Guide FGFR3 inhibtion- epiphyseal plates and bone growth (4 Viewers)

[reazy]

So ??

can not find anything, or any site without customs, only anti-histamine getting sold is Dimenhydrinat

 

[Biomaxx]

Introduction:
Growth Plates and FGFR3

View attachment 22765​

Epiphyseal (growth) plates are zones of proliferating and hypertrophic chondrocytes near the ends of long bones. These regions drive longitudinal growth during childhood and adolescence.

Fibroblast growth factor receptor 3 (FGFR3) is a membrane receptor that modulates growth by binding fibroblast growth factors such as FGF18 and FGF9. Once activated, FGFR3 triggers MAPK and STAT signaling cascades that decrease chondrocyte proliferation and accelerate differentiation.

Too much FGFR3 signaling shortens bones (as in achondroplasia). Removing FGFR3 function lengthens bones in animal models.

In mid‑puberty (Tanner stage IV), estrogen rises and pushes the growth plates toward senescence and closure.
(Which I why aromatase inhibitors should be paired but ill get into that another time)

Blocking FGFR3 at this stage could prolong chondrocyte proliferation, slow epiphyseal fusion, and increase final height. Preclinical studies with selective FGFR3 inhibitors have shown increases in femur and tibia length when given before closure.

View attachment 22767
(Refer to meclozine-
FGFR3 Inhibitors (paragraph 5 ))



FGFR3 Inhibitors​

Recifercept – a soluble decoy receptor that binds FGF ligands and prevents them from activating FGFR3. It was administered by weekly subcutaneousinjections at roughly 1 mg/kg in early trials. Development halted after phase II.

Infigratinib – an oral tyrosine kinase inhibitor of FGFR1–3. In achondroplasia children, about 0.128 mg/kg/day increased height velocity by ~1.5 cm/year. Doses up to 0.25 mg/kg/day are being tested.

Vofatamab – a monoclonal antibody that blocks the extracellular domain of FGFR3. It was used in oncology at 10–20 mg/kg IV every few weeks. Proposed for growth plate modulation but not trialed in adolescents.

Vosoritide – a C‑type natriuretic peptide analog that activates guanylate cyclase and inhibits the MAPK pathway downstream of FGFR3. Approved for achondroplasia; 15 µg/kg/day subcutaneously increases growth velocity by ~1.6 cm/year.
(Ill get into cnp analogs in another thread)

Meclozine – an antihistamine found to attenuate FGFR3 signaling in cell models. Doses around 1–2 mg/kg twice daily increased long‑bone length in mice. Safety in adolescents for height is untested.

Statins – cholesterol‑lowering drugs that improved chondrogenesis and bone growth in achondroplasia models. Mechanism may involve BMP signaling. Typical cholesterol doses were used in animal studies; human data are lacking.

InhibitorMechanismTypical Dosage​

Recifercept
Decoy receptor for FGF ligands~1 mg/kg weeklySubcutaneousDiscontinued development

Infigratinib
FGFR1–3 tyrosine kinase inhibitor0.128–0.25 mg/kg/dayOralPhase II pediatric trials

Vofatamab
FGFR3 monoclonal antibody10–20 mg/kg every few weeksIntravenousUsed in oncology

VosoritideC‑type natriuretic peptide analog
15 µg/kg/daySubcutaneousApproved for achondroplasia

MeclozineAntihistamine;
downstream MAPK inhibition1–2 mg/kg twice dailyOralAnimal data only

Statins
Cholesterol synthesis inhibitors; possible BMP modulationStandard dosesOralExperimental use

Predicted Effect by Bone Age
View attachment 22768View attachment 22770​

Bone age influences how much additional height can be gained by blocking FGFR3.
Estrogen exposure increases with age, driving plates toward closure.
The earlier the intervention, the greater the potential gain.

14 years – Mid‑puberty
Growth plates are thick and proliferative; FGFR3 blockade could add several centimeters. This stage offers the highest potential.

15 years – Mid‑late puberty
Plates are thinning; growth slows. FGFR3 inhibition still helps but estrogen now accelerates closure.

16 years – Late puberty
Plates are nearly exhausted; benefits are modest unless estrogen production is suppressed (e.g., with aromatase inhibitors).

17 years - typically end of puberty
Most plates have fused; little to no height can be added by inhibiting FGFR3.

Safety, Monitoring, and Supportive Measures
View attachment 22769​

Hyperphosphatemia and mineral imbalance –

FGFR signaling affects kidney handling of phosphate via FGF23. Inhibitors can cause phosphate retention and lower vitamin D levels. Check serum phosphate, calcium, and vitamin D during treatment.

Hepatic and renal function –

FGFR inhibitors are metabolized and excreted through liver and kidneys. Routine liver function tests and serum creatinine are prudent.

Gastrointestinal and appetite changes –

Mild dyspepsia, decreased appetite, and flatulence have been reported. Monitor weight and nutritional status.

Osteochondromas and abnormal growth


FGFR3 normally restricts chondrocyte proliferation. Complete suppression can lead to benign cartilage tumors and dysregulated bone overgrowth. Orthopedic evaluation and imaging help detect such problems early.

Hormonal modulation –

Estrogen drives epiphyseal closure. Combining FGFR3 inhibitors with aromatase inhibitors delays estrogen formation and can further prolong growth plates. Testosterone is converted to estrogen via aromatase, suppressing this step slows closure.

Supportive nutrition –

Adequate calcium, protein, and vitamin D are required for osteoblast function and bone mineralization. Ensure dietary intake meets increased growth demands.


0nce the growth plates have fused, further inhibition of FGFR3 does not provide additional height. Terminate therapy when radiographs confirm epiphyseal closure and continue regular follow‑up to monitor bone health.

TheCoolDude2000 for the idea

Spoiler: Tags

Mandy B BastiHgH Godveil Heir Primalwontsaveme Circadex howdoi T Testicular O ogre
birthdefect acromegalic

rip section-
9Dino
Ogre_cel
longhairedChad
hide
Mirilow

Bump

 

[khanlite]

good thing i found this 2 years too late

 

[weedforinhib]

Introduction:
Growth Plates and FGFR3

View attachment 22765​

Epiphyseal (growth) plates are zones of proliferating and hypertrophic chondrocytes near the ends of long bones. These regions drive longitudinal growth during childhood and adolescence.

Fibroblast growth factor receptor 3 (FGFR3) is a membrane receptor that modulates growth by binding fibroblast growth factors such as FGF18 and FGF9. Once activated, FGFR3 triggers MAPK and STAT signaling cascades that decrease chondrocyte proliferation and accelerate differentiation.

Too much FGFR3 signaling shortens bones (as in achondroplasia). Removing FGFR3 function lengthens bones in animal models.

In mid‑puberty (Tanner stage IV), estrogen rises and pushes the growth plates toward senescence and closure.
(Which I why aromatase inhibitors should be paired but ill get into that another time)

Blocking FGFR3 at this stage could prolong chondrocyte proliferation, slow epiphyseal fusion, and increase final height. Preclinical studies with selective FGFR3 inhibitors have shown increases in femur and tibia length when given before closure.

View attachment 22767
(Refer to meclozine-
FGFR3 Inhibitors (paragraph 5 ))



FGFR3 Inhibitors​

Recifercept – a soluble decoy receptor that binds FGF ligands and prevents them from activating FGFR3. It was administered by weekly subcutaneousinjections at roughly 1 mg/kg in early trials. Development halted after phase II.

Infigratinib – an oral tyrosine kinase inhibitor of FGFR1–3. In achondroplasia children, about 0.128 mg/kg/day increased height velocity by ~1.5 cm/year. Doses up to 0.25 mg/kg/day are being tested.

Vofatamab – a monoclonal antibody that blocks the extracellular domain of FGFR3. It was used in oncology at 10–20 mg/kg IV every few weeks. Proposed for growth plate modulation but not trialed in adolescents.

Vosoritide – a C‑type natriuretic peptide analog that activates guanylate cyclase and inhibits the MAPK pathway downstream of FGFR3. Approved for achondroplasia; 15 µg/kg/day subcutaneously increases growth velocity by ~1.6 cm/year.
(Ill get into cnp analogs in another thread)

Meclozine – an antihistamine found to attenuate FGFR3 signaling in cell models. Doses around 1–2 mg/kg twice daily increased long‑bone length in mice. Safety in adolescents for height is untested.

Statins – cholesterol‑lowering drugs that improved chondrogenesis and bone growth in achondroplasia models. Mechanism may involve BMP signaling. Typical cholesterol doses were used in animal studies; human data are lacking.

InhibitorMechanismTypical Dosage​

Recifercept
Decoy receptor for FGF ligands~1 mg/kg weeklySubcutaneousDiscontinued development

Infigratinib
FGFR1–3 tyrosine kinase inhibitor0.128–0.25 mg/kg/dayOralPhase II pediatric trials

Vofatamab
FGFR3 monoclonal antibody10–20 mg/kg every few weeksIntravenousUsed in oncology

VosoritideC‑type natriuretic peptide analog
15 µg/kg/daySubcutaneousApproved for achondroplasia

MeclozineAntihistamine;
downstream MAPK inhibition1–2 mg/kg twice dailyOralAnimal data only

Statins
Cholesterol synthesis inhibitors; possible BMP modulationStandard dosesOralExperimental use

Predicted Effect by Bone Age
View attachment 22768View attachment 22770​

Bone age influences how much additional height can be gained by blocking FGFR3.
Estrogen exposure increases with age, driving plates toward closure.
The earlier the intervention, the greater the potential gain.

14 years – Mid‑puberty
Growth plates are thick and proliferative; FGFR3 blockade could add several centimeters. This stage offers the highest potential.

15 years – Mid‑late puberty
Plates are thinning; growth slows. FGFR3 inhibition still helps but estrogen now accelerates closure.

16 years – Late puberty
Plates are nearly exhausted; benefits are modest unless estrogen production is suppressed (e.g., with aromatase inhibitors).

17 years - typically end of puberty
Most plates have fused; little to no height can be added by inhibiting FGFR3.

Safety, Monitoring, and Supportive Measures
View attachment 22769​

Hyperphosphatemia and mineral imbalance –

FGFR signaling affects kidney handling of phosphate via FGF23. Inhibitors can cause phosphate retention and lower vitamin D levels. Check serum phosphate, calcium, and vitamin D during treatment.

Hepatic and renal function –

FGFR inhibitors are metabolized and excreted through liver and kidneys. Routine liver function tests and serum creatinine are prudent.

Gastrointestinal and appetite changes –

Mild dyspepsia, decreased appetite, and flatulence have been reported. Monitor weight and nutritional status.

Osteochondromas and abnormal growth


FGFR3 normally restricts chondrocyte proliferation. Complete suppression can lead to benign cartilage tumors and dysregulated bone overgrowth. Orthopedic evaluation and imaging help detect such problems early.

Hormonal modulation –

Estrogen drives epiphyseal closure. Combining FGFR3 inhibitors with aromatase inhibitors delays estrogen formation and can further prolong growth plates. Testosterone is converted to estrogen via aromatase, suppressing this step slows closure.

Supportive nutrition –

Adequate calcium, protein, and vitamin D are required for osteoblast function and bone mineralization. Ensure dietary intake meets increased growth demands.


0nce the growth plates have fused, further inhibition of FGFR3 does not provide additional height. Terminate therapy when radiographs confirm epiphyseal closure and continue regular follow‑up to monitor bone health.

TheCoolDude2000 for the idea

Spoiler: Tags

Mandy B BastiHgH Godveil Heir Primalwontsaveme Circadex howdoi T Testicular O ogre
birthdefect acromegalic

rip section-
9Dino
Ogre_cel
longhairedChad
hide
Mirilow

mirin

 

[weedforinhib]

Introduction:
Growth Plates and FGFR3

View attachment 22765​

Epiphyseal (growth) plates are zones of proliferating and hypertrophic chondrocytes near the ends of long bones. These regions drive longitudinal growth during childhood and adolescence.

Fibroblast growth factor receptor 3 (FGFR3) is a membrane receptor that modulates growth by binding fibroblast growth factors such as FGF18 and FGF9. Once activated, FGFR3 triggers MAPK and STAT signaling cascades that decrease chondrocyte proliferation and accelerate differentiation.

Too much FGFR3 signaling shortens bones (as in achondroplasia). Removing FGFR3 function lengthens bones in animal models.

In mid‑puberty (Tanner stage IV), estrogen rises and pushes the growth plates toward senescence and closure.
(Which I why aromatase inhibitors should be paired but ill get into that another time)

Blocking FGFR3 at this stage could prolong chondrocyte proliferation, slow epiphyseal fusion, and increase final height. Preclinical studies with selective FGFR3 inhibitors have shown increases in femur and tibia length when given before closure.

View attachment 22767
(Refer to meclozine-
FGFR3 Inhibitors (paragraph 5 ))



FGFR3 Inhibitors​

Recifercept – a soluble decoy receptor that binds FGF ligands and prevents them from activating FGFR3. It was administered by weekly subcutaneousinjections at roughly 1 mg/kg in early trials. Development halted after phase II.

Infigratinib – an oral tyrosine kinase inhibitor of FGFR1–3. In achondroplasia children, about 0.128 mg/kg/day increased height velocity by ~1.5 cm/year. Doses up to 0.25 mg/kg/day are being tested.

Vofatamab – a monoclonal antibody that blocks the extracellular domain of FGFR3. It was used in oncology at 10–20 mg/kg IV every few weeks. Proposed for growth plate modulation but not trialed in adolescents.

Vosoritide – a C‑type natriuretic peptide analog that activates guanylate cyclase and inhibits the MAPK pathway downstream of FGFR3. Approved for achondroplasia; 15 µg/kg/day subcutaneously increases growth velocity by ~1.6 cm/year.
(Ill get into cnp analogs in another thread)

Meclozine – an antihistamine found to attenuate FGFR3 signaling in cell models. Doses around 1–2 mg/kg twice daily increased long‑bone length in mice. Safety in adolescents for height is untested.

Statins – cholesterol‑lowering drugs that improved chondrogenesis and bone growth in achondroplasia models. Mechanism may involve BMP signaling. Typical cholesterol doses were used in animal studies; human data are lacking.

InhibitorMechanismTypical Dosage​

Recifercept
Decoy receptor for FGF ligands~1 mg/kg weeklySubcutaneousDiscontinued development

Infigratinib
FGFR1–3 tyrosine kinase inhibitor0.128–0.25 mg/kg/dayOralPhase II pediatric trials

Vofatamab
FGFR3 monoclonal antibody10–20 mg/kg every few weeksIntravenousUsed in oncology

VosoritideC‑type natriuretic peptide analog
15 µg/kg/daySubcutaneousApproved for achondroplasia

MeclozineAntihistamine;
downstream MAPK inhibition1–2 mg/kg twice dailyOralAnimal data only

Statins
Cholesterol synthesis inhibitors; possible BMP modulationStandard dosesOralExperimental use

Predicted Effect by Bone Age
View attachment 22768View attachment 22770​

Bone age influences how much additional height can be gained by blocking FGFR3.
Estrogen exposure increases with age, driving plates toward closure.
The earlier the intervention, the greater the potential gain.

14 years – Mid‑puberty
Growth plates are thick and proliferative; FGFR3 blockade could add several centimeters. This stage offers the highest potential.

15 years – Mid‑late puberty
Plates are thinning; growth slows. FGFR3 inhibition still helps but estrogen now accelerates closure.

16 years – Late puberty
Plates are nearly exhausted; benefits are modest unless estrogen production is suppressed (e.g., with aromatase inhibitors).

17 years - typically end of puberty
Most plates have fused; little to no height can be added by inhibiting FGFR3.

Safety, Monitoring, and Supportive Measures
View attachment 22769​

Hyperphosphatemia and mineral imbalance –

FGFR signaling affects kidney handling of phosphate via FGF23. Inhibitors can cause phosphate retention and lower vitamin D levels. Check serum phosphate, calcium, and vitamin D during treatment.

Hepatic and renal function –

FGFR inhibitors are metabolized and excreted through liver and kidneys. Routine liver function tests and serum creatinine are prudent.

Gastrointestinal and appetite changes –

Mild dyspepsia, decreased appetite, and flatulence have been reported. Monitor weight and nutritional status.

Osteochondromas and abnormal growth


FGFR3 normally restricts chondrocyte proliferation. Complete suppression can lead to benign cartilage tumors and dysregulated bone overgrowth. Orthopedic evaluation and imaging help detect such problems early.

Hormonal modulation –

Estrogen drives epiphyseal closure. Combining FGFR3 inhibitors with aromatase inhibitors delays estrogen formation and can further prolong growth plates. Testosterone is converted to estrogen via aromatase, suppressing this step slows closure.

Supportive nutrition –

Adequate calcium, protein, and vitamin D are required for osteoblast function and bone mineralization. Ensure dietary intake meets increased growth demands.


0nce the growth plates have fused, further inhibition of FGFR3 does not provide additional height. Terminate therapy when radiographs confirm epiphyseal closure and continue regular follow‑up to monitor bone health.

TheCoolDude2000 for the idea

Spoiler: Tags

Mandy B BastiHgH Godveil Heir Primalwontsaveme Circadex howdoi T Testicular O ogre
birthdefect acromegalic

rip section-
9Dino
Ogre_cel
longhairedChad
hide
Mirilow

where do i get this stuff

 

[Biomaxx]

where do i get this stuff

The deepest depths of China and India, super hard to find apart from meclizine

 

[Testicular]

Introduction:
Growth Plates and FGFR3

View attachment 22765​

Epiphyseal (growth) plates are zones of proliferating and hypertrophic chondrocytes near the ends of long bones. These regions drive longitudinal growth during childhood and adolescence.

Fibroblast growth factor receptor 3 (FGFR3) is a membrane receptor that modulates growth by binding fibroblast growth factors such as FGF18 and FGF9. Once activated, FGFR3 triggers MAPK and STAT signaling cascades that decrease chondrocyte proliferation and accelerate differentiation.

Too much FGFR3 signaling shortens bones (as in achondroplasia). Removing FGFR3 function lengthens bones in animal models.

In mid‑puberty (Tanner stage IV), estrogen rises and pushes the growth plates toward senescence and closure.
(Which I why aromatase inhibitors should be paired but ill get into that another time)

Blocking FGFR3 at this stage could prolong chondrocyte proliferation, slow epiphyseal fusion, and increase final height. Preclinical studies with selective FGFR3 inhibitors have shown increases in femur and tibia length when given before closure.

View attachment 22767
(Refer to meclozine-
FGFR3 Inhibitors (paragraph 5 ))



FGFR3 Inhibitors​

Recifercept – a soluble decoy receptor that binds FGF ligands and prevents them from activating FGFR3. It was administered by weekly subcutaneousinjections at roughly 1 mg/kg in early trials. Development halted after phase II.

Infigratinib – an oral tyrosine kinase inhibitor of FGFR1–3. In achondroplasia children, about 0.128 mg/kg/day increased height velocity by ~1.5 cm/year. Doses up to 0.25 mg/kg/day are being tested.

Vofatamab – a monoclonal antibody that blocks the extracellular domain of FGFR3. It was used in oncology at 10–20 mg/kg IV every few weeks. Proposed for growth plate modulation but not trialed in adolescents.

Vosoritide – a C‑type natriuretic peptide analog that activates guanylate cyclase and inhibits the MAPK pathway downstream of FGFR3. Approved for achondroplasia; 15 µg/kg/day subcutaneously increases growth velocity by ~1.6 cm/year.
(Ill get into cnp analogs in another thread)

Meclozine – an antihistamine found to attenuate FGFR3 signaling in cell models. Doses around 1–2 mg/kg twice daily increased long‑bone length in mice. Safety in adolescents for height is untested.

Statins – cholesterol‑lowering drugs that improved chondrogenesis and bone growth in achondroplasia models. Mechanism may involve BMP signaling. Typical cholesterol doses were used in animal studies; human data are lacking.

InhibitorMechanismTypical Dosage​

Recifercept
Decoy receptor for FGF ligands~1 mg/kg weeklySubcutaneousDiscontinued development

Infigratinib
FGFR1–3 tyrosine kinase inhibitor0.128–0.25 mg/kg/dayOralPhase II pediatric trials

Vofatamab
FGFR3 monoclonal antibody10–20 mg/kg every few weeksIntravenousUsed in oncology

VosoritideC‑type natriuretic peptide analog
15 µg/kg/daySubcutaneousApproved for achondroplasia

MeclozineAntihistamine;
downstream MAPK inhibition1–2 mg/kg twice dailyOralAnimal data only

Statins
Cholesterol synthesis inhibitors; possible BMP modulationStandard dosesOralExperimental use

Predicted Effect by Bone Age
View attachment 22768View attachment 22770​

Bone age influences how much additional height can be gained by blocking FGFR3.
Estrogen exposure increases with age, driving plates toward closure.
The earlier the intervention, the greater the potential gain.

14 years – Mid‑puberty
Growth plates are thick and proliferative; FGFR3 blockade could add several centimeters. This stage offers the highest potential.

15 years – Mid‑late puberty
Plates are thinning; growth slows. FGFR3 inhibition still helps but estrogen now accelerates closure.

16 years – Late puberty
Plates are nearly exhausted; benefits are modest unless estrogen production is suppressed (e.g., with aromatase inhibitors).

17 years - typically end of puberty
Most plates have fused; little to no height can be added by inhibiting FGFR3.

Safety, Monitoring, and Supportive Measures
View attachment 22769​

Hyperphosphatemia and mineral imbalance –

FGFR signaling affects kidney handling of phosphate via FGF23. Inhibitors can cause phosphate retention and lower vitamin D levels. Check serum phosphate, calcium, and vitamin D during treatment.

Hepatic and renal function –

FGFR inhibitors are metabolized and excreted through liver and kidneys. Routine liver function tests and serum creatinine are prudent.

Gastrointestinal and appetite changes –

Mild dyspepsia, decreased appetite, and flatulence have been reported. Monitor weight and nutritional status.

Osteochondromas and abnormal growth


FGFR3 normally restricts chondrocyte proliferation. Complete suppression can lead to benign cartilage tumors and dysregulated bone overgrowth. Orthopedic evaluation and imaging help detect such problems early.

Hormonal modulation –

Estrogen drives epiphyseal closure. Combining FGFR3 inhibitors with aromatase inhibitors delays estrogen and can further prolong growth plates. Testosterone is converted to estrogen via aromatase, suppressing this step slows closure.

Supportive nutrition –

Adequate calcium, protein, and vitamin D are required for osteoblast function and bone mineralization. Ensure dietary intake meets increased growth demands.


0nce the growth plates have fused, further inhibition of FGFR3 does not provide additional height. Terminate therapy when radiographs confirm epiphyseal closure and continue regular follow‑up to monitor bone health.

TheCoolDude2000 for the idea

Spoiler: Tags

Mandy B BastiHgH Godveil Heir Primalwontsaveme Circadex howdoi T Testicular O ogre
birthdefect acromegalic

rip section-
9Dino
Ogre_cel
longhairedChad
hide
Mirilow

No studies? Thanks for the tag tho.I think this is a very interesting topic I will do further research.

 

[Biomaxx]

No studies? Thanks for the tag tho.I think this is a very interesting topic I will do further research.

I dont rlly link studied but I should start

 

[birthdefect]

The deepest depths of China and India, super hard to find apart from meclizine

found a source in like 20 min tbh
infigratinib brutally mogs meclizine obviously, but i really doubt its gonna do much on someone who doesnt have the mutation
perhaps itll act as an amplifier to agents that increase growth velocity, like proviron to androgens

 

[Biomaxx]

found a source in like 20 min tbh
infigratinib brutally mogs meclizine obviously, but i really doubt its gonna do much on someone who doesnt have the mutation
perhaps itll act as an amplifier to agents that increase growth velocity, like proviron to androgens

U dont need a mutation for FGFR3 inhibitors to work?? Im looking more into vosoritide aswell tho. Gonna try find some sourced tn

 

[birthdefect]

U dont need a mutation for FGFR3 inhibitors to work?? Im looking more into vosoritide aswell tho. Gonna try find some sourced tn

i really doubt it man, id imagine it would work the way i said in my previous method
vosoritide has a broader moa, so it does work for idiopathic short stature, which is why its in clinical trials for idiopathic short stature and will most likely be combined with gh.

 

[TheCoolDude2000]

wasn’t that hard to source found a source to for vos and infig only it’s pretty expensive. Overall infig is just a little better but more sides compared to voso

 

[birthdefect]

wasn’t that hard to source found a source to for vos and infig only it’s pretty expensive. Overall infig is just a little better but more sides compared to voso

if you have a mutation infigratinib is significantly better than vosoritide, but if you dont have any mutations vosoritide brutally mogs
i only found a source for vosoritide because like 3 people all gave a source at the same time tbh

 

[Biomaxx]

i really doubt it man, id imagine it would work the way i said in my previous method
vosoritide has a broader moa, so it does work for idiopathic short stature, which is why its in clinical trials for idiopathic short stature and will most likely be combined with gh.

Previous method ?? Also that is mb I had assumed people would pair hgh with it so I didnt mention it, honest mistake, I dont rlly get what ur saying tho

 

[Biomaxx]

if you have a mutation infigratinib is significantly better than vosoritide, but if you dont have any mutations vosoritide brutally mogs
i only found a source for vosoritide because like 3 people all gave a source at the same time tbh

Yes yes yes yes we are arguing the same point

 

[Biomaxx]

wasn’t that hard to source found a source to for vos and infig only it’s pretty expensive. Overall infig is just a little better but more sides compared to voso

If im honest i js guessed bc icba to look

 

[birthdefect]

Previous method ?? Also that is mb I had assumed people would pair hgh with it so I didnt mention it, honest mistake, I dont rlly get what ur saying tho

you're all good bro by previous method i meant my previous post, i fucked it up tbh
and yea it should definitely be paired with gh, otherwise its gonna be negligible. fgfr3 inhibition just removes the ceiling, but doesnt actually push velocity further in non overactive models. i would use vosoritide tbh, perhaps even combine the 2 with gh and oxandrolone, then to mitigate bone aging, ky, arimidex, and maybe pthrp analogues.

 

[Biomaxx]

you're all good bro by previous method i meant my previous post, i fucked it up tbh
and yea it should definitely be paired with gh, otherwise its gonna be negligible. fgfr3 inhibition just removes the ceiling, but doesnt actually push velocity further in non overactive models. i would use vosoritide tbh, perhaps even combine the 2 with gh and oxandrolone, then to mitigate bone aging, ky, arimidex, and maybe pthrp analogues.

Yh im throwing vosoritide into my stack. Why Arimidex and not aromasin ?? I was thinking of abalo but ended up taking it out

 

[birthdefect]

Yh im throwing vosoritide into my stack. Why Arimidex and not aromasin ?? I was thinking of abalo but ended up taking it out

im only considering abalo as a way to keep chondrocytes proliferating and prevent them from hypertophying
doing that for a few months while dosing growth velocity promoting compounds at a higher dose than usual would probably be beneficial

 

[Biomaxx]

im only considering abalo as a way to keep chondrocytes proliferating and prevent them from hypertophying
doing that for a few months while dosing growth velocity promoting compounds at a higher dose than usual would probably be beneficial

I would be taking for the same reason. Js took it out bc I dont wanna pin like 5× a day

 

[birthdefect]

I would be taking for the same reason. Js took it out bc I dont wanna pin like 5× a day

valid
you pinning androgens as well?

 

[Biomaxx]

valid
you pinning androgens as well?

Cycle is pinned on my profile

 

[birthdefect]

Cycle is pinned on my profile

ah alr, i had read somewhere that you werent using androgens but it likely was an old post
my mistake

 

[Synapzyzz]

mirin the very high iq and insane effort, this is actual useful info.

 

[Biomaxx]

mirin the very high iq and insane effort, this is actual useful info.

Ty bhai