGFR3 inhibition and HDAC6 inhibition at a decent rate but of course not full blown inhibition as the selective drugs achieve

over 10 iu? what like 12-15? isnt my heart gonna explode while I develop diabetesprob the best choice regardless

 

[Zagro]

over 10 iu? what like 12-15? isnt my heart gonna explode while I develop diabetesprob the best choice regardless

Systemic/hepatic igf will already almost plateau at these dosages but that’s fucking useless anyways increasing dose helps with more free igf which is the goal and we can override the pathways more

I’m on 18 and my heart is still intact, but cardiomegaly can indeed be a little concern if you plan to take it upwards of a year potentially but no one here has like 2-3 years of growth left anyways

 

[cyrixxy]

Systemic/hepatic igf will already almost plateau at these dosages but that’s fucking useless anyways increasing dose helps with more free igf which is the goal and we can override the pathways more

I’m on 18 and my heart is still intact, but cardiomegaly can indeed be a little concern if you plan to take it upwards of a year potentially but no one here has like 2-3 years of growth left anyways

18how is ur blood glucose levels not crazy high. I heard things like berebine can help keep it in check but also heard its cope , i try to cut out most sugar now anyway i guess.
Also, if i do want to do a dose like 12-14iu etc, how fast can i accelerate it, like start on 6 and go up by 2iu every week until i reach my target?

 

[infrainfra]

It inhibits FGFR1 and FGFR2 and although FGFR1 is a negative factor for growth inhibiting FGFR2 is insanely bad for you

Also the consequences of inhibiting 1 and 2 are:

“The mean bone density value for the lumbar spine measured 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.”

View attachment 4809396

how do you know these „decrease FAH”
anyway in vitro studies dont matter too much if you got in vivo studies. every time kids take erdafitinib they get insane growth spurts even causes scoliosis in one case. and yeah acting like you can get tyra even though its like 500$ per gram from sketchy sources lmao. just because in vitro infig/erda supress fgfr2 doesnt mean they will cause negative effects on height. you need to look wt the drugs half-life , delivery to growth plates etc.

also infig is being used in children with achondroplasia and its giving good results +3cm yearly as far as i remember

 

[Zagro]

how do you know these „decrease FAH”
anyway in vitro studies dont matter too much if you got in vivo studies. every time kids take erdafitinib they get insane growth spurts even causes scoliosis in one case. and yeah acting like you can get tyra even though its like 500$ per gram from sketchy sources lmao. just because in vitro infig/erda supress fgfr2 doesnt mean they will cause negative effects on height. you need to look wt the drugs half-life , delivery to growth plates etc.

also infig is being used in children with achondroplasia and its giving good results +3cm yearly as far as i remember

Are you okay bro?

“Yeah bro i pay 500$ for my fake (guaranteed) sketchy tyra-300 haha”

Omg children with FGFR mutations see an increase in growth when the mutation is reversed no way!!! So rhGH given to GHD also is guaranteed to work the same way right we don’t even need to look into it everything that gives height will work

“Just because in vitro” please tell me you know that infigratinib is literally a known proven FGFR 1-3 inhibitor, and i did not cherry-pick studies or extrapolate this is literally what it is.

“you need to look wt the drugs half-life , delivery to growth plates etc”

yes bro infigratinib works systemically and inhibits FGFR3 and works in achondroplasia models but it somehow when it comes to FGFR2 it wont reach the plates very correct

Do not talk back to me man you don’t understand anything I’m losing braincells. “BUT BRO ANTON VERADA TOLD ME IT WORKS”

 

[infrainfra]

Omg children with FGFR mutations see an increase in growth when the mutation is reversed no way!!! So rhGH given to GHD also is guaranteed to work the same way right we don’t even need to look into it everything that gives height will work

no a child with brain cancer not a fgfr3 mutation received erdafitnib and got a massive growth spurt without changes in serum testosterone or igf-1 (pre puberty) and the authors of the study clearly stated that the unnatural growth is due to the drug.

Just because in vitro” please tell me you know that infigratinib is literally a known proven FGFR 1-3 inhibitor, and i did not cherry-pick studies or extrapolate this is literally what it is.

yeah erda is signficantly better in vivo despite looking as potent as infig in vitro while not being as selective, maybe its the molecular structure penetrating the hypoxic cartilage better or just different in vivo selectivity; there are studies showing erda induces growth at even 4mg, there was a case on a kid with cancer, gave him erda and he had severe hyperphosphatemia, they got him down to 4mg to manage hyperphosphatemia, and he still had a significant growth spurt which is something infigratinib cant even come close to IN ACH KIDS, so if its more potent in healthy humans than infig is on ach kids, u can sum it up, there really isnt that many studies to prove why its that much better but it has to do with the molecule itself or just being more potent at fgfr3 than they thought it was in a petri dish „b - but it inhibits fgfr2 which is needed for growth”

yes bro infigratinib works systemically and inhibits FGFR3 and works in achondroplasia models but it somehow when it comes to FGFR2 it wont reach the plates very correct

first of all infig <erda second off all thats why in vivo and in vitro studies exist and in vivo erda always causes abnormal growth i so does infig but not as much. doesnt take a lot of time to look at pubmed

 

[Zagro]

no a child with brain cancer not a fgfr3 mutation received erdafitnib and got a massive growth spurt without changes in serum testosterone or igf-1 (pre puberty) and the authors of the study clearly stated that the unnatural growth is due to the drug.

yeah erda is signficantly better in vivo despite looking as potent as infig in vitro while not being as selective, maybe its the molecular structure penetrating the hypoxic cartilage better or just different in vivo selectivity; there are studies showing erda induces growth at even 4mg, there was a case on a kid with cancer, gave him erda and he had severe hyperphosphatemia, they got him down to 4mg to manage hyperphosphatemia, and he still had a significant growth spurt which is something infigratinib cant even come close to IN ACH KIDS, so if its more potent in healthy humans than infig is on ach kids, u can sum it up, there really isnt that many studies to prove why its that much better but it has to do with the molecule itself or just being more potent at fgfr3 than they thought it was in a petri dish „b - but it inhibits fgfr2 which is needed for growth”

first of all infig <erda second off all thats why in vivo and in vitro studies exist and in vivo erda always causes abnormal growth i so does infig but not as much. doesnt take a lot of time to look at pubmed

“https://pubmed.ncbi.nlm.nih.gov/39555818/?utm_source“

Okay now tell me why your last post has this study link, hmm what does the utm source mean here? With with ai did you get this information retard

whilst the normal link looks like this https://pubmed.ncbi.nlm.nih.gov/39555818/

Before tryna larp high, try to interpret studies yourself and i wont even waste time here

You’re a real big retard but not the biggest, shitty ahh logic “But anastrozole treated kids grew 0.6cm taller compared to letrozole so it should mean that it’s better” same shit as “erda showed 0.1cm more growth velocity compared to infig in a case-report so it’s better”.

Omg one case report shows growth, but did you know if it was a growth spurt and then a sudden stop which is basically shorter FAH, Because FGFR2 is like a reservoir pool typa thing like RZCs

 

[infrainfra]

Okay now tell me why your last post has this study link, hmm what does the utm source mean here? With with ai did you get this information retard

yeah ok i type in a „show me _____ studies and send links” to save time. this is irrelevant if i read these through ai or google. or i get a pubmed study and copy paste to summorize it because my attention span is cooked. as i said completely irrelevant i still got the knowledge.

my last posts where just a rough draft of the knowledge i have now and ive completely changed my entire approach. im still limited by money so ill be using erda if i can get ny hands on it.

Omg one case report shows growth, but did you know if it was a growth spurt and then a sudden stop which is basically shorter FAH, Because FGFR2 is like a reservoir pool typa thing like RZCs

how would you know its a „sudden stop” and that one study where a kids plates closed after they stopped erda wasn’t because of the drug it was because they started testosterone without an ai. you should know what happens then. and no fgfr2 doesnt even come close to a reservoir pool wtf are you even talking about. RZCs store cells over time and self-renew fgfr2 is just a receptor sitting on cells it controls shit like how fast cells divide and when they differentiate it doesnt act like a supply tank.

 

[Zagro]

yeah ok i type in a „show me _____ studies and send links” to save time. this is irrelevant if i read these through ai or google. or i get a pubmed study and copy paste to summorize it because my attention span is cooked. as i said completely irrelevant i still got the knowledge.

Straight to my ignores son, "yes i have no knowledge and rely on whatever google or ChatGPT tells me, i cant interpret study nor read them myself, i also find every single study and form my counter-arguments through GPT, but i still have the knowledge yeah".

GTFO bro

"doesnt take a lot of time to look at pubmed"

HHHHHHHHAAAAHAHHHHahahaaaaaaaaaahahhhhhhhhhhhhahaha you are the biggest retard now, you have that title now nws.

"and no fgfr2 doesnt even come close to a reservoir pool wtf are you even talking about. RZCs store cells over time and self-renew fgfr2 is just a receptor sitting on cells it controls shit like how fast cells divide and when they differentiate it doesnt act like a supply tank."

No bro FGFR2 isn't a reservoir like RZCs, but yeah both are relevant to how fast differentiation is achieved but yeah RZCs depleting and FGFR2 regulating the same thing isn't comparable no. Also you said it yourself you FUCKING IDIOT it regulates how fast they divide and regulate meaning it regulates proliferation and differentiation, you get a sudden increase in height short-term but plates close faster=the final height is lower because of how fast you go through stages like proliferation and differentiation

 

[childishkillah]

Orc’s boen scratching method

What da hell is that?