THE MOST UP TO DATE HEIGHTMAXXING STACK

"heightmaxxing"
Afkgaming 2021 08 79649079 d0e7 4acd 853b 6a2b92797da3 copium png
 
Take igf1-lr3 and aromasin (this is self explanatory)

and lastly add ky19382 and vosoritide

ky19382 inhibits the cxxc5 gene that regulates the wnt signaling pathway.

chatgpt summary of what the wnt signaling pathway does:

Wnt signaling pathway plays a significant role in the regulation of growth plates and ultimately influences a person's height. Here's how it works:

  1. Chondrocyte Proliferation: Growth plates, also known as epiphyseal plates, are found at the ends of long bones in the body and are responsible for longitudinal bone growth. Within these plates, specialized cells called chondrocytes are responsible for producing new cartilage, which then turns into bone. The Wnt signaling pathway is involved in regulating the proliferation (multiplication) of these chondrocytes. Activation of Wnt signaling can promote chondrocyte proliferation, leading to bone growth.
  2. Chondrocyte Differentiation: In addition to promoting cell proliferation, the Wnt pathway also influences the differentiation (maturation) of chondrocytes. Proper chondrocyte differentiation is essential for the orderly transition of cartilage to bone in the growth plates. Dysregulation of the Wnt pathway can disrupt this process and potentially impact bone growth.
  3. Bone Remodeling: The Wnt signaling pathway also plays a role in the process of bone remodeling, which continues throughout life. This pathway helps maintain the balance between bone formation and bone resorption. Imbalances can affect overall bone density and potentially impact height.
Overall, the Wnt signaling pathway is crucial for the regulation of growth plates and, consequently, for determining a person's height. Dysregulation of this pathway can lead to growth disorders and skeletal abnormalities that can affect an individual's final height. However, it's important to note that the Wnt pathway is just one of many factors that influence height, and genetics, nutrition, hormones, and other factors also play significant roles.



the cxxc5 gene:

The CXXC5 gene, also known as IDAX (Inhibition of the Dvl and Axin complex protein), primarily functions as a regulator of the Wnt signaling pathway, as mentioned earlier. Here's a summary of what the CXXC5 gene does:

  1. Negative Regulation of Wnt Signaling: CXXC5/IDAX acts as a negative regulator of the Wnt signaling pathway. It does so by interacting with key components of the pathway, including Disheveled (Dvl) and Axin. This interaction helps inhibit the Wnt signaling cascade, which is involved in various cellular processes, including cell proliferation and differentiation.





the cxxc5 gene is like the myostatin of chondrocyte proliferation and differentiation.




now vosoritide is this:

Vosoritide (BMN 111) is a modified recombinant CNP (C-type natriuretic peptide) analogue, binds to NPR-B (natriuretic peptide receptor type B) and reduces the activity of FGFR3 (fibroblast growth factor receptor 3). Vosoritide can be used in achondroplasia and dwarfism research[1][2][3].
In VitroVosoritide (0.1 μM; 1 h) decreases NPR2 phosphorylation in chondrocytes[2].
Vosoritide (0.1 μM; 6 d) improves chondrocyte differentiation and increases the proliferative growth plate area of cultured Fgfr3Y367C/+ femurs[2].
Vosoritide (10 μM; overnight) reduces ERK1/2 activation in ACH growth-plate chondrocytes[






the only problem is that you are going to have to work around the "For research use only. We do not sell to patients." thing.
and yeah normal vosoridite costs like $10,000+ usd but vosoritide acetate (its the same thing but instead of being in a liquid, its just powder/salt form) which is beneficial for dosing, can cost like $600 usd for 10mg. normal injection dose is 0.4mg.
So yeah all we need is to find out a way to bypass the "For research use only. We do not sell to patients."
LINKS
theory no one will do that irl
 
Take igf1-lr3 and aromasin (this is self explanatory)

and lastly add ky19382 and vosoritide

ky19382 inhibits the cxxc5 gene that regulates the wnt signaling pathway.

chatgpt summary of what the wnt signaling pathway does:

Wnt signaling pathway plays a significant role in the regulation of growth plates and ultimately influences a person's height. Here's how it works:

  1. Chondrocyte Proliferation: Growth plates, also known as epiphyseal plates, are found at the ends of long bones in the body and are responsible for longitudinal bone growth. Within these plates, specialized cells called chondrocytes are responsible for producing new cartilage, which then turns into bone. The Wnt signaling pathway is involved in regulating the proliferation (multiplication) of these chondrocytes. Activation of Wnt signaling can promote chondrocyte proliferation, leading to bone growth.
  2. Chondrocyte Differentiation: In addition to promoting cell proliferation, the Wnt pathway also influences the differentiation (maturation) of chondrocytes. Proper chondrocyte differentiation is essential for the orderly transition of cartilage to bone in the growth plates. Dysregulation of the Wnt pathway can disrupt this process and potentially impact bone growth.
  3. Bone Remodeling: The Wnt signaling pathway also plays a role in the process of bone remodeling, which continues throughout life. This pathway helps maintain the balance between bone formation and bone resorption. Imbalances can affect overall bone density and potentially impact height.
Overall, the Wnt signaling pathway is crucial for the regulation of growth plates and, consequently, for determining a person's height. Dysregulation of this pathway can lead to growth disorders and skeletal abnormalities that can affect an individual's final height. However, it's important to note that the Wnt pathway is just one of many factors that influence height, and genetics, nutrition, hormones, and other factors also play significant roles.



the cxxc5 gene:

The CXXC5 gene, also known as IDAX (Inhibition of the Dvl and Axin complex protein), primarily functions as a regulator of the Wnt signaling pathway, as mentioned earlier. Here's a summary of what the CXXC5 gene does:

  1. Negative Regulation of Wnt Signaling: CXXC5/IDAX acts as a negative regulator of the Wnt signaling pathway. It does so by interacting with key components of the pathway, including Disheveled (Dvl) and Axin. This interaction helps inhibit the Wnt signaling cascade, which is involved in various cellular processes, including cell proliferation and differentiation.





the cxxc5 gene is like the myostatin of chondrocyte proliferation and differentiation.




now vosoritide is this:

Vosoritide (BMN 111) is a modified recombinant CNP (C-type natriuretic peptide) analogue, binds to NPR-B (natriuretic peptide receptor type B) and reduces the activity of FGFR3 (fibroblast growth factor receptor 3). Vosoritide can be used in achondroplasia and dwarfism research[1][2][3].
In VitroVosoritide (0.1 μM; 1 h) decreases NPR2 phosphorylation in chondrocytes[2].
Vosoritide (0.1 μM; 6 d) improves chondrocyte differentiation and increases the proliferative growth plate area of cultured Fgfr3Y367C/+ femurs[2].
Vosoritide (10 μM; overnight) reduces ERK1/2 activation in ACH growth-plate chondrocytes[






the only problem is that you are going to have to work around the "For research use only. We do not sell to patients." thing.
and yeah normal vosoridite costs like $10,000+ usd but vosoritide acetate (its the same thing but instead of being in a liquid, its just powder/salt form) which is beneficial for dosing, can cost like $600 usd for 10mg. normal injection dose is 0.4mg.
So yeah all we need is to find out a way to bypass the "For research use only. We do not sell to patients."
LINKS
bro vosoritide on a 62kg guy is like 0.9mcg which is almost 1mg; meaning you would only get 10 days before it runs out even though its fricking 600$
 
Nice, hope it makes a difference
 
Take igf1-lr3 and aromasin (this is self explanatory)

and lastly add ky19382 and vosoritide

ky19382 inhibits the cxxc5 gene that regulates the wnt signaling pathway.

chatgpt summary of what the wnt signaling pathway does:

Wnt signaling pathway plays a significant role in the regulation of growth plates and ultimately influences a person's height. Here's how it works:

  1. Chondrocyte Proliferation: Growth plates, also known as epiphyseal plates, are found at the ends of long bones in the body and are responsible for longitudinal bone growth. Within these plates, specialized cells called chondrocytes are responsible for producing new cartilage, which then turns into bone. The Wnt signaling pathway is involved in regulating the proliferation (multiplication) of these chondrocytes. Activation of Wnt signaling can promote chondrocyte proliferation, leading to bone growth.
  2. Chondrocyte Differentiation: In addition to promoting cell proliferation, the Wnt pathway also influences the differentiation (maturation) of chondrocytes. Proper chondrocyte differentiation is essential for the orderly transition of cartilage to bone in the growth plates. Dysregulation of the Wnt pathway can disrupt this process and potentially impact bone growth.
  3. Bone Remodeling: The Wnt signaling pathway also plays a role in the process of bone remodeling, which continues throughout life. This pathway helps maintain the balance between bone formation and bone resorption. Imbalances can affect overall bone density and potentially impact height.
Overall, the Wnt signaling pathway is crucial for the regulation of growth plates and, consequently, for determining a person's height. Dysregulation of this pathway can lead to growth disorders and skeletal abnormalities that can affect an individual's final height. However, it's important to note that the Wnt pathway is just one of many factors that influence height, and genetics, nutrition, hormones, and other factors also play significant roles.



the cxxc5 gene:

The CXXC5 gene, also known as IDAX (Inhibition of the Dvl and Axin complex protein), primarily functions as a regulator of the Wnt signaling pathway, as mentioned earlier. Here's a summary of what the CXXC5 gene does:

  1. Negative Regulation of Wnt Signaling: CXXC5/IDAX acts as a negative regulator of the Wnt signaling pathway. It does so by interacting with key components of the pathway, including Disheveled (Dvl) and Axin. This interaction helps inhibit the Wnt signaling cascade, which is involved in various cellular processes, including cell proliferation and differentiation.





the cxxc5 gene is like the myostatin of chondrocyte proliferation and differentiation.




now vosoritide is this:

Vosoritide (BMN 111) is a modified recombinant CNP (C-type natriuretic peptide) analogue, binds to NPR-B (natriuretic peptide receptor type B) and reduces the activity of FGFR3 (fibroblast growth factor receptor 3). Vosoritide can be used in achondroplasia and dwarfism research[1][2][3].
In VitroVosoritide (0.1 μM; 1 h) decreases NPR2 phosphorylation in chondrocytes[2].
Vosoritide (0.1 μM; 6 d) improves chondrocyte differentiation and increases the proliferative growth plate area of cultured Fgfr3Y367C/+ femurs[2].
Vosoritide (10 μM; overnight) reduces ERK1/2 activation in ACH growth-plate chondrocytes[






the only problem is that you are going to have to work around the "For research use only. We do not sell to patients." thing.
and yeah normal vosoridite costs like $10,000+ usd but vosoritide acetate (its the same thing but instead of being in a liquid, its just powder/salt form) which is beneficial for dosing, can cost like $600 usd for 10mg. normal injection dose is 0.4mg.
So yeah all we need is to find out a way to bypass the "For research use only. We do not sell to patients."
LINKS
So what would be the best stack ???
 
bro vosoritide on a 62kg guy is like 0.9mcg which is almost 1mg; meaning you would only get 10 days before it runs out even though its fricking 600$
Same for igf-1
 
I have pretty cheap (as in comparison to the 12-14,000$ sources) pharma vosoritide links.
does this work for post puberty? (closed growth plates)
 
how much lr3 per day?
 
can i still use ts when im 18
 
Lr3 is worst you can do for height otherwise valid
 
Take igf1-lr3 and aromasin (this is self explanatory)

and lastly add ky19382 and vosoritide

ky19382 inhibits the cxxc5 gene that regulates the wnt signaling pathway.

chatgpt summary of what the wnt signaling pathway does:

Wnt signaling pathway plays a significant role in the regulation of growth plates and ultimately influences a person's height. Here's how it works:

  1. Chondrocyte Proliferation: Growth plates, also known as epiphyseal plates, are found at the ends of long bones in the body and are responsible for longitudinal bone growth. Within these plates, specialized cells called chondrocytes are responsible for producing new cartilage, which then turns into bone. The Wnt signaling pathway is involved in regulating the proliferation (multiplication) of these chondrocytes. Activation of Wnt signaling can promote chondrocyte proliferation, leading to bone growth.
  2. Chondrocyte Differentiation: In addition to promoting cell proliferation, the Wnt pathway also influences the differentiation (maturation) of chondrocytes. Proper chondrocyte differentiation is essential for the orderly transition of cartilage to bone in the growth plates. Dysregulation of the Wnt pathway can disrupt this process and potentially impact bone growth.
  3. Bone Remodeling: The Wnt signaling pathway also plays a role in the process of bone remodeling, which continues throughout life. This pathway helps maintain the balance between bone formation and bone resorption. Imbalances can affect overall bone density and potentially impact height.
Overall, the Wnt signaling pathway is crucial for the regulation of growth plates and, consequently, for determining a person's height. Dysregulation of this pathway can lead to growth disorders and skeletal abnormalities that can affect an individual's final height. However, it's important to note that the Wnt pathway is just one of many factors that influence height, and genetics, nutrition, hormones, and other factors also play significant roles.



the cxxc5 gene:

The CXXC5 gene, also known as IDAX (Inhibition of the Dvl and Axin complex protein), primarily functions as a regulator of the Wnt signaling pathway, as mentioned earlier. Here's a summary of what the CXXC5 gene does:

  1. Negative Regulation of Wnt Signaling: CXXC5/IDAX acts as a negative regulator of the Wnt signaling pathway. It does so by interacting with key components of the pathway, including Disheveled (Dvl) and Axin. This interaction helps inhibit the Wnt signaling cascade, which is involved in various cellular processes, including cell proliferation and differentiation.





the cxxc5 gene is like the myostatin of chondrocyte proliferation and differentiation.




now vosoritide is this:

Vosoritide (BMN 111) is a modified recombinant CNP (C-type natriuretic peptide) analogue, binds to NPR-B (natriuretic peptide receptor type B) and reduces the activity of FGFR3 (fibroblast growth factor receptor 3). Vosoritide can be used in achondroplasia and dwarfism research[1][2][3].
In VitroVosoritide (0.1 μM; 1 h) decreases NPR2 phosphorylation in chondrocytes[2].
Vosoritide (0.1 μM; 6 d) improves chondrocyte differentiation and increases the proliferative growth plate area of cultured Fgfr3Y367C/+ femurs[2].
Vosoritide (10 μM; overnight) reduces ERK1/2 activation in ACH growth-plate chondrocytes[






the only problem is that you are going to have to work around the "For research use only. We do not sell to patients." thing.
and yeah normal vosoridite costs like $10,000+ usd but vosoritide acetate (its the same thing but instead of being in a liquid, its just powder/salt form) which is beneficial for dosing, can cost like $600 usd for 10mg. normal injection dose is 0.4mg.
So yeah all we need is to find out a way to bypass the "For research use only. We do not sell to patients."
LINKS
stopped reading as i saw igf1lr3 is so cope it has no effects on bones or very minimal take hgh
 
stopped reading as i saw igf1lr3 is so cope it has no effects on bones or very minimal take hgh
nigga ts was made 2 years ago, none of this works. maybe for some fat loss

but none if it works
 
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Reactions: PhonecianCell12
nigga ts was made 2 years ago, none of this works. maybe for some fat loss

but none if it works
ky19382 for sure works, tons of mice studies showing cxxc5 is the primary upregulated gene expression during puberty correlating with gp thinning.
the only con is how expensive it is
 
ky19382 for sure works, tons of mice studies showing cxxc5 is the primary upregulated gene expression during puberty correlating with gp thinning.
the only con is how expensive it is
how abt voso
 
how abt voso
wdym? ur askin if voso works? yeah it does but its inferior to fgfr3 inhibition ( thru potent kinase inhibitors not fucking meclizine ) and its expensive asf
 
have anyone actually tried it
also if you want to apply it on humans you should only care about vivo results
In VivoVosoritide (subcutaneous injection; 800 μg/kg; once daily; 20 d) treatment leads to improvement in skeletal parameters in Fgfr3 gain-of-function mutation mouse[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:Fgfr3Y367C/+ mice[3]
Dosage:800 μg/kg
Administration:Subcutaneous injection; 800 μg/kg; once daily; 20 days
Result:Observed phenotypic changes including flattening of the skull, elongation of the snout, improvement of the anterior crossbite, larger paws and digits, and longer and straightened tibias and femurs.

Dosage is 800 μg/kg which is 0.06g for someone who weights 75Kg also it is was taken everyday for 20 days as a subcutaneous injection

For KY19382:

In VivoKY19382 (0.1 mg/kg; i.p. once daily for 2 weeks) delays growth plate senescence in older mice and promotes growth plate maturation in rapidly growing young mice[1].
KY19382 (0.1 mg/kg; i.p. once daily for 10 weeks) significantly increases the length of tibiae in mice[1].
KY19382 (5 mg/kg; i.p.) displays a relatively favorable bioavailability (F=16.74%), showing half-life of 16.20 h and an exposure level of 6,555.79 ng•h/ml[1].
KY19382 (A3051) (25 mg/kg; p.o. once daily for 16 weeks) shows reduction in adipocyte size and anti-inflammatory effects[2].
A3051 (25 mg/kg; p.o. once daily for 5 days) reduces fasting glucose in mice[2].
A3051 (25 mg/kg; p.o. once daily for 3 weeks) reduces the hepatosteatosis in mice[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:C57BL/6 male mice (7-weeks-old or 3-weeks-old)[1]
Dosage:0.1 mg/kg
Administration:I.p. once daily for 2 weeks
Result:Increased nuclear β-catenin in the growth plate chondrocytes dramatically.
Elevated the height of each growth plate zone and BrdU-positive cells.
Did not affect the cartilage resorption of rapidly growing young mice.
the dosage is 0.1 mg/kg which will be 7.5mg for someone who weights 75kg taken once daily for 2 weeks
The problem is there is no enough results for human use and the instructions is not very clear
price is not really a problem since the results would be life changing if this actually applicable
How do you think it should be cycled?
 
have anyone actually tried it
also if you want to apply it on humans you should only care about vivo results
In VivoVosoritide (subcutaneous injection; 800 μg/kg; once daily; 20 d) treatment leads to improvement in skeletal parameters in Fgfr3 gain-of-function mutation mouse[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:Fgfr3Y367C/+ mice[3]
Dosage:800 μg/kg
Administration:Subcutaneous injection; 800 μg/kg; once daily; 20 days
Result:Observed phenotypic changes including flattening of the skull, elongation of the snout, improvement of the anterior crossbite, larger paws and digits, and longer and straightened tibias and femurs.

Dosage is 800 μg/kg which is 0.06g for someone who weights 75Kg also it is was taken everyday for 20 days as a subcutaneous injection

For KY19382:

In VivoKY19382 (0.1 mg/kg; i.p. once daily for 2 weeks) delays growth plate senescence in older mice and promotes growth plate maturation in rapidly growing young mice[1].
KY19382 (0.1 mg/kg; i.p. once daily for 10 weeks) significantly increases the length of tibiae in mice[1].
KY19382 (5 mg/kg; i.p.) displays a relatively favorable bioavailability (F=16.74%), showing half-life of 16.20 h and an exposure level of 6,555.79 ng•h/ml[1].
KY19382 (A3051) (25 mg/kg; p.o. once daily for 16 weeks) shows reduction in adipocyte size and anti-inflammatory effects[2].
A3051 (25 mg/kg; p.o. once daily for 5 days) reduces fasting glucose in mice[2].
A3051 (25 mg/kg; p.o. once daily for 3 weeks) reduces the hepatosteatosis in mice[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:C57BL/6 male mice (7-weeks-old or 3-weeks-old)[1]
Dosage:0.1 mg/kg
Administration:I.p. once daily for 2 weeks
Result:Increased nuclear β-catenin in the growth plate chondrocytes dramatically.
Elevated the height of each growth plate zone and BrdU-positive cells.
Did not affect the cartilage resorption of rapidly growing young mice.
the dosage is 0.1 mg/kg which will be 7.5mg for someone who weights 75kg taken once daily for 2 weeks
The problem is there is no enough results for human use and the instructions is not very clear
price is not really a problem since the results would be life changing if this actually applicable
A HED of 0.1mg/kg for a 75kg human would be 0.6mg??
 

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