Fulvestrant is Dog Piss for Height.

[Kojo]

Just a topic I want to shortly touch on that I'm surprised I forgot to even mention before.

Tissue diffusion

I'm going to keep this short and low effort, but I presume anyone that talks about pharma/biology understands the foundational concept of diffusion.

Now, with certain compounds they have to diffuse into tissues to obviously exhibit their effects and bind to what they want to bind to like I covered BINDING in my recent thread..

So a lot of these lipophilic compounds that we love to use bind to fatty plasma proteins in the blood and use them as carriers to get into tissues they want to get to, (albumin/vldl/ldl/hdl) being prior examples.

However, for anyone to make claims on specific compounds for height must address it's natural physiological purpose, but ALSO it's purpose in the growth plate. If your compound cannot even diffuse into the growth plate properly to exhibit it's effects, it is useless.

The Growth Plate is a cartilagenous tissue that is avascular meaning it lacks blood vessels. Those plasma proteins want to travel and diffuse into tissues using blood vessels but you cannot do this for the growth plate given it's avascular. This means they have to get in very slowly through PASSIVE DIFFUSION.

Fulvestrants relevance to this comes here, it is a highly lipophilic compound such that 99% of it binds to lipoproteins which have an absurd amount of mass beyond the cutoff the growth plate allows for passive diffusion. Making fulvestrant too large of a molecule to even get into the growth plate and degrade the receptors.

So make sure when you check some of these compounds you are using, you factor something like this in.

Side note: This also could explain why fulvestrant administration in mice did not change bone maturation at all. Ignore the trash conclusion that the study derives, what I'm saying about fulvestrant in this thread fully debunks the "androgens may fuse on their own" no fulvestrant is just shit -- https://hero.epa.gov/reference/6319620/

As always, do your own research. Everything I've said can be completely fact checked. I will never make a thread without learning/studying the topic for every pixel I type on this site

@AtrophicPyra @Paul.jnxy @flowiza @zanenenene + anyone else who cares idk

 

[AtrophicPyra]

Just a topic I want to shortly touch on that I'm surprised I forgot to even mention before.

Tissue diffusion

I'm going to keep this short and low effort, but I presume anyone that talks about pharma/biology understands the foundational concept of diffusion.

Now, with certain compounds they have to diffuse into tissues to obviously exhibit their effects and bind to what they want to bind to like I covered BINDING in my recent thread..

So a lot of these lipophilic compounds that we love to use bind to fatty plasma proteins in the blood and use them as carriers to get into tissues they want to get to, (albumin/vldl/ldl/hdl) being prior examples.

However, for anyone to make claims on specific compounds for height must address it's natural physiological purpose, but ALSO it's purpose in the growth plate. If your compound cannot even diffuse into the growth plate properly to exhibit it's effects, it is useless.

The Growth Plate is a cartilagenous tissue that is avascular meaning it lacks blood vessels. Those plasma proteins want to travel and diffuse into tissues using blood vessels but you cannot do this for the growth plate given it's avascular. This means they have to get in very slowly through PASSIVE DIFFUSION.

Fulvestrants relevance to this comes here, it is a highly lipophilic compound such that 99% of it binds to lipoproteins which have an absurd amount of mass beyond the cutoff the growth plate allows for passive diffusion. Making fulvestrant too large of a molecule to even get into the growth plate and degrade the receptors.

So make sure when you check some of these compounds you are using, you factor something like this in.

Side note: This also could explain why fulvestrant administration in mice did not change bone maturation at all. Ignore the trash conclusion that the study derives, what I'm saying about fulvestrant in this thread fully debunks the "androgens may fuse on their own" no fulvestrant is just shit -- https://hero.epa.gov/reference/6319620/

As always, do your own research. Everything I've said can be completely fact checked. I will never make a thread without learning/studying the topic for every pixel I type on this site

@AtrophicPyra @Paul.jnxy @flowiza @zanenenene + anyone else who cares idk

Androgen-accelerated bone maturation in mice is not attenuated by Faslodex, an estrogen receptor blocker

HERO

hero.epa.gov

am i tripping..
doesnt this study prove that androgens express maturation genes to bone and that they cause maturation?

or what ur implying is that it fulvestrant cant diffuse into the gp.. but the study was using bone not cartillage..

do u have the studies on fulvestrant? how can it be an er antagonist and not antagonize?

 

[fraudster#1]

Androgen-accelerated bone maturation in mice is not attenuated by Faslodex, an estrogen receptor blocker

HERO

hero.epa.gov

am i tripping..
doesnt this study prove that androgens express maturation genes to bone and that they cause maturation?

or what ur implying is that it fulvestrant cant diffuse into the gp.. but the study was using bone not cartillage..

do u have the studies on fulvestrant? how can it be an er antagonist and not antagonize?

i though fulvestrant was a ER degrader not a antagonist

 

[AtrophicPyra]

i though fulvestrant was a ER degrader not a antagonist

if it degrades doesnt it antagonize

 

[Kojo]

if it degrades doesnt it antagonize

Functionally, if you use antagonise as a broad term for simply stopping an effect then yeah it’s technically an antagonist.

 

[Kojo]

i though fulvestrant was a ER degrader not a antagonist

Yes it’s a degrader

 

[Kojo]

Androgen-accelerated bone maturation in mice is not attenuated by Faslodex, an estrogen receptor blocker

HERO

hero.epa.gov

am i tripping..
doesnt this study prove that androgens express maturation genes to bone and that they cause maturation?

or what ur implying is that it fulvestrant cant diffuse into the gp.. but the study was using bone not cartillage..

do u have the studies on fulvestrant? how can it be an er antagonist and not antagonize?

No, the study simply says that adding in fulv did nothing. Hence they come to the conclusion that Ar can potentially mature bone since the maturation continued occurring compared to controls. Using only test.

Study was on bone maturation, bone maturation like definitively is endochondral ossification

The reason is because another thing I haven’t made a thread about is tissues. Tissues act different and interact with different drugs differently. People don’t account for compounds intended usage anymore when it actually means a lot.

Fulvestrant is made for women to act on the breast, those tissues are all very vascular and easy to instantly penetrate. Whereas an atypical usage for growth plates wasn’t its intended utility hence it fails at being a serd there

 

[goonadict]

if it degrades doesnt it antagonize

it is

 

[AtrophicPyra]

No, the study simply says that adding in fulv did nothing. Hence they come to the conclusion that Ar can potentially mature bone since the maturation continued occurring compared to controls. Using only test.

Study was on bone maturation, bone maturation like definitively is endochondral ossification

The reason is because another thing I haven’t made a thread about is tissues. Tissues act different and interact with different drugs differently. People don’t account for compounds intended usage anymore when it actually means a lot.

Fulvestrant is made for women to act on the breast, those tissues are all very vascular and easy to instantly penetrate. Whereas an atypical usage for growth plates wasn’t its intended utility hence it fails at being a serd there

ye i got what u meant, that study has to be involved in some sort of money laundering scheme

 

[Paul.jnxy]

Good thread. Most SERDs suck anyway

 

[Niebvll]

Ok interesting

 

[Paul.jnxy]

Ok interesting

Mirin new avi

 

[Niebvll]

Mirin new avi

Thanks mommy

 

[flowiza]

i dnrd but as far as i know fulverestant stops aromatisation in the place you pinned it

 

[Zagro]

Oh my god what a dumb nigger

 

[Paul.jnxy]

Oh my god what a dumb nigger

Haven’t seen you in a while nigha.

 

[Kojo]

Oh my god what a dumb nigger

Counterargument?

 

[Kojo]

i dnrd but as far as i know fulverestant stops aromatisation in the place you pinned it

Doesn't target aromatase

 

[Paul.jnxy]

Doesn't target aromatase

It’s literally a SERD lmao

Counterargument?

He just here cause he missed us

 

[Zagro]

Counterargument?

“Average rates of bone age advancement (ΔBA/ΔCA) decreased from 1.99 pre-treatment to 1.06 on treatment (mean change -0.93, 95% CI -1.43, -0.43; p = 0.0007).”

This is at 30-40% of clinical dosages

 

[Paul.jnxy]

“Average rates of bone age advancement (ΔBA/ΔCA) decreased from 1.99 pre-treatment to 1.06 on treatment (mean change -0.93, 95% CI -1.43, -0.43; p = 0.0007).”

This is at 30-40% of clinical dosages

thoughts on oral SERDs?

Also this was on girls McCune Albright syndrome or sum. I skimmed the study a while ago I got no clue