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

[hemingway_the_mercenary]

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?

 

[Francky85]

Of all the things ive tried to combat hair loss, Ru-58841 is the worst; it made me feel like death and I had the worst chest pains on it....something 100x stronger would probably kill me....to me that approach is like using a nuclear bomb to crack a nut.

 

[hemingway_the_mercenary]

Welcome to 10 years ago.

Many tried it. It's a mess to make an a lot noticed side effects. It works though.

lolwut

there is not one thread about this on all of the internet. Im not sure if your talking about ru58841 or what but there are many different drugs that start with RU and I strongly doubt youd be able to recognize the name just by looking at it. Go google it, try to find one thread about this on hairloss forums. I think your mistaken this for something else

but, if you could find me any threads of people trying this, Id greatly appreciate it

btw just cause its from 10 years ago doesnt mean its useless/old. Enzalutamide which is the strongest marketed anti anrogen today was discovered in 2003/2004. It takes forverever for drugs to pass through FDA regulations

 

[jared garnith]

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

 

[Recon_s]

all these are great in theory but never work look at RU enzo daro etc no one has had success

 

[hemingway_the_mercenary]

all these are great in theory but never work look at RU enzo daro etc no one has had success

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

 

[Sanchez1234]

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...

On this RU or the RU-58841 version everybody is using?

 

[Thebaldcel]

Honestly, if enzalutamide and darolutamide doesn't work then antiandrogens probably aren't the answer. Throwing in a stronger one is going to do nothing more than maybe marginally slowing down progression at the risk of increased sides. The only way is to turn into a female and even then it isn't guaranteed because females also suffer from Androgenetic Alopecia.

 

[abcdefg]

Honestly, if enzalutamide and darolutamide doesn't work then antiandrogens probably aren't the answer. Throwing in a stronger one is going to do nothing more than maybe marginally slowing down progression at the risk of increased sides. The only way is to turn into a female and even then it isn't guaranteed because females also suffer from Androgenetic Alopecia.

Why do women go bald? Its not androgens so what else is it?
I do think stronger AAs are good if done safely, but again castration prevents male pattern baldness. It doesnt reverse or regrow it. No AA no matter how powerful will ever top castration. Prevention is the absolute best your going to get going down this road.

 

[disfiguredyoungman]

Why do women go bald? Its not androgens so what else is it?
I do think stronger AAs are good if done safely, but again castration prevents male pattern baldness. It doesnt reverse or regrow it. No AA no matter how powerful will ever top castration. Prevention is the absolute best your going to get going down this road.

HRT can regrow hair on basically a chrome dome.

 

[hemingway_the_mercenary]

The old RU.

Lmao which one are you talking about. I still can’t tell

@Thebaldcel yes androgens are not the problem for androgenic alopecia...

I already explained how weak enza and Daro are compared to testosterone. Compared to DHT they are nothing

 

[hemingway_the_mercenary]

Honestly, if enzalutamide and darolutamide doesn't work then antiandrogens probably aren't the answer. Throwing in a stronger one is going to do nothing more than maybe marginally slowing down progression at the risk of increased sides. The only way is to turn into a female and even then it isn't guaranteed because females also suffer from Androgenetic Alopecia.

Castrations crashes both testosterone and estradiol levels. The ratio between theM is key for regrowth. Doesn’t mean castrations doesn’t work.

Regardless this version of RU is stronger than castration

 

[jamesbooker1975]

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?

You are forgueting the most important thing. Do this drug go systemic ? There is not a single human study showing that will not.

 

[hemingway_the_mercenary]

You are forgueting the most important thing. Do this drug go systemic ? There is not a single human study showing that will not.

All drugs go systemic. You either accept going bald and stay off all meds or you have a threshold to which point you are willing to accept the possiblity of side effects. Everyone takes that risk when they take even something as weak as finasteride

 

[Thebaldcel]

Why do women go bald? Its not androgens so what else is it?
I do think stronger AAs are good if done safely, but again castration prevents male pattern baldness. It doesnt reverse or regrow it. No AA no matter how powerful will ever top castration. Prevention is the absolute best your going to get going down this road.

By answer I mean throwing stronger antiandrogens at your body is not the answer to reversing hair loss unless you're fine with becoming transsexual. And I'm saying even having female levels of androgens sometimes isn't enough considering some females suffer from Androgenetic Alopecia too. Androgens are the main culprit but the ultimate cause is the immune response that occurs when androgens bind. There is something that is causing the receptors themselves to be upregulated even when androgen levels are crippled.

Lmao which one are you talking about. I still can’t tell

@Thebaldcel yes androgens are not the problem for androgenic alopecia...

I already explained how weak enza and Daro are compared to testosterone. Compared to DHT they are nothing

Wikipedia says enzalutamide only has 2-3 fold less binding affinity to the AR compared to DHT (citation checked). This is similar to testosterone or even stronger. Darolutamide has significantly stronger binding affinity than enza, with a Ki of 11nM, while enzalutamide has a Ki of 86 nM.

For comparison, ru-59063 had a Ki of 2.23 SD 0.5 nM in rat AR. Ru58841 26 SD 5 nM. Not the huge difference as you made it seem, and not to mention it's actually a partial agonist. There's a chance it would actually accelerate hair loss.

Meanwhile, the cancer drugs enza and darolutamide silences AR signaling and aren't just antagonists. There is a reason why ru59063 was abandoned and why daro is being researched for castration resistant prostate cancer. But even then, there has been limited success with daro and enza for hair loss.

 

[hemingway_the_mercenary]

By answer I mean throwing stronger antiandrogens at your body is not the answer to reversing hair loss unless you're fine with becoming transsexual. And I'm saying even having female levels of androgens sometimes isn't enough considering some females suffer from Androgenetic Alopecia too. Androgens are the main culprit but the ultimate cause is the immune response that occurs when androgens bind. There is something that is causing the receptors themselves to be upregulated even when androgen levels are crippled.



Wikipedia says enzalutamide only has 2-3 fold less binding affinity to the AR compared to DHT (citation checked). This is similar to testosterone or even stronger. Darolutamide has significantly stronger binding affinity than enza, with a Ki of 11nM, while enzalutamide has a Ki of 86 nM.

For comparison, ru-59063 had a Ki of 2.23 SD 0.5 nM in rat AR. Ru58841 26 SD 5 nM. Not the huge difference as you made it seem, and not to mention it's actually a partial agonist. There's a chance it would actually accelerate hair loss.

Meanwhile, the cancer drugs enza and darolutamide silences AR signaling and aren't just antagonists. There is a reason why ru59063 was abandoned and why daro is being researched for castration resistant prostate cancer. But even then, there has been limited success with daro and enza for hair loss.

Actually here are the real numbers for the strenght of Daro vs DHT. It about 20-80x weaker. Not even close. I strongly dislike when people spew out misinformation like this. Your source for Enza being 2-3 weaker than Testosterone is Wikipedia...

ORM-15341: (Ki) of 8 nM and an IC50 of 38 nM
Darolutamide: (Ki) of 11 nM and an IC50 of 26 nM
DHT: (Kd) of 0.25 to 0.5 nM and an EC50 for activation of the AR is 0.13 nM
Testosterone: Kd = 0.4 to 1.0 nM and an EC50 of 0.66 nM

So as everyone can see there is a HUGE difference between this RU and all the other mentioned drugs.

 

[Thebaldcel]

Actually here are the real numbers for the strenght of Daro vs DHT. It about 20-80x weaker. Not even close. I strongly dislike when people spew out misinformation like this. Your source for Enza being 2-3 weaker than Testosterone is Wikipedia...

ORM-15341: (Ki) of 8 nM and an IC50 of 38 nM
Darolutamide: (Ki) of 11 nM and an IC50 of 26 nM
DHT: (Kd) of 0.25 to 0.5 nM and an EC50 for activation of the AR is 0.13 nM
Testosterone: Kd = 0.4 to 1.0 nM and an EC50 of 0.66 nM

So as everyone can see there is a HUGE difference between this RU and all the other mentioned drugs.

I checked the citation, but it's ironic how you mention wikipedia when you pulled that table from wikipedia, and then pulled the Kd values from wikipedia lol. Here is something contradicting. Your intro states relative binding affinity of ru 59063 as 300, while DHT is 180. The Ki of ru-59063 is 2.2nm while stated Kd of dht is 0.25.

But let's conveniently forget the fact that ru-59063 is actually androgenic and not antiandrogenic. That Ki should probably be actually Kd.

Yup, Ru-59063 was discontinued because it activates the AR rather than inhibit it. There is a plain reason why enzalutamide and darolutamide are being researched for prostate cancer and not ru-59063. Applying that ru to your scalp will likely cause hair loss. Binding affinity is only a single property.

 

[hemingway_the_mercenary]

I checked the citation, but it's ironic how you mention wikipedia when you pulled that table from wikipedia, and then pulled the Kd values from wikipedia lol. Here is something contradicting. Your intro states relative binding affinity of ru 59063 as 300, while DHT is 180. The Ki of ru-59063 is 2.2nm while stated Kd of dht is 0.25.

But let's conveniently forget the fact that ru-59063 is actually androgenic and not antiandrogenic. That Ki should probably be actually Kd.

Yup, Ru-59063 was discontinued because it activates the AR rather than inhibit it. There is a plain reason why enzalutamide and darolutamide are being researched for prostate cancer and not ru-59063. Applying that ru to your scalp will likely cause hair loss. Binding affinity is only a single property.

I checked all the sources before posting, the source for enza beiing 2-3 weaker than DHT was not active, so theres no way you checked it

you apparantly dont understand what a partial agonist is, cyperatone ace is a partial agonist too, doesnt mean it doesnt work. Youre obviously not the kind of person who will be intrested in trying out this drug. Why are you commenting on this thread?

all the info you put out is half assed research you never actually bothered to look into. That table I posted was also on a pubmed publication, which I actually bothered to read before posting this thread.

What you dont understand about Ki and Kd values is they change during experiments depending on testing conditons so in order for the Ki and Kd to be valid when comparing 2 different drugs they need to be tested during the same experiment. Thats why I posted the relative binding affinity which is much more valid when comparing different drugs.

Heres a study in which it prevents the effects of 6x the amount of testosterone measured by prostate weight.

This is what I mean when I say this is in a world of its own. Any other drug would need to be administered at dosages at least 20x the dose of testosterone to inhibit the testosterone meanwhile this is able to inhib the androgenic effect of testosterone at 6x lower concentrations. Insane

For reference the medium dose for daro is 200-250mg 2x daily, meaning 400-500mg per day, while a man with high testosterone will only be producing at max 20mg per day

"Thus, RU 56187, given orally in castrated male animals, prevented in a dose-dependent manner the effects of 3 mg/kg testosterone propionate (TP) on mouse renal ornithine decarboxylase (acute test) and of 0.5 mg/kg TP on rat prostate weight (chronic test). In these two models, its ED50 was 0.6 and 1 mg/kg, respectively. In the intact rat, when given alone, it inhibited dose-dependently the effect of endogenous androgens on the seminal vesicles (ED50 approximately 1 mg/kg) and prostate (ED50 approximately 3 mg/kg) weights. These results suggest that these new compounds may be useful as specific markers for the androgen receptor as well as for the treatment of androgen-dependent diseases or disorders such as prostate cancer, acne, hirsutism and male pattern baldness."

enza and daro are made for castration resistant prostate cancer during which the Ars of the cancer cells have mutated and are able to use bicalutamide as an androgen. There is incentive to market this RU when it likely wont stop mutated forms of cancer cells and also cause more side effects than bicalutamide because it is anti androgenic in every tissue including the testicles. There are already sufficient drugs for regualr forms of prostate cancer with great safety profiles.

none of this has any relation to male pattern baldness which no one has bothered to research this drug for.

 

[Thebaldcel]

I checked all the sources before posting, the source for enza beiing 2-3 weaker than DHT was not active, so theres no way you checked it

you apparantly dont understand what a partial agonist is, cyperatone ace is a partial agonist too, doesnt mean it doesnt work. Youre obviously not the kind of person who will be intrested in trying out this drug. Why are you commenting on this thread?

all the info you put out is half assed research you never actually bothered to look into. That table I posted was also on a pubmed publication, which I actually bothered to read before posting this thread.

What you dont understand about Ki and Kd values is they change during experiments depending on testing conditons so in order for the Ki and Kd to be valid when comparing 2 different drugs they need to be tested during the same experiment. Thats why I posted the relative binding affinity which is much more valid when comparing different drugs.

Heres a study in which it prevents the effects of 6x the amount of testosterone measured by prostate weight.

This is what I mean when I say this is in a world of its own. Any other drug would need to be administered at dosages at least 20x the dose of testosterone to inhibit the testosterone meanwhile this is able to inhib the androgenic effect of testosterone at 6x lower concentrations. Insane

For reference the medium dose for daro is 200-250mg 2x daily, meaning 400-500mg per day, while a man with high testosterone will only be producing at max 20mg per day

"Thus, RU 56187, given orally in castrated male animals, prevented in a dose-dependent manner the effects of 3 mg/kg testosterone propionate (TP) on mouse renal ornithine decarboxylase (acute test) and of 0.5 mg/kg TP on rat prostate weight (chronic test). In these two models, its ED50 was 0.6 and 1 mg/kg, respectively. In the intact rat, when given alone, it inhibited dose-dependently the effect of endogenous androgens on the seminal vesicles (ED50 approximately 1 mg/kg) and prostate (ED50 approximately 3 mg/kg) weights. These results suggest that these new compounds may be useful as specific markers for the androgen receptor as well as for the treatment of androgen-dependent diseases or disorders such as prostate cancer, acne, hirsutism and male pattern baldness."

enza and daro are made for castration resistant prostate cancer during which the Ars of the cancer cells have mutated and are able to use bicalutamide as an androgen. There is incentive to market this RU when it likely wont stop mutated forms of cancer cells and also cause more side effects than bicalutamide because it is anti androgenic in every tissue including the testicles. There are already sufficient drugs for regualr forms of prostate cancer with great safety profiles.

none of this has any relation to male pattern baldness which no one has bothered to research this drug for.

You're right I did half assed research, because it doesn't take extensive research to see this won't cure your hair loss. All the studies calculating the Ki values have had the same range of value, which is higher than the known Kds of test and dht.

I'm posting here because this is potentially dangerous and it likely won't work. I'm not sure why you are clinging to this, but I don't want you dragging in other baldcels into your fool's errand.

Cypro has a very weak binding affinity to the AR, so I don't see how you can compare its partial agonism to Ru-59063. Ru59063 is actually more than a partial agonist, and may be a full agonist, albeit weaker than DHT. In fact, it may be considered a SARM. Have you checked out the data on this study?

https://www.ncbi.nlm.nih.gov/m/pubmed/10966753/?i=2&from=ru 59063

It has dose dependent androgenic effects. That study you quoted says ru 56187, not 59063. If you read the paper it's because 59063 had less than stellar antiandrogen function.

Certain anabolic SARMs also have protective effects on the prostate, but it doesn't mean they are AR antagonists.

Also you are underestimating the significance of enza and daro compared to ru59063. They are actually full antagonists of the AR. In addition, they block binding to DNA and coactivators. They are in a class above ru 59063, which actually activates the AR anand isn't an antagonist.

I hope anyone reading this can see that a combo of activating the AR+high binding affinity= bad news for hair.

Also, I'm doing you a favor. You are on a fool's errand. The trend of flocking to the next strongest antiandrogen is already bad enough, but you didn't even pick a good one

 

[hemingway_the_mercenary]

You're right I did half assed research, because it doesn't take extensive research to see this won't cure your hair loss. All the studies calculating the Ki values have had the same range of value, which is higher than the known Kds of test and dht.

I'm posting here because this is potentially dangerous and it likely won't work. I'm not sure why you are clinging to this, but I don't want you dragging in other baldcels into your fool's errand.

Cypro has a very weak binding affinity to the AR, so I don't see how you can compare its partial agonism to Ru-59063. Ru59063 is actually more than a partial agonist, and may be a full agonist, albeit weaker than DHT. In fact, it may be considered a SARM. Have you checked out the data on this study?

https://www.ncbi.nlm.nih.gov/m/pubmed/10966753/?i=2&from=ru 59063

It has dose dependent androgenic effects. That study you quoted says ru 56187, not 59063. If you read the paper it's because 59063 had less than stellar antiandrogen function.

Certain anabolic SARMs also have protective effects on the prostate, but it doesn't mean they are AR antagonists.

Also you are underestimating the significance of enza and daro compared to ru59063. They are actually full antagonists of the AR. In addition, they block binding to DNA and coactivators. They are in a class above ru 59063, which actually activates the AR anand isn't an antagonist.

I hope anyone reading this can see that a combo of activating the AR+high binding affinity= bad news for hair.

Also, I'm doing you a favor. You are on a fool's errand. The trend of flocking to the next strongest antiandrogen is already bad enough, but you didn't even pick a good one

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