Ru-59063- Strongest Antiandrogen Ever Created, Stronger Binding Affinity Than Even Dht

[Thebaldcel]

Hoy f*** you are a hopeless idiot. That study is not on ru-59... it’s a modification that they made to it to make a molecule almost as androgenic as DHT

Also I did read the study no where does it say the ru-59... is not a good anti androgen

Get out of this thread you idiot. You don’t have the ability to understand anything you’re reading

All you’re doing is spreading mid information. You claim to read studies but you skim over them in 3 seconds and don’t understand anything about them.

People like you are why this forum sucks

Lol, I tried to be nice and let you figure it out yourself by linking to the study but you had to attack my intelligence.

"ALso I dId REad ThE StuDY NO wheRE dOeS it sAy ThE Ru-59... Is Not A GOod AntI AndROgEn"

It really doesn't look good to attack someone's intelligence when you're blatantly wrong lol. I'm saving you from yourself, you can thank me later.

 

[hemingway_the_mercenary]

@TheBaldcell This is a perfect example of you posting research without fully understanding it.

Do you know what Chloramphenicol acetyltransferase even is. Do you understand what CAT activity% means? Because I hardly understand it, and yes I've read the study.

Do you know that thats not even an androgen receptor. Do you know that there are many variations of androgen receptors and when testing drugs for their anti androgenic effect they look on its effect on various different ARs before coming to any conclusions? I mean how could you be so smart seriously? That study in very inconclusive.

Read these links
https://www.researchgate.net/public...f_Amino-_and_carboxyl-terminal_and_the_ligand

http://www.jbc.org/content/272/25/15973/F6.expansion.html

It takes a deep understanding of the research and more than one weak study to comdiscreditdiscrdit a compound when other studies have shown that its sister compound was effectve at blocking testosterone with a 6x lesser dose.

you do not have experiance with the compounds that I have tried. Unlike you have tried daro, bicalutamide and a few others. And from my and many others experiances bica was much stronger for hairloss than Daro. So you see that its not always so clear whether a compound will work for male pattern baldness or not. Research done on prostate ARs that are transplanted into the kidneys is not enough to dismiss a compound

EDIT: also read this you can learn alot about wild type AR
https://www.sciencedirect.com/science/article/pii/S0014579398007017

I dont have fully access to that paper you cited, do you? If so can you check which prostate cancer cell lines the experiment was done for CAT activity%.

 

[zinny999]

If you have sides on fina/duta, then stay away. If not, try it out.

Friend I know did it and had great results on RU but he also had side effects...

Which RU?

My Friend went from NW2 to NW0 on RU 58841

 

[alibaba92]

Which RU?

My Friend went from NW2 to NW0 on RU 58841

Hey, can ask your friend to share his story here ?

 

[Georgie]

What is it
Ru-59063 is simillar in its structure to Ru-58841 however its over a 100x or more strong.

It was found to have a binding affinity to the AR even higher than DHT but it was never marketed because it showed some very slight androgenic effects which could be problematic for prostate cancer AR proliferation but likely will have a very little effect on male pattern baldness as this drug will be guaranteed to block the follicle from testosterone and even DHT.

I dont think the partial agonism of this drug is to be convered with because even drugs like Cyperatone Acetate which is known to be one of the strongest anti androgens is also a partial agonist. If this drug can block testosterone it will be doing 100x more good than harm.

As I have explained before in other threads, there are no marketed drugs which can bind to the AR with anywhere near the affinity of Testosterone. This creates a limitation because at equal levels Testosterone will render the compounds useless. As a result, extremely high dosages of these drugs are needed to even have a chance of competing with testosterone.

Additionally, it is possible that testosterone has the ability to rip off drugs like Darolutamide/Enzalutamdie off the AR and bind itself instead thus resulting in androgenic gene expression.

Relative Binding Affinity of Know Compounds
Metribolone 290
Dihydrotestosterone 180
Testosterone 100
Cyproterone acetate 10
Bicalutamide 1.8
Nilutamide 0.8
Hydroxyflutamide 0.8
RU-59063 300
RU-57073 163
RU-56187 92

As you can see DHT has one of the strongest binding affinity to the AR of any know substances. Powerful drugs like bicalutamide only have a binding affinity of 1.8. That is unbelievably low compared with DHT. Even cyperatone acetate only has a binding affinity of 10. RU-59063 will overpower DHT has potential to be the greatest compound of all time for hair loss, because due to its incredible binding affinity, every single molecule will bind to the first AR it comes across. This means that the chance for systemic absorption is quite low as a very low dosage can be used for a great effect.

Unlike all other AR antagonists talked about on this site it does not need higher concentration than DHT to bind to the AR.


This drug is it its own realm. It is significantly stronger than Enzalutamide, Darolutamide, over 150x stronger than Bicalutamide.

Sharing this for all the sufferers of aggressive androgenic alopecia. Would anyone be interested in doing a group buy?

Here are some sources where you can get more info on how amazing this drug has potential to be:

https://books.google.ca/books?id=vc...4Q6AEwFXoECA8QAQ#v=onepage&q=RU 59063&f=false

https://www.ncbi.nlm.nih.gov/pubmed/8136296 - source for being stronger than DHT



So many people are willing to try out RU-58841, would anyone be willing to try this?

I’d try it simply out of curiosity because up to know I have proven to be 100% catraste resistant. I’d love to know where you would plan of obtaining it however. Also, we are unaware of appropriate dosing no?

 

[furrydome]

I’d try it simply out of curiosity because up to know I have proven to be 100% catraste resistant. I’d love to know where you would plan of obtaining it however. Also, we are unaware of appropriate dosing no?

I hope this post means we're heading back to science and civility. Please be true... please be true...

 

[hemingway_the_mercenary]

Hey, can ask your friend to share his story here ?

He replied to me in pm and said he was mistaken and talking about another ru

 

[hemingway_the_mercenary]

I’d try it simply out of curiosity because up to know I have proven to be 100% catraste resistant. I’d love to know where you would plan of obtaining it however. Also, we are unaware of appropriate dosing no?

We are completely unaware of the doseing and half life. This makes it very challenging. I am trying to reach out to the researchers who did studies on it but their contact info is very hard to find

 

[Thebaldcel]

@TheBaldcell This is a perfect example of you posting research without fully understanding it.

Do you know what Chloramphenicol acetyltransferase even is. Do you understand what CAT activity% means? Because I hardly understand it, and yes I've read the study.

Do you know that thats not even an androgen receptor. Do you know that there are many variations of androgen receptors and when testing drugs for their anti androgenic effect they look on its effect on various different ARs before coming to any conclusions? I mean how could you be so smart seriously? That study in very inconclusive.

Read these links
https://www.researchgate.net/public...f_Amino-_and_carboxyl-terminal_and_the_ligand

http://www.jbc.org/content/272/25/15973/F6.expansion.html

It takes a deep understanding of the research and more than one weak study to comdiscreditdiscrdit a compound when other studies have shown that its sister compound was effectve at blocking testosterone with a 6x lesser dose.

you do not have experiance with the compounds that I have tried. Unlike you have tried daro, bicalutamide and a few others. And from my and many others experiances bica was much stronger for hairloss than Daro. So you see that its not always so clear whether a compound will work for male pattern baldness or not. Research done on prostate ARs that are transplanted into the kidneys is not enough to dismiss a compound

EDIT: also read this you can learn alot about wild type AR
https://www.sciencedirect.com/science/article/pii/S0014579398007017

I dont have fully access to that paper you cited, do you? If so can you check which prostate cancer cell lines the experiment was done for CAT activity%.

Jesus christ you're still clinging onto this and still being condescending lol.

Tell me again what studies show potent antiandrogen properties? There are only 4 studies that involves RU-59063. The very first study in 1994 was the only study to show it being a strong antiandrogen.

The 1997 study you linked to did not study RU specifically, but that study was slightly flawed in that the reporter was slightly antagonized by the ARs themselves used in the study in a ligand independent fashion. But still, even this study showed Ru 59063 had androgen receptor agonist properties. Here is one table: http://m.jbc.org/content/272/25/15973/T1.expansion.html
This study is inconclusive but foreshadows whats to come.

Next comes the 2000 study I cited, using a CAT assay to show the AR agonist properties of RU 59063 and the derivative. It doesn't take a deep understanding of the procedures and mechanisms to know what it does lol. They used the cytosol from the ventral prostate of castrated Wistar rats.

The general idea of a CAT assay is relatively straightforward. The CAT gene produces an enzyme, and the gene is attached to a reporter gene, such as one for the AR. When an agonist binds to the AR, it activates it. What happens? The AR binds to DNA and upregulates genes. In an assay, the reporter gene is transcripted and the enzyme is produced. The level of agonism is determined by measuring the activity of the produced enzyme, or any other marker.

The CV-1 cell line (derived from kidney cells) is suitable for cotransfection, which is why it is used.

An antiandrogen would result in ZERO CAT activity, but guess what they found? A level of CAT activity induced by RU-59063 comparable to DHT. This study is pretty conclusive, but you are calling it insignificant lol.

The scientific community has the consensus that it is an androgen receptor agonist, and research on the compound itself was abandoned after this in favor of its derivatives.

You are the only one clinging to the hope that it is actually an antiandrogen for scalp AR just because there have been no studies on its effects on scalp AR.

Did you know that the SARM RAD-140 exerted protective effects on the prostate against testosterone in rats? It doesn't make it an antiandrogen. It's what happens when a ligand with weaker effects competes with a stronger ligand for the same receptor.

Go ahead and keep being condescending.

Keep in mind for anyone that wants to try this, you are paying big money for an abandoned compound that has been shown to activate the androgen receptor in the most recent study, and has had zero safety studies done on it.

You can try it if you want, not going to stop you. I find it funny how you are continually being condscending and attacking my intelligence despite the burden of proof being higher for you.

 

[hemingway_the_mercenary]

Jesus christ you're still clinging onto this and still being condescending lol.

Tell me again what studies show potent antiandrogen properties? There are only 4 studies that involves RU-59063. The very first study in 1994 was the only study to show it being a strong antiandrogen.

The 1997 study you linked to did not study RU specifically, but that study was slightly flawed in that the reporter was slightly antagonized by the ARs themselves used in the study in a ligand independent fashion. But still, even this study showed Ru 59063 had androgen receptor agonist properties. Here is one table: http://m.jbc.org/content/272/25/15973/T1.expansion.html
This study is inconclusive but foreshadows whats to come.

Next comes the 2000 study I cited, using a CAT assay to show the AR agonist properties of RU 59063 and the derivative. It doesn't take a deep understanding of the procedures and mechanisms to know what it does lol. They used the cytosol from the ventral prostate of castrated Wistar rats.

The general idea of a CAT assay is relatively straightforward. The CAT gene produces an enzyme, and the gene is attached to a reporter gene, such as one for the AR. When an agonist binds to the AR, it activates it. What happens? The AR binds to DNA and upregulates genes. In an assay, the reporter gene is transcripted and the enzyme is produced. The level of agonism is determined by measuring the activity of the produced enzyme, or any other marker.

The CV-1 cell line (derived from kidney cells) is suitable for cotransfection, which is why it is used.

An antiandrogen would result in ZERO CAT activity, but guess what they found? A level of CAT activity induced by RU-59063 comparable to DHT. This study is pretty conclusive, but you are calling it insignificant lol.

The scientific community has the consensus that it is an androgen receptor agonist, and research on the compound itself was abandoned after this in favor of its derivatives.

You are the only one clinging to the hope that it is actually an antiandrogen for scalp AR just because there have been no studies on its effects on scalp AR.

Did you know that the SARM RAD-140 exerted protective effects on the prostate against testosterone in rats? It doesn't make it an antiandrogen. It's what happens when a ligand with weaker effects competes with a stronger ligand for the same receptor.

Go ahead and keep being condescending.

Keep in mind for anyone that wants to try this, you are paying big money for an abandoned compound that has been shown to activate the androgen receptor in the most recent study, and has had zero safety studies done on it.

You can try it if you want, not going to stop you. I find it funny how you are continually being condscending and attacking my intelligence despite the burden of proof being higher for you.

you still dont get it. lol first of all true anti androgens resultted in higher CAT activity % not zero! Look at your table.

Hydroxyflutamdie 99.5% and bicalutamide 77%.

So your whole theory of zero CAT activity goes straight out the window.

Even cyperatone acetate which is a very powerfull androgen recptor blocker has a lower CAT activity than the RU molecules and even Testosterone. Assuming high CAT activity means no AR expression this is certainly strange because that would make it more androgenic than testosterone and as a result any male taking it would go bald. Yes I know it also shut down your bodies natural testosterone production but if it were more androgenic than testosterone this would still be irrelevant, you would go bald quickly from taking it. Obviously this is not the case

I dont know everything, but at least I dont try to pretend lke you. Waiting for your reply

 

[Thebaldcel]

you still dont get it. lol first of all true anti androgens resultted in higher CAT activity % not zero! Look at your table.

Hydroxyflutamdie 99.5% and bicalutamide 77%.

So your whole theory of zero CAT activity goes straight out the window.

Even cyperatone acetate which is a very powerfull androgen recptor blocker has a lower CAT activity than the RU molecules and even Testosterone. Assuming high CAT activity means no AR expression this is certainly strange because that would make it more androgenic than testosterone and as a result any male taking it would go bald. Yes I know it also shut down your bodies natural testosterone production but if it were more androgenic than testosterone this would still be irrelevant, you would go bald quickly from taking it. Obviously this is not the case

I dont know everything, but at least I dont try to pretend lke you. Waiting for your reply

Did you even read the study you linked? The table comes from the 1997 paper which you yourself told me to go read. In this experiment, control CAT activity starts at 100%, with the androgen receptors they used slightly interfering with the reporter activity independent of any ligands.

Androgen receptor agonists will decrease % activity, hence the 46% activity when exposed to testosterone. In comparison, the vehicle control is 85.5% and RU-59063 is 42.5%. See the values of the full androgen antagonists in comparison to control and testosterone?

The 2000 study is different, and all you needed to do was compare the results to native ligand DHT. CAT activity starts at 0 and will stay at 0 unless the AR is activated and DNA is transcripted. Again, DHT, RU-59063, and the derivative showed dosed dependent AR agonism. No negative control needed because it's self explanatory.

 

[hemingway_the_mercenary]

Did you even read the study you linked? The table comes from the 1997 paper which you yourself told me to go read. In this experiment, control CAT activity starts at 100%, with the androgen receptors they used slightly interfering with the reporter activity independent of any ligands.

Androgen receptor agonists will decrease % activity, hence the 46% activity when exposed to testosterone. In comparison, the vehicle control is 85.5% and RU-59063 is 42.5%. See the values of the full androgen antagonists in comparison to control and testosterone?

The 2000 study is different, and all you needed to do was compare the results to native ligand DHT. CAT activity starts at 0 and will stay at 0 unless the AR is activated and DNA is transcripted. Again, DHT, RU-59063, and the derivative showed dosed dependent AR agonism. No negative control needed because it's self explanatory.

Explain then why cyperatone ace had a lower CAT activity than even RU-59063

 

[Thebaldcel]

Explain then why cyperatone ace had a lower CAT activity than even RU-59063

Because it's a partial agonist for the AR? Why does this have to be explained? Like I said before, the 1997 study warranted further investigation, and the 2000 study confirmed it.

I'm not sure why you are so desperately clinging to this unknown drug when there are more promising compounds like way 31606 and ptd-dbm

 

[hemingway_the_mercenary]

Because it's a partial agonist for the AR? Why does this have to be explained? Like I said before, the 1997 study warranted further investigation, and the 2000 study confirmed it.

I'm not sure why you are so desperately clinging to this unknown drug when there are more promising compounds like way 31606 and ptd-dbm

It a partial agonist that is a stronger agonist than testosterone yet is frequently used for mtf trans and even some here use it for hairloss and it stops balding... this is why it is inconclusive.

If cyp ace can be used for hairloss and etc and has a lower CAT activity than Ru-59063 than there is potential that RU-59063 can be used as an anti androgen that has the ablity to block testosterone from the receptor with only mind agonistic effects. This is what I have been saying from the beggining. If cyp ace had a higher CAT activity like flut or bica I would give up on RU-59063 but so far its very unclear just how agonistic it is.

check out this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC22623/
Depending on the AR variant anti androgens can act as agonists. So the question is which AR variant did they use in the CAT activity% study. Keep in mind that this drug was being researched into for Flutamide and Hydroxyflutamide resistant prostate cancer not male pattern baldness. The ARs of the human scalp react very differently than prostate cancer ARs

 

[Thebaldcel]

It a partial agonist that is a stronger agonist than testosterone yet is frequently used for mtf trans and even some here use it for hairloss and it stops balding... this is why it is inconclusive.

If cyp ace can be used for hairloss and etc and has a lower CAT activity than Ru-59063 than there is potential that RU-59063 can be used as an anti androgen that has the ablity to block testosterone from the receptor with only mind agonistic effects. This is what I have been saying from the beggining. If cyp ace had a higher CAT activity like flut or bica I would give up on RU-59063 but so far its very unclear just how agonistic it is.

check out this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC22623/
Depending on the AR variant anti androgens can act as agonists. So the question is which AR variant did they use in the CAT activity% study. Keep in mind that this drug was being researched into for Flutamide and Hydroxyflutamide resistant prostate cancer not male pattern baldness. The ARs of the human scalp react very differently than prostate cancer ARs

The 1997 study used a mutant AR variant for that study. We can't take the result values as absolute.
Cypro is unique in that it is a steroid, and also a progestin which acts on the progesterone receptor. Progesterone has a large amount of functions. Cypro also decreases natural sex hormone production which explains why it is such a strong antiandrogen.

The difference with RU 59063 is the high selectivity for AR. With high selectivity, and high affinity, an agonist property would not be ideal for antiandrogen usage.

The 2000 study did not use a prostate cancer cell line. The AR was isolated from castrated prostates of Wistar rats, no cancer. Prostate cancer AR is a different beast.

Setting the agonist/antagonist argument aside, the next question is would this likely be good enough to reverse hair loss?

My honest take is it will confer a protective effect if you have supraphysiological levels of DHT or androgenic steroids, like certain sarms in low doses.

If you have low androgen levels such as being on a 5ar inhibitor, or female, then it will likely accelerate hair loss.

All in all, probably not the cure you're looking for. Much more promise with careful wounding combined with way316606 and ptd-dbm

 

[hemingway_the_mercenary]

The 1997 study used a mutant AR variant for that study. We can't take the result values as absolute.
Cypro is unique in that it is a steroid, and also a progestin which acts on the progesterone receptor. Progesterone has a large amount of functions. Cypro also decreases natural sex hormone production which explains why it is such a strong antiandrogen.

The difference with RU 59063 is the high selectivity for AR. With high selectivity, and high affinity, an agonist property would not be ideal for antiandrogen usage.

The 2000 study did not use a prostate cancer cell line. The AR was isolated from castrated prostates of Wistar rats, no cancer. Prostate cancer AR is a different beast.

Setting the agonist/antagonist argument aside, the next question is would this likely be good enough to reverse hair loss?

My honest take is it will confer a protective effect if you have supraphysiological levels of DHT or androgenic steroids, like certain sarms in low doses.

If you have low androgen levels such as being on a 5ar inhibitor, or female, then it will likely accelerate hair loss.

All in all, probably not the cure you're looking for. Much more promise with careful wounding combined with way316606 and ptd-dbm

Do have full access to this study? https://pubs.acs.org/doi/abs/10.1021/jm000163y

Because I can only read the abstact. If you have the full study can you pm the pdf. I need to do more reseach before coming to any conclusions. I believe one of the three RU molecules has potential for hairloss. The one used in the study to inhib the effects of testosterone on prostate weight is also interesting.

 

[Cody1212]

Any hormone altering path is not the best course. As a long time finasteride user, screwing with your hormones is a nightmare in the long run.

 

[random phone charger]

I might be interested in this, combining it with daro might be interesting.

Being interested in this, is like being interested in standing in front of a pack of traveling Hyenas covered in Gazelle blood, whilst trying to get them to display signs of good table etiquette.

 

[Recon_s]

Ru is weak as piss and this is 10-30 times stronger than both Daro and Enza.

I explained that the problem with all those drugs is that they are weaker than Testosterone not to mention DHT. This is stronger than DHT. That makes a world of s differencd

Ok so where are your results? oh wait that's right its just theory

 

[hemingway_the_mercenary]

Ok so where are your results? oh wait that's right its just theory

wtf lmao

this forum I swear