Does Anyone Try Oral Ru58841 For Aggressive Balding?

DHTcel

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Maave

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RU is a non-selective androgen receptor binding agent with a half life of 1 hour, and after 1 hour 1% of it has a half life of 20 hours. Say you drank 10mL of RU. That’s like 500mg. After 20 hours, you’d still have 5mg of RU in your system. Remember we dose finasteride at 1mg and Dutasteride at 0.25mg. But RU doesn’t just block 5AR like finasteride and dutasteride, it’s non-selective. You know what else in your body has androgen receptors? Literally everything. Your heart muscle, you brain, the cilia in your lungs. RU doesn’t give a f***. It’ll block all of them for 48 hours. Can you live for 48 hours with a heart that won’t beat? Can you hold your breath for an hour? If you start having a seizure because your brain can’t produce dopamine will you be able to call an ambulance before you bite your tongue off and drown in your own blood?

But f*** all that. Say you miraculously survived the onslaught on your vital organs. What happens when it all leaves your system and your pituitary-hypothalmic-adrenal axis has to reboot itself? If I had to guess I’d say the worst PFS in history, or coming off a 10,000ng/dL exogenous test cruise after ten years cold turkey. In other words, you’d be functionally retarded, infertile and impotent.

Your call tho
This sh*t makes no sense. NSAAs are frequently used for prostate cancer treatment. Your heart isn't going to stop from blocking testosterone, you're not going to die, your organs aren't going to shut down. NSAAs don't even downregulate the HPG axis, it's not cypro or lupron. It upregulates it due to blocked feedback. You're pulling all this out of your ***. Don't give people advice if you can't even read wikipedia.
 

DHTcel

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SuperDPAsteve

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This sh*t makes no sense. NSAAs are frequently used for prostate cancer treatment. Your heart isn't going to stop from blocking testosterone, you're not going to die, your organs aren't going to shut down. NSAAs don't even downregulate the HPG axis, it's not cypro or lupron. It upregulates it due to blocked feedback. You're pulling all this out of your ***. Don't give people advice if you can't even read wikipedia.

With respect, you’re completely wrong on this.

Your first mistake is to conflate RU, an NSARM, with prostate cancer drugs, NSAAs. Androgen deprivation therapy used in prostate cancer or gender transition differs from a non-selective androgen receptor inhibitor in two major ways.

Firstly, ADT blocks only the production of male sex hormones - i.e. test and DHT, and in rare cases, other androgens. Certain other drugs may even non-selectively inhibit aromatase. What ADT does not do is bind to or effect androgen receptors.

Secondly, their effect on the HPG axis is very different than any effect NSAAs might have. Yes, you are correct in that your HPG axis will upregulate itself when androgens are blocked. What you failed to realize was that the production of those androgens aren’t blocked, their receptors are. And what do we all know happens in the presence of an abundance of free androgens? Downregulation. Ask any bodybuilder on gear or TRT doctor.

The next point I’d like to make has to do with ADT. The more obvious misrepresentation you’ve made about the actual nature of RU58841 notwithstanding (it is not an NSAA), ADT in and of itself is not without its risks. Say the chemical structure of RU magically changed so it had the properties you thought it did. ADT has been associated with as high as a 25% chance of coronary artery disease. Impotence and infertility are obligatory. Long term degenerative brain tissue changes are seen in most patients on ADT for longer than two years (however in neglible amounts). The name ADT is also a little misleading. Except for in the most aggressive metastatic cases of prostate cancer, ADT focuses around depriving the cancer cells of testosterone and DHT through the use of 5AR and various testosterone reducing drugs as well as specific, selective aromatase inhibitors. What it does not remove are ALL of the androgens from the human body. It is undisputed that this would cause unacceptable harm or even death.

You’ve heard of SARMs - ever wonder why NSARMs aren’t a thing?

As a balding guy who has used RU58841 in the past and who currently uses a 5AR2I, I do my research on the chemicals I put into my body. I don’t just “pull things out of my ***” as you’ve suggested. However from your post it seems like you formulated your opinion based on a quick and inaccurate Wikipedia search so I won’t fault you for your swing & miss.

At the risk of jumping to conclusions it looks like you might be a transgender individual. While radical, the therapeutic approach to gender transition has nothing to do with NSARMS.
 

DHTcel

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With respect, you’re completely wrong on this.

Your first mistake is to conflate RU, an NSARM, with prostate cancer drugs, NSAAs. Androgen deprivation therapy used in prostate cancer or gender transition differs from a non-selective androgen receptor inhibitor in two major ways.

Firstly, ADT blocks only the production of male sex hormones - i.e. test and DHT, and in rare cases, other androgens. Certain other drugs may even non-selectively inhibit aromatase. What ADT does not do is bind to or effect androgen receptors.

Secondly, their effect on the HPG axis is very different than any effect NSAAs might have. Yes, you are correct in that your HPG axis will upregulate itself when androgens are blocked. What you failed to realize was that the production of those androgens aren’t blocked, their receptors are. And what do we all know happens in the presence of an abundance of free androgens? Downregulation. Ask any bodybuilder on gear or TRT doctor.

The next point I’d like to make has to do with ADT. The more obvious misrepresentation you’ve made about the actual nature of RU58841 notwithstanding (it is not an NSAA), ADT in and of itself is not without its risks. Say the chemical structure of RU magically changed so it had the properties you thought it did. ADT has been associated with as high as a 25% chance of coronary artery disease. Impotence and infertility are obligatory. Long term degenerative brain tissue changes are seen in most patients on ADT for longer than two years (however in neglible amounts). The name ADT is also a little misleading. Except for in the most aggressive metastatic cases of prostate cancer, ADT focuses around depriving the cancer cells of testosterone and DHT through the use of 5AR and various testosterone reducing drugs as well as specific, selective aromatase inhibitors. What it does not remove are ALL of the androgens from the human body. It is undisputed that this would cause unacceptable harm or even death.

You’ve heard of SARMs - ever wonder why NSARMs aren’t a thing?

As a balding guy who has used RU58841 in the past and who currently uses a 5AR2I, I do my research on the chemicals I put into my body. I don’t just “pull things out of my ***” as you’ve suggested. However from your post it seems like you formulated your opinion based on a quick and inaccurate Wikipedia search so I won’t fault you for your swing & miss.

At the risk of jumping to conclusions it looks like you might be a transgender individual. While radical, the therapeutic approach to gender transition has nothing to do with NSARMS.
I have an idea, what if I make a protein powder shake with 200mg of RU58841 and see what happens?
 

SuperDPAsteve

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DHTcel

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Maave

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With respect, you’re completely wrong on this.

Your first mistake is to conflate RU, an NSARM, with prostate cancer drugs, NSAAs. Androgen deprivation therapy used in prostate cancer or gender transition differs from a non-selective androgen receptor inhibitor in two major ways.

Firstly, ADT blocks only the production of male sex hormones - i.e. test and DHT, and in rare cases, other androgens. Certain other drugs may even non-selectively inhibit aromatase. What ADT does not do is bind to or effect androgen receptors.

Secondly, their effect on the HPG axis is very different than any effect NSAAs might have. Yes, you are correct in that your HPG axis will upregulate itself when androgens are blocked. What you failed to realize was that the production of those androgens aren’t blocked, their receptors are. And what do we all know happens in the presence of an abundance of free androgens? Downregulation. Ask any bodybuilder on gear or TRT doctor.

The next point I’d like to make has to do with ADT. The more obvious misrepresentation you’ve made about the actual nature of RU58841 notwithstanding (it is not an NSAA), ADT in and of itself is not without its risks. Say the chemical structure of RU magically changed so it had the properties you thought it did. ADT has been associated with as high as a 25% chance of coronary artery disease. Impotence and infertility are obligatory. Long term degenerative brain tissue changes are seen in most patients on ADT for longer than two years (however in neglible amounts). The name ADT is also a little misleading. Except for in the most aggressive metastatic cases of prostate cancer, ADT focuses around depriving the cancer cells of testosterone and DHT through the use of 5AR and various testosterone reducing drugs as well as specific, selective aromatase inhibitors. What it does not remove are ALL of the androgens from the human body. It is undisputed that this would cause unacceptable harm or even death.

You’ve heard of SARMs - ever wonder why NSARMs aren’t a thing?

As a balding guy who has used RU58841 in the past and who currently uses a 5AR2I, I do my research on the chemicals I put into my body. I don’t just “pull things out of my ***” as you’ve suggested. However from your post it seems like you formulated your opinion based on a quick and inaccurate Wikipedia search so I won’t fault you for your swing & miss.

At the risk of jumping to conclusions it looks like you might be a transgender individual. While radical, the therapeutic approach to gender transition has nothing to do with NSARMS.

RU-58841 an NSAA. Every study says so. I don't know where you're getting your information.

https://www.ncbi.nlm.nih.gov/pubmed/9415227
"A controlled study of the effects of RU58841, a non-steroidal antiandrogen"

https://www.ncbi.nlm.nih.gov/pubmed/9798729
"The effect of androgen receptor transcriptional activation by RU58841, a nonsteroidal anti-androgen"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2072875/

Another series of hydantoin analogs are nilutamide derivatives like RU58642 [4-(3-Cyanomethyl-4,4-dimethyl-2,5-dioxo-imidazolidin-1-yl)-2-trifluoromethyl-benzonitrile] and RU58841 [1-(4-Hydroxy-butyl)-3-(4-isocyano-3-trifluoromethyl-phenyl)-5,5-dimethyl-imidazolidine-2,4-dione]. RU58841 (Tables (TablesII and andII)II) was developed in Europe for topical treatment of acne and alopecia (42,43), due to its short half life in vivo (less than one hour). Topical application not only avoids extensive hepatic metabolism (N-dealkylation) but also provides for effective regional treatment without systemic antiandrogen activity due to the formation of active metabolite

I don't recommend oral RU58841. The reason RU58841 is useful topically is because its half life is short and its metabolites are weak, so once its absorbed systemically it becomes weaker, as mentioned above. Its metabolites are similar to nilutamide (an outdated NSAA with more side effects) so if you manage to take enough to be effective you're risking side effects.

Firstly, ADT blocks only the production of male sex hormones - i.e. test and DHT, and in rare cases, other androgens. Certain other drugs may even non-selectively inhibit aromatase. What ADT does not do is bind to or effect androgen receptors.

NSAAs are a frequent part of ADT. Like just google "adt" and NSAAs are part of it.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1831539/

The addition of an antiandrogen provides maximum androgen blockade.
...
MAB can be achieved pharmacologically by combining an LHRH agonist with an antiandrogen. The antiandrogens flutamide, bicalutamide, and nilutamide block the effects of adrenal androgens at the androgen receptor. There is a general consensus that MAB has a role in the treatment of advanced prostate cancer.30 The controversy is whether MAB should be the initial form of ADT or whether the antiandrogen should be offered after the patient has had disease progression with LHRH agonist treatment.

"ADT" it's a catch all and includes medical castration (GnRH agonists / LHRH agonists), surgical castration, and anti-androgens including NSAAs. But you can't lump NSAA monotherapy with other forms of ADT, the side effects are completely different. The difference is that NSAAs don't lower serum testosterone, so all the hormones and neurosteroids derived from T are still produced and reach your brain and bones. Search "bicalutamide monotherapy" if you want an idea of NSAA side effects and rates. Here are some examples

https://onlinelibrary.wiley.com/doi/full/10.1046/j.1464-410X.2003.04026.x
The mainstay of hormonal therapy in prostate cancer has been medical or surgical castration, both of which are associated with loss of libido and impotence, and may not always be acceptable to the patient. Antiandrogen monotherapy is an alternative treatment option to castration.
....
Large phase III trials have established that monotherapy with bicalutamide 150 mg once daily provides a survival outcome that is not significantly different to that after castration in men with locally advanced, non-metastatic disease, while conferring significant advantages for sexual interest and physical capacity.
...
Bicalutamide has a more favourable side effect-profile than the other antiandrogens and is more likely to promote compliance.



I have medical sources for days. Come back with sources for your claims.
 

Maave

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I have an idea, what if I make a protein powder shake with 200mg of RU58841 and see what happens?
Don't bother. It's ineffective and you'll get side effects like nilutamide.
 

hemingway_the_mercenary

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With respect, you’re completely wrong on this.

Your first mistake is to conflate RU, an NSARM, with prostate cancer drugs, NSAAs. Androgen deprivation therapy used in prostate cancer or gender transition differs from a non-selective androgen receptor inhibitor in two major ways.

Firstly, ADT blocks only the production of male sex hormones - i.e. test and DHT, and in rare cases, other androgens. Certain other drugs may even non-selectively inhibit aromatase. What ADT does not do is bind to or effect androgen receptors.

Secondly, their effect on the HPG axis is very different than any effect NSAAs might have. Yes, you are correct in that your HPG axis will upregulate itself when androgens are blocked. What you failed to realize was that the production of those androgens aren’t blocked, their receptors are. And what do we all know happens in the presence of an abundance of free androgens? Downregulation. Ask any bodybuilder on gear or TRT doctor.

The next point I’d like to make has to do with ADT. The more obvious misrepresentation you’ve made about the actual nature of RU58841 notwithstanding (it is not an NSAA), ADT in and of itself is not without its risks. Say the chemical structure of RU magically changed so it had the properties you thought it did. ADT has been associated with as high as a 25% chance of coronary artery disease. Impotence and infertility are obligatory. Long term degenerative brain tissue changes are seen in most patients on ADT for longer than two years (however in neglible amounts). The name ADT is also a little misleading. Except for in the most aggressive metastatic cases of prostate cancer, ADT focuses around depriving the cancer cells of testosterone and DHT through the use of 5AR and various testosterone reducing drugs as well as specific, selective aromatase inhibitors. What it does not remove are ALL of the androgens from the human body. It is undisputed that this would cause unacceptable harm or even death.

You’ve heard of SARMs - ever wonder why NSARMs aren’t a thing?

As a balding guy who has used RU58841 in the past and who currently uses a 5AR2I, I do my research on the chemicals I put into my body. I don’t just “pull things out of my ***” as you’ve suggested. However from your post it seems like you formulated your opinion based on a quick and inaccurate Wikipedia search so I won’t fault you for your swing & miss.

At the risk of jumping to conclusions it looks like you might be a transgender individual. While radical, the therapeutic approach to gender transition has nothing to do with NSARMS.


WOW, I cant believe people actually believe this crap and your post actually has likes

ADT- androgen deprivation therapy doesnt only block the production of testosterone, almost always AR blocking drugs are included and even the most common drug which shuts down the production of testosterone in cyp ace is also a AR blocker as well

Bicalutamide, Enzalutamide, Darolutamide, Spirinolactone, Cyp Ace and etc ALL block the AR non selectively just like RU. Your post isnt even worth my time.


you are seriously a clueless moron
 

SuperDPAsteve

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RU-58841 an NSAA. Every study says so. I don't know where you're getting your information.

https://www.ncbi.nlm.nih.gov/pubmed/9415227
"A controlled study of the effects of RU58841, a non-steroidal antiandrogen"

https://www.ncbi.nlm.nih.gov/pubmed/9798729
"The effect of androgen receptor transcriptional activation by RU58841, a nonsteroidal anti-androgen"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2072875/



I don't recommend oral RU58841. The reason RU58841 is useful topically is because its half life is short and its metabolites are weak, so once its absorbed systemically it becomes weaker, as mentioned above. Its metabolites are similar to nilutamide (an outdated NSAA with more side effects) so if you manage to take enough to be effective you're risking side effects.



NSAAs are a frequent part of ADT. Like just google "adt" and NSAAs are part of it.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1831539/



"ADT" it's a catch all and includes medical castration (GnRH agonists / LHRH agonists), surgical castration, and anti-androgens including NSAAs. But you can't lump NSAA monotherapy with other forms of ADT, the side effects are completely different. The difference is that NSAAs don't lower serum testosterone, so all the hormones and neurosteroids derived from T are still produced and reach your brain and bones. Search "bicalutamide monotherapy" if you want an idea of NSAA side effects and rates. Here are some examples

https://onlinelibrary.wiley.com/doi/full/10.1046/j.1464-410X.2003.04026.x




I have medical sources for days. Come back with sources for your claims.

Cool post but you failed to address the mode of action of RU - receptor modulation. Studies may call it an antiandrogen but are you going to tell me that RU actually inhibits the production of androgens? If so, please post a link because I’m totally unaware. It seems like the disagreement is going nowhere and I don’t want to debate semantics. A cursory read of this very website’s info page on RU should explain exactly why systemic application is extremely dangerous.

OP - please do your own research and our safety first
 

Grim

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I'm not familiar with alot of the medications that are being talked about here, but if you're desperate then maybe oral spironolactone could help. But it has a risk for gyno and feminization. If dutasteride isn't enough maybe spironolactone could help.
 

el_duterino

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@DHTcel
do you a actually have hair loss?
From one of the photo you posted before you seem to have perfect thick hair

That may explain why none of these drugs work for you
 

DHTcel

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I just tried 200mg orally, my heart has been hurting for the past 15 minutes. when I apply it topically my heart only beats fast for like a minute or two but orally its worse. Ill let u guys know if it made a difference by tomorrow when I take a shower.
 

hz123456

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Y’all this guy doesn’t have hairloss from earlier photos I’ve seen. The stuff I’ve seen posted is extemely dangerous for a 16 year old... especially one who might not even need finasteride
 

Grim

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Its none of my business but if you're not balding and taking alot of stuff it can cause alot of damage. Maybe you have ocd. I sure as heck do. It sucks.
 

FCKW36

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RU58841 is basically snake oil tbh, I'm thinking about using topical estradiol next but if that doesn't work then idk tbh


RU is definitely not snake oil. I got regrowth in my temples from RU alone and I can back this with photos. I also paused RU vor 2 month after 4 years of usage last year because I had some problems with my supplier and that led to the biggest shedding I ever head in my life.
 

FCKW36

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I just tried 200mg orally, my heart has been hurting for the past 15 minutes. when I apply it topically my heart only beats fast for like a minute or two but orally its worse. Ill let u guys know if it made a difference by tomorrow when I take a shower.

Omg you are so retarded... Unbelievable.
 
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