The Cure For Hair Loss - The Truth About 5α-Reductase Inhibitors and Topical Anti-Androgens

View attachment 3683815

The Cure For Hair Loss - The Truth about 5α-Reductase Inhibitors and Topical Anti-Androgens - Part 2
(excuse the shit formatting, I don't normally write threads, so I can't format for shit)

What does this thread include?
In this thread I will be covering the different treatments depending on your age and situation for hair loss, as well as what impact each of these drugs will have on your development.

1) Introduction
2) Why are you balding in the first place?
3) What can we do about DHT at the scalp?
4) Distinguishing between Type 1 isoenzyme and Type 2 isoenzyme
5) Should I be worried about side effects from FInasteride?
6) Hair loss treatment if you are over 18
7) Hair loss treatment if you are under 18
8) What do do if you still experience hair loss on 5α-Reductase inhibitors
9) Is RU58841 safe for use, since it's a research chemical
10) How to make RU58841 solution
11) Drug dosages


Introduction.
We all know, hair is life, if you have no hair, you have no life.

Once you down the rabbit hole of finding a "cure" for hair loss, you will find that you have only 2 real options in term of halting the actual hair loss itself. Those options would be Finasteride/Dutasteride (5α-Reductase inhibitor) or research produces like ru58841. In this thread I will go into depth about these, and which one people should use depending on their situation, or if they should use one at all.

Why are you balding in the first place?
The vast majority of men go bald because of a hereditary condition called Androgenic Alopecia (AGA). Unfortunately, the number of men that do not have condition are in the minority, so do not assume that you are safe from the norwood reaper, ever. Everyone's hair follicles has a different sensitivity to androgens. The androgens binding to the hair follicles will make the Anagen phase shorter and shorter until a permanent state of anagen phase is present and the hair follicle is deactivated. The strongest hormone that shorten the Anagen phase is DHT (dihydrotestosteron) and Testosterone. Some woman are so sensitive to DHT and Testosterone that the small amount they produce is sufficient enough to cause hair loss.

What can we do about DHT at the scalp?
As I mentioned above, there is a very limited number of things we can do to combat this, however using the protocols I will outline in this thread will leave you having you hair for life. First we have to take care of the main androgen in causing hair loss, which already outlined above, is DHT. There is only one safe way to decrease the amount of DHT in your body, and that is taking a 5α-Reductase inhibitor such as Finasteride or Dutasteride. In taking on of these 5α-Reductase inhibitors, we are systematically decreasing the amount of DHT in out body, and subsequently decreasing the amount of scalp DHT we have, which is what we want to reduce as much as possible. I will outline which is best to take for each individual, since it's dependant on your age, if you use certain compounds to "pubertymaxx" etc.

Will 5α-Reductase inhibitors stunt bone development?
Is taking 5α-Reductase inhibitors going to keep you boneless forever? Lets find out.

Study:
Results: Patients with dihydrotestosterone deficiency present normal bone mineral density, suggesting that dihydrotestosterone is not the main androgen acting in bone.

Study:
Results:
View attachment 3683851

The two guys on the left have 0 DHT (literally) and they still have a normal bone structure and an identical height, bone density and skeletal mass to their healthy siblings, it have a higher binding affinity to the androgen receptor but it doesn't cause the same physiological response.
The pubertal growth spurt (for men) is also induced by testosterone and not DHT.

Also 5AR is not very active in bone tissues and DHT is mainly a paracrine hormone (i.e it acts where it's produced while testosterone acts on the whole body despite being produced in the testes).

So, does that mean we should all just take the strongest 5α-Reductase inhibitor (Dutasteride) and call it a day? Well, no. First we have to distinguish between the two forms of DHT, as these studies to not distinguish between them, so it is not the full picture.

Distinguishing between Type 1 isoenzyme and Type 1 isoenzyme.

Both these studies show that DHT doesn't have an effect on bones, right? So, we should all just take Dutasteride? Wrong.

These studies have not differentiated between type 1 isoenzyme, and type 2 isoenzyme.

So, first we have to see where type 1 DHT and type 2 DHT are expressed in the body.

Type 2 DHT is not expressed in bones at all, it's only expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles, and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys.

However, Type 1 DHT is actually expressed in bones. This matters because the studies I have shown above, are actually only deficient in the type 2 isoenzyme, which is the one that is not present in bones. This is the reason they present with normal bone mineral density, bone structure etc. If they were also deficient in Type 1 DHT, this would likely not be the case at all.

"5α-Reductase type 1 inactivated male mice have reduced bone mass and forelimb muscle grip strength, which has been proposed to be due to lack of 5α-reductase type 1 expression in bone and muscle.[29] In 5 alpha reductase type 2 deficient males, the type 1 isoenzyme is thought to be responsible for their virilization at puberty.[6]"

Bone growth and change will be minimal after 18, I definitely agree, but it still does happen. Facial bones are flat bones. They do not fuse, so they will continue to change forever, obviously to a lesser extent the older you get. Bones development/growth “stops” when resorption becomes greater than formation. As you age, this is more likely to happen, and will happen at a certain age most likely. Taking Dut with inhibits type 1, which is active in bones would likely have a negative impact, and speed up this process. You also won't achieve the slight bone changes that maybe desirable. It's true you don't know if you will have any noticeable change. Even in terms of BMD, doesn't effect aesthetics, it is still somewhat important for health. I would feel more comfortable to take Finasteride over Dutasteride if natural, since enhanced individuals would probably be able to compensate with supraphysiological Test levels and compensate for the lack of Type 1 DHT. The only thing I can really think of that have possibly comparable DHT type 1 levels to men on Dutasteride, would be women, who do actually have lower bone mass and lower BMD than men, and are at a greater risk of developing osteoporosis compared to men. That is not me saying if you take Dut your bones are going to melt and dissolve off your face.

Should I be worried about side effects from Finasteride?
I am not going to say that side effects do not exist, there are going to be the very unfortunate minority that may get side effects, but most of the people that are reporting side effects are schizo, especially if you go to places like r/tressless. They are basically all mentally ill. I’m not saying PFS or side effects in general aren't real, but I am saying that side effects, including PFS, are very much exaggerated in 2025.

Even in long-term studies (10 yr +) in Asians, no evidence of PFS symptoms were ever discovered. Only 1-3% get sexual sides, which wasn't even significantly different from the placebo arm in the original trials.

View attachment 3683840


Only after social media started popping off side effect reports started skyrocketing, and no, it’s not because there were fewer users back in the 2000s, millions of men were already on it back then.

There is some evidence for the existence of PFS and I will link a post here:
Personally, I would take the chance 10/10 times.

Hair loss treatment if you're over 18.
If you are above the age of 18, and are natural, which means you DO NOT take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Finasteride at 1mg ever day.
If you are above the age of 18, and are enhanced, which means you DO take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Dutasteride at 2.5mg a day.

Hair loss treatment if you're under 18.
If you are younger than, you don't want to reduce your serum DHT levels since you are obliviously still growing, and DHT does play an important role in puberty. This means we are going to have to deal with scalp DH and Testosterone through compounds that will not effect your systematic levels. This can be accomplished through the use to the research chemical RU58841. This is a anti androgen which is applied topically to the scalp. To put it simply, it binds to the androgen receptors instead of DHT and Testosterone. Since hormones like DHT and Testosterone will not be able to bind, your hair will be safe from the norwood reaper, at least until you are old enough to get on approved treatments.

What should I do if you still experience hair loss while taking a 5α-Reductase inhibitor?
So you may have taken a 5α-Reductase inhibitor and are still seeing hair loss after a few months on treatment. You are probably very sensitive to androgens at the scalp, since for a large majority, 5α-Reductase inhibitors will be enough. If you still experience loss, it is because 5α-Reductase inhibitors will not completely remove scalp DHT, there is still some present at the scalp. As well as this, 5α-Reductase inhibitors don't decrease scalp Testosterone. The only way to deal with any residual DHT at the scalp, and the scalp Testosterone is by using ru58841. I already mentioned above that it does. Adding this on top of 5α-Reductase inhibitors will mean that your scalp will have as little androgens present that is currently possible, and will give your hair the best chance of survival.

Is RU58841 safe for use, since it's a research chemical?
This next part is not my words, it's from a post else where.
I found out about a clinical researcher that worked on the compound.
I wrote him two e-mails, but he didn't answer.
Therefore I tried to call him on the phone. It was quite hard to get to him since his secretaries apparently don't speak English. But the third time I was calling, I was lucky enough to get himself on the phone.
When I mentioned PSK-3841 he knew immediately what I was talking about. Apparently he got at least 10 phone calls in the last 3 years about this subject.
I asked him wether he remembers major safety concerns and he said no. He thinks the research was stopped because of financial issues or bad marketability.
He also said he tried to contact Prostrakan about it, but they are not interested in continuing the research.

He said that PSK-3841 was quite effective when he used it in the 6 month trial. He even suggested crowdfunding to make Prostrakan release the data or continue research.
This corresponds with the following statement, that was released by Prostrakan.

Topical anti-androgen
This is an innovative molecule with a unique mechanism of action for the treatment of androgen-dependent conditions, such as alopecia and acne.
In pre-clinical studies, it has shown promising activity in various models of acne, alopecia and hirsutism. The product has good systemic and dermal tolerance.
In human clinical pharmacology, there was no systemic anti-androgenic activity and again good general and dermal tolerance.
The molecule has completed several Phase I studies and a Proof of Concept Phase II study for alopecia.
It has demonstrated similar efficacy after 6 months treatment as that observed with current oral therapy for alopecia after twelve months, based on the increase in net hair count. Again, no systemic anti-androgenic effect was observed (n=90).
This product is available for licensing.


PS: English is not my native language so I may have not understood everything 100% correctly. But I asked him about the safety concerns 2 times, so I'm quite sure about that.

Edit: I don't want the researcher to get into legal trouble. Therefore I have deleted the name from the post. He has not shared confidential Data with me but I want him to be safe.

How to make an RU58841 solution.
You can either use a premade solution or you can home brew your own, which is much cheaper.
I will outline how to make your own now.

You will need: Precisions measuring scale 0.001g, Propylene Glycol, Ethanol 95%, RU58841 raw powder, glass measuring beakers.

I will outline how to make a 5% solution.
This will contain 50mg RU58841 per mL. And it will be a 50mL solution.
70% Ethanol 30% Propylene Glycol is the best ratio for the solution.
You can use DMSO if you wish instead of Propylene Gylycol, with the same 70% 30% ratio.

Steps
1) Get the precision scale and put a measuring beaker on it, and set the weight to 0
2) Put the RU58841 powder into the beaker, measuring out 2.5g
3) Using the measuring beaker, measure out 35mL of ethanol 95%, and add that to the one with the RU58841 powder in it.
4) Using the measuring beaker and measure out 15mL of Propylene Glycol and add that to the beaker with the RU58841 and ethanol.
5) Stir until the RU dissolves.
Store the ready made solution in the fridge. Store the raw RU58841 powder in the freezer.

Here is a video from Reddit if you wish to follow that instead:


Drug Dosages.
Why 1mg of FInasteride and not 0.1mg or 5mg?

View attachment 3683969
Why 2.5mg Dutasteride and not the standard dosage of 0.5mg?
You are taking supraphysiological amounts of Testosterone, which as a result means you are going to have high DHT levels, and if you are particularly prone to androgens raping your hair follicles, you need to be as nuclear as you can be.
Serum DHT inhibition is not that different (about 4% more with 2.5mg) but the Scalp DHT inhibition is almost 80% at 2.5mg compared to 50% with 0.5mg.
Best RU58841 dosage?
I will clarify, by dosage I mean the amount of ru58841 that is applied to your scalp. You are not drinking it or taking it orally, you will be a Testosteroneless creature.
Apply between 50-100mg of RU58841 to the scalp. I would recommend not exceeding 100mg as it will increase the chances of systematic absorption.
If you still lose hair on the stack mentioned in this thread, you are likely not balding due to AGA.

Also go check out @Jonas2k7 thread about Minoxidil:

TAGS
@Drugsmaxxer @Hexmask @spectrumaesthetics2

@imontheloose (I will respond on dc to you, I just haven't gotten round to it yet)

chad wakes up with a full head of hair everyday next to stacies
mirin gud thread
 
good thread. although nuking DHT with something as powerful as dutasteride will have inevitable side effects. no medication is free.

however, losing your hair is a death sentence to dating prospects. immediately lowers your looks by 2 to 3 points (you are not jeremy meeks, but even he descended when he lost his hairline)

you have two options:
- inhibit DHT to slow down hair loss (side effects? stop taking!)
- keep DHT and let norwood reaper rape hair follicles, for potentially 0.01 mm of bone growth

don’t take in puberty, ideally not before 25
 
im natty, can I still hop on dut? im using 1mg fin and topical minox since 2 years. minox regrowth is so fucking ass so I started .5mg dut a few days ago, you reckon I should continue with dut? my hair's stable from fin tho with 0 sides and im satisfied with my current hair condition if there are potential downsides with dut
 
im natty, can I still hop on dut? im using 1mg fin and topical minox since 2 years. minox regrowth is so fucking ass so I started .5mg dut a few days ago, you reckon I should continue with dut? my hair's stable from fin tho with 0 sides and im satisfied with my current hair condition if there are potential downsides with dut
@jonas2k7 @Jonasㅤㅤ⠀
 
im natty, can I still hop on dut? im using 1mg fin and topical minox since 2 years. minox regrowth is so fucking ass so I started .5mg dut a few days ago, you reckon I should continue with dut? my hair's stable from fin tho with 0 sides and im satisfied with my current hair condition if there are potential downsides with dut
Yes, you can use Dut. Or add in RU with your Fin, it would mog Dut alone to Mumbai and back.
 
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Reactions: killyourselfASAP, Jonasㅤㅤ⠀ and Arthur the Egyptian
1747660677285
Doesn't this prove that 0.2Mg is also effective? and would a lower dose lower the risks of sexual side effects?
 
https://pubmed.ncbi.nlm.nih.gov/11163596/ wb this

btw 2.5mg dut lowers scalp dht by 79% while 40mg lowers it by 98% so that guy that was on 40mg might not be that dumb
I already made a post about this but no one reacted. So according to this graph i would say 20mg DUT Powder would be optimal.
Beyond that its just 2% more so not worth the risk.

But 13% more than 2.5mg is still something and DUT is generally a safe drug
 

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I already made a post about this but no one reacted. So according to this graph i would say 20mg DUT Powder would be optimal.
Beyond that its just 2% more so not worth the risk.

But 13% more than 2.5mg is still something and DUT is generally a safe drug
It is diminishing returns after 2.5mg. You can achieve drastically better results by using RU which will deal with any residual DHT and deal with scalp T (which Dut does nothing for. If anything, it increases scalp T). Not to mention the cost.
 
It is diminishing returns after 2.5mg. You can achieve drastically better results by using RU which will deal with any residual DHT and deal with scalp T (which Dut does nothing for. If anything, it increases scalp T). Not to mention the cost.
scalp t doesnt cause bald
 
I already made a post about this but no one reacted. So according to this graph i would say 20mg DUT Powder would be optimal.
Beyond that its just 2% more so not worth the risk.

But 13% more than 2.5mg is still something and DUT is generally a safe drug
yeah the guy even used 500mg dut to see what would happen and nothing happened
 
It is diminishing returns after 2.5mg. You can achieve drastically better results by using RU which will deal with any residual DHT and deal with scalp T (which Dut does nothing for. If anything, it increases scalp T). Not to mention the cost.
I agree with you thats why i am on 8% RU as well. But despite that i will still increase my 2.5mg dosage to 20mg and see what will happen.

Idk what you mean with cost but i have 100gramm of powder (like u i think) and it would still be enough for years.
 
Idk what you mean with cost but i have 100gramm of powder (like u i think) and it would still be enough for years.
where do u get this shit from can u dm me where
 
Idk what you mean with cost but i have 100gramm of powder (like u i think) and it would still be enough for years.
Yeah that's what I do. Many niggas don't do that and would be extortion other wise.

I agree with you thats why i am on 8% RU as well. But despite that i will still increase my 2.5mg dosage to 20mg and see what will happen.
Mirin the RU. Personally I think upping to 20mg won't give many benefits. Your scalp is basically androgen free with 2.5mg Dut and 8% RU IMO.

idk also if dht doesnt grow bone wb this https://pubmed.ncbi.nlm.nih.gov/11163596/

"growing mice"​

Mice are much more dependant on DHT than humans. For humans the main mediators of bone growth are Test, Estrogen, GH and IGF1.
 
idk also if dht doesnt grow bone wb this https://pubmed.ncbi.nlm.nih.gov/11163596/
@HEXEDRONE what do u think of dht and do u think, for instance, loox would've gotten the growth he got if he had inhibited dht from the start
and are the positive mental effects of dht largely correlated with allopregnanolone rather than dht in and of itself and can thus be mitigated by suplementation for ppl who are reliant on these neurosteroids (who probably are the victims of the side effect profile)
 
@
HEXEDRONE
@HEXEDRONE what do u think of dht and do u think, for instance, loox would've gotten the growth he got if he had inhibited dht from the start
He is on Dutasteride and RU
and are the positive mental effects of dht largely correlated with allopregnanolone rather than dht in and of itself and can thus be mitigated by suplementation for ppl who are reliant on these neurosteroids (who probably are the victims of the side effect profile)
I've had no issues. It is fearmongering.
 
Mice are much more dependant on DHT than humans. For humans the main mediators of bone growth are Test, Estrogen, GH and IGF1.
don't the endicrinological systems of all mammals work pretty much the same way but ur probably right
 
Mirin the RU. Personally I think upping to 20mg won't give many benefits. Your scalp is basically androgen free with 2.5mg Dut and 8% RU IMO.
You are right, but when it comes to hair loss im mentally a bit ill so thats why i experiment with high dosages.
But for 99,99% of people 2.5mg DUT and 50mg of RU will be the cure for AGA
 
He is on Dutasteride and RU
dutasteride is anti neuro inflammatory right
and abt it's effects on fertility would you just transition from dutasteride to fin to a topical antiandrogen when yuo want to conceive
I've had no issues. It is fearmongering.
yeah ik my friend is on fin and he's still a gooner it's probably placebo for the most part but considering the lower incidence of side effects on dutasteride than finasteride and the fact that dutasteride is positively correlated with allopregnanolone at 0.5mg while finasteride shows an inverse correlation with it at 1mg there might be a correlation with some people
 
View attachment 3683815

The Cure For Hair Loss - The Truth about 5α-Reductase Inhibitors and Topical Anti-Androgens - Part 2
(excuse the shit formatting, I don't normally write threads, so I can't format for shit)

What does this thread include?
In this thread I will be covering the different treatments depending on your age and situation for hair loss, as well as what impact each of these drugs will have on your development.

1) Introduction
2) Why are you balding in the first place?
3) What can we do about DHT at the scalp?
4) Distinguishing between Type 1 isoenzyme and Type 2 isoenzyme
5) Should I be worried about side effects from FInasteride?
6) Hair loss treatment if you are over 18
7) Hair loss treatment if you are under 18
8) What do do if you still experience hair loss on 5α-Reductase inhibitors
9) Is RU58841 safe for use, since it's a research chemical
10) How to make RU58841 solution
11) Drug dosages


Introduction.
We all know, hair is life, if you have no hair, you have no life.

Once you down the rabbit hole of finding a "cure" for hair loss, you will find that you have only 2 real options in term of halting the actual hair loss itself. Those options would be Finasteride/Dutasteride (5α-Reductase inhibitor) or research produces like ru58841. In this thread I will go into depth about these, and which one people should use depending on their situation, or if they should use one at all.

Why are you balding in the first place?
The vast majority of men go bald because of a hereditary condition called Androgenic Alopecia (AGA). Unfortunately, the number of men that do not have condition are in the minority, so do not assume that you are safe from the norwood reaper, ever. Everyone's hair follicles has a different sensitivity to androgens. The androgens binding to the hair follicles will make the Anagen phase shorter and shorter until a permanent state of anagen phase is present and the hair follicle is deactivated. The strongest hormone that shorten the Anagen phase is DHT (dihydrotestosteron) and Testosterone. Some woman are so sensitive to DHT and Testosterone that the small amount they produce is sufficient enough to cause hair loss.

What can we do about DHT at the scalp?
As I mentioned above, there is a very limited number of things we can do to combat this, however using the protocols I will outline in this thread will leave you having you hair for life. First we have to take care of the main androgen in causing hair loss, which already outlined above, is DHT. There is only one safe way to decrease the amount of DHT in your body, and that is taking a 5α-Reductase inhibitor such as Finasteride or Dutasteride. In taking on of these 5α-Reductase inhibitors, we are systematically decreasing the amount of DHT in out body, and subsequently decreasing the amount of scalp DHT we have, which is what we want to reduce as much as possible. I will outline which is best to take for each individual, since it's dependant on your age, if you use certain compounds to "pubertymaxx" etc.

Will 5α-Reductase inhibitors stunt bone development?
Is taking 5α-Reductase inhibitors going to keep you boneless forever? Lets find out.

Study:
Results: Patients with dihydrotestosterone deficiency present normal bone mineral density, suggesting that dihydrotestosterone is not the main androgen acting in bone.

Study:
Results:
View attachment 3683851

The two guys on the left have 0 DHT (literally) and they still have a normal bone structure and an identical height, bone density and skeletal mass to their healthy siblings, it have a higher binding affinity to the androgen receptor but it doesn't cause the same physiological response.
The pubertal growth spurt (for men) is also induced by testosterone and not DHT.

Also 5AR is not very active in bone tissues and DHT is mainly a paracrine hormone (i.e it acts where it's produced while testosterone acts on the whole body despite being produced in the testes).

So, does that mean we should all just take the strongest 5α-Reductase inhibitor (Dutasteride) and call it a day? Well, no. First we have to distinguish between the two forms of DHT, as these studies to not distinguish between them, so it is not the full picture.

Distinguishing between Type 1 isoenzyme and Type 1 isoenzyme.

Both these studies show that DHT doesn't have an effect on bones, right? So, we should all just take Dutasteride? Wrong.

These studies have not differentiated between type 1 isoenzyme, and type 2 isoenzyme.

So, first we have to see where type 1 DHT and type 2 DHT are expressed in the body.

Type 2 DHT is not expressed in bones at all, it's only expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles, and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys.

However, Type 1 DHT is actually expressed in bones. This matters because the studies I have shown above, are actually only deficient in the type 2 isoenzyme, which is the one that is not present in bones. This is the reason they present with normal bone mineral density, bone structure etc. If they were also deficient in Type 1 DHT, this would likely not be the case at all.

"5α-Reductase type 1 inactivated male mice have reduced bone mass and forelimb muscle grip strength, which has been proposed to be due to lack of 5α-reductase type 1 expression in bone and muscle.[29] In 5 alpha reductase type 2 deficient males, the type 1 isoenzyme is thought to be responsible for their virilization at puberty.[6]"

Bone growth and change will be minimal after 18, I definitely agree, but it still does happen. Facial bones are flat bones. They do not fuse, so they will continue to change forever, obviously to a lesser extent the older you get. Bones development/growth “stops” when resorption becomes greater than formation. As you age, this is more likely to happen, and will happen at a certain age most likely. Taking Dut with inhibits type 1, which is active in bones would likely have a negative impact, and speed up this process. You also won't achieve the slight bone changes that maybe desirable. It's true you don't know if you will have any noticeable change. Even in terms of BMD, doesn't effect aesthetics, it is still somewhat important for health. I would feel more comfortable to take Finasteride over Dutasteride if natural, since enhanced individuals would probably be able to compensate with supraphysiological Test levels and compensate for the lack of Type 1 DHT. The only thing I can really think of that have possibly comparable DHT type 1 levels to men on Dutasteride, would be women, who do actually have lower bone mass and lower BMD than men, and are at a greater risk of developing osteoporosis compared to men. That is not me saying if you take Dut your bones are going to melt and dissolve off your face.

Should I be worried about side effects from Finasteride?
I am not going to say that side effects do not exist, there are going to be the very unfortunate minority that may get side effects, but most of the people that are reporting side effects are schizo, especially if you go to places like r/tressless. They are basically all mentally ill. I’m not saying PFS or side effects in general aren't real, but I am saying that side effects, including PFS, are very much exaggerated in 2025.

Even in long-term studies (10 yr +) in Asians, no evidence of PFS symptoms were ever discovered. Only 1-3% get sexual sides, which wasn't even significantly different from the placebo arm in the original trials.

View attachment 3683840


Only after social media started popping off side effect reports started skyrocketing, and no, it’s not because there were fewer users back in the 2000s, millions of men were already on it back then.

There is some evidence for the existence of PFS and I will link a post here:
Personally, I would take the chance 10/10 times.

Hair loss treatment if you're over 18.
If you are above the age of 18, and are natural, which means you DO NOT take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Finasteride at 1mg ever day.
If you are above the age of 18, and are enhanced, which means you DO take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Dutasteride at 2.5mg a day.

Hair loss treatment if you're under 18.
If you are younger than, you don't want to reduce your serum DHT levels since you are obliviously still growing, and DHT does play an important role in puberty. This means we are going to have to deal with scalp DH and Testosterone through compounds that will not effect your systematic levels. This can be accomplished through the use to the research chemical RU58841. This is a anti androgen which is applied topically to the scalp. To put it simply, it binds to the androgen receptors instead of DHT and Testosterone. Since hormones like DHT and Testosterone will not be able to bind, your hair will be safe from the norwood reaper, at least until you are old enough to get on approved treatments.

What should I do if you still experience hair loss while taking a 5α-Reductase inhibitor?
So you may have taken a 5α-Reductase inhibitor and are still seeing hair loss after a few months on treatment. You are probably very sensitive to androgens at the scalp, since for a large majority, 5α-Reductase inhibitors will be enough. If you still experience loss, it is because 5α-Reductase inhibitors will not completely remove scalp DHT, there is still some present at the scalp. As well as this, 5α-Reductase inhibitors don't decrease scalp Testosterone. The only way to deal with any residual DHT at the scalp, and the scalp Testosterone is by using ru58841. I already mentioned above that it does. Adding this on top of 5α-Reductase inhibitors will mean that your scalp will have as little androgens present that is currently possible, and will give your hair the best chance of survival.

Is RU58841 safe for use, since it's a research chemical?
This next part is not my words, it's from a post else where.
I found out about a clinical researcher that worked on the compound.
I wrote him two e-mails, but he didn't answer.
Therefore I tried to call him on the phone. It was quite hard to get to him since his secretaries apparently don't speak English. But the third time I was calling, I was lucky enough to get himself on the phone.
When I mentioned PSK-3841 he knew immediately what I was talking about. Apparently he got at least 10 phone calls in the last 3 years about this subject.
I asked him wether he remembers major safety concerns and he said no. He thinks the research was stopped because of financial issues or bad marketability.
He also said he tried to contact Prostrakan about it, but they are not interested in continuing the research.

He said that PSK-3841 was quite effective when he used it in the 6 month trial. He even suggested crowdfunding to make Prostrakan release the data or continue research.
This corresponds with the following statement, that was released by Prostrakan.

Topical anti-androgen
This is an innovative molecule with a unique mechanism of action for the treatment of androgen-dependent conditions, such as alopecia and acne.
In pre-clinical studies, it has shown promising activity in various models of acne, alopecia and hirsutism. The product has good systemic and dermal tolerance.
In human clinical pharmacology, there was no systemic anti-androgenic activity and again good general and dermal tolerance.
The molecule has completed several Phase I studies and a Proof of Concept Phase II study for alopecia.
It has demonstrated similar efficacy after 6 months treatment as that observed with current oral therapy for alopecia after twelve months, based on the increase in net hair count. Again, no systemic anti-androgenic effect was observed (n=90).
This product is available for licensing.


PS: English is not my native language so I may have not understood everything 100% correctly. But I asked him about the safety concerns 2 times, so I'm quite sure about that.

Edit: I don't want the researcher to get into legal trouble. Therefore I have deleted the name from the post. He has not shared confidential Data with me but I want him to be safe.

How to make an RU58841 solution.
You can either use a premade solution or you can home brew your own, which is much cheaper.
I will outline how to make your own now.

You will need: Precisions measuring scale 0.001g, Propylene Glycol, Ethanol 95%, RU58841 raw powder, glass measuring beakers.

I will outline how to make a 5% solution.
This will contain 50mg RU58841 per mL. And it will be a 50mL solution.
70% Ethanol 30% Propylene Glycol is the best ratio for the solution.
You can use DMSO if you wish instead of Propylene Gylycol, with the same 70% 30% ratio.

Steps
1) Get the precision scale and put a measuring beaker on it, and set the weight to 0
2) Put the RU58841 powder into the beaker, measuring out 2.5g
3) Using the measuring beaker, measure out 35mL of ethanol 95%, and add that to the one with the RU58841 powder in it.
4) Using the measuring beaker and measure out 15mL of Propylene Glycol and add that to the beaker with the RU58841 and ethanol.
5) Stir until the RU dissolves.
Store the ready made solution in the fridge. Store the raw RU58841 powder in the freezer.

Here is a video from Reddit if you wish to follow that instead:


Drug Dosages.
Why 1mg of FInasteride and not 0.1mg or 5mg?

View attachment 3683969
Why 2.5mg Dutasteride and not the standard dosage of 0.5mg?
You are taking supraphysiological amounts of Testosterone, which as a result means you are going to have high DHT levels, and if you are particularly prone to androgens raping your hair follicles, you need to be as nuclear as you can be.
Serum DHT inhibition is not that different (about 4% more with 2.5mg) but the Scalp DHT inhibition is almost 80% at 2.5mg compared to 50% with 0.5mg.
Best RU58841 dosage?
I will clarify, by dosage I mean the amount of ru58841 that is applied to your scalp. You are not drinking it or taking it orally, you will be a Testosteroneless creature.
Apply between 50-100mg of RU58841 to the scalp. I would recommend not exceeding 100mg as it will increase the chances of systematic absorption.
If you still lose hair on the stack mentioned in this thread, you are likely not balding due to AGA.

Also go check out @Jonas2k7 thread about Minoxidil:

TAGS
@Drugsmaxxer @Hexmask @spectrumaesthetics2

@imontheloose (I will respond on dc to you, I just haven't gotten round to it yet)

Dnr
 
@chadisbeingmade
What do you think of Spironolactone instead of RU5884?
 
@chadisbeingmade
extremely high iq thread.

will fin be able to regrow hair in terms of thickness specifically?i have no slick bald areas/dead zones and my hairline is damn near perfect thank god, but im thinning on top (noticable only when wet) and especially on the crown when its kinda noticable even when dry, the hair is blonder and scalp is more visible.

been on fin for 9 months and im definetly seeing some regrowth but very slowly after i recovered from a brutal shed,i guess my question is wheter or not its normal to only see mediocre results now and if its only gonna get better from now on?when should we expect very noticabe results?
 
View attachment 3683815

The Cure For Hair Loss - The Truth about 5α-Reductase Inhibitors and Topical Anti-Androgens - Part 2
(excuse the shit formatting, I don't normally write threads, so I can't format for shit)

What does this thread include?
In this thread I will be covering the different treatments depending on your age and situation for hair loss, as well as what impact each of these drugs will have on your development.

1) Introduction
2) Why are you balding in the first place?
3) What can we do about DHT at the scalp?
4) Distinguishing between Type 1 isoenzyme and Type 2 isoenzyme
5) Should I be worried about side effects from FInasteride?
6) Hair loss treatment if you are over 18
7) Hair loss treatment if you are under 18
8) What do do if you still experience hair loss on 5α-Reductase inhibitors
9) Is RU58841 safe for use, since it's a research chemical
10) How to make RU58841 solution
11) Drug dosages


Introduction.
We all know, hair is life, if you have no hair, you have no life.

Once you down the rabbit hole of finding a "cure" for hair loss, you will find that you have only 2 real options in term of halting the actual hair loss itself. Those options would be Finasteride/Dutasteride (5α-Reductase inhibitor) or research produces like ru58841. In this thread I will go into depth about these, and which one people should use depending on their situation, or if they should use one at all.

Why are you balding in the first place?
The vast majority of men go bald because of a hereditary condition called Androgenic Alopecia (AGA). Unfortunately, the number of men that do not have condition are in the minority, so do not assume that you are safe from the norwood reaper, ever. Everyone's hair follicles has a different sensitivity to androgens. The androgens binding to the hair follicles will make the Anagen phase shorter and shorter until a permanent state of anagen phase is present and the hair follicle is deactivated. The strongest hormone that shorten the Anagen phase is DHT (dihydrotestosteron) and Testosterone. Some woman are so sensitive to DHT and Testosterone that the small amount they produce is sufficient enough to cause hair loss.

What can we do about DHT at the scalp?
As I mentioned above, there is a very limited number of things we can do to combat this, however using the protocols I will outline in this thread will leave you having you hair for life. First we have to take care of the main androgen in causing hair loss, which already outlined above, is DHT. There is only one safe way to decrease the amount of DHT in your body, and that is taking a 5α-Reductase inhibitor such as Finasteride or Dutasteride. In taking on of these 5α-Reductase inhibitors, we are systematically decreasing the amount of DHT in out body, and subsequently decreasing the amount of scalp DHT we have, which is what we want to reduce as much as possible. I will outline which is best to take for each individual, since it's dependant on your age, if you use certain compounds to "pubertymaxx" etc.

Will 5α-Reductase inhibitors stunt bone development?
Is taking 5α-Reductase inhibitors going to keep you boneless forever? Lets find out.

Study:
Results: Patients with dihydrotestosterone deficiency present normal bone mineral density, suggesting that dihydrotestosterone is not the main androgen acting in bone.

Study:
Results:
View attachment 3683851

The two guys on the left have 0 DHT (literally) and they still have a normal bone structure and an identical height, bone density and skeletal mass to their healthy siblings, it have a higher binding affinity to the androgen receptor but it doesn't cause the same physiological response.
The pubertal growth spurt (for men) is also induced by testosterone and not DHT.

Also 5AR is not very active in bone tissues and DHT is mainly a paracrine hormone (i.e it acts where it's produced while testosterone acts on the whole body despite being produced in the testes).

So, does that mean we should all just take the strongest 5α-Reductase inhibitor (Dutasteride) and call it a day? Well, no. First we have to distinguish between the two forms of DHT, as these studies to not distinguish between them, so it is not the full picture.

Distinguishing between Type 1 isoenzyme and Type 1 isoenzyme.

Both these studies show that DHT doesn't have an effect on bones, right? So, we should all just take Dutasteride? Wrong.

These studies have not differentiated between type 1 isoenzyme, and type 2 isoenzyme.

So, first we have to see where type 1 DHT and type 2 DHT are expressed in the body.

Type 2 DHT is not expressed in bones at all, it's only expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles, and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys.

However, Type 1 DHT is actually expressed in bones. This matters because the studies I have shown above, are actually only deficient in the type 2 isoenzyme, which is the one that is not present in bones. This is the reason they present with normal bone mineral density, bone structure etc. If they were also deficient in Type 1 DHT, this would likely not be the case at all.

"5α-Reductase type 1 inactivated male mice have reduced bone mass and forelimb muscle grip strength, which has been proposed to be due to lack of 5α-reductase type 1 expression in bone and muscle.[29] In 5 alpha reductase type 2 deficient males, the type 1 isoenzyme is thought to be responsible for their virilization at puberty.[6]"

Bone growth and change will be minimal after 18, I definitely agree, but it still does happen. Facial bones are flat bones. They do not fuse, so they will continue to change forever, obviously to a lesser extent the older you get. Bones development/growth “stops” when resorption becomes greater than formation. As you age, this is more likely to happen, and will happen at a certain age most likely. Taking Dut with inhibits type 1, which is active in bones would likely have a negative impact, and speed up this process. You also won't achieve the slight bone changes that maybe desirable. It's true you don't know if you will have any noticeable change. Even in terms of BMD, doesn't effect aesthetics, it is still somewhat important for health. I would feel more comfortable to take Finasteride over Dutasteride if natural, since enhanced individuals would probably be able to compensate with supraphysiological Test levels and compensate for the lack of Type 1 DHT. The only thing I can really think of that have possibly comparable DHT type 1 levels to men on Dutasteride, would be women, who do actually have lower bone mass and lower BMD than men, and are at a greater risk of developing osteoporosis compared to men. That is not me saying if you take Dut your bones are going to melt and dissolve off your face.

Should I be worried about side effects from Finasteride?
I am not going to say that side effects do not exist, there are going to be the very unfortunate minority that may get side effects, but most of the people that are reporting side effects are schizo, especially if you go to places like r/tressless. They are basically all mentally ill. I’m not saying PFS or side effects in general aren't real, but I am saying that side effects, including PFS, are very much exaggerated in 2025.

Even in long-term studies (10 yr +) in Asians, no evidence of PFS symptoms were ever discovered. Only 1-3% get sexual sides, which wasn't even significantly different from the placebo arm in the original trials.

View attachment 3683840


Only after social media started popping off side effect reports started skyrocketing, and no, it’s not because there were fewer users back in the 2000s, millions of men were already on it back then.

There is some evidence for the existence of PFS and I will link a post here:
Personally, I would take the chance 10/10 times.

Hair loss treatment if you're over 18.
If you are above the age of 18, and are natural, which means you DO NOT take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Finasteride at 1mg ever day.
If you are above the age of 18, and are enhanced, which means you DO take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Dutasteride at 2.5mg a day.

Hair loss treatment if you're under 18.
If you are younger than, you don't want to reduce your serum DHT levels since you are obliviously still growing, and DHT does play an important role in puberty. This means we are going to have to deal with scalp DH and Testosterone through compounds that will not effect your systematic levels. This can be accomplished through the use to the research chemical RU58841. This is a anti androgen which is applied topically to the scalp. To put it simply, it binds to the androgen receptors instead of DHT and Testosterone. Since hormones like DHT and Testosterone will not be able to bind, your hair will be safe from the norwood reaper, at least until you are old enough to get on approved treatments.

What should I do if you still experience hair loss while taking a 5α-Reductase inhibitor?
So you may have taken a 5α-Reductase inhibitor and are still seeing hair loss after a few months on treatment. You are probably very sensitive to androgens at the scalp, since for a large majority, 5α-Reductase inhibitors will be enough. If you still experience loss, it is because 5α-Reductase inhibitors will not completely remove scalp DHT, there is still some present at the scalp. As well as this, 5α-Reductase inhibitors don't decrease scalp Testosterone. The only way to deal with any residual DHT at the scalp, and the scalp Testosterone is by using ru58841. I already mentioned above that it does. Adding this on top of 5α-Reductase inhibitors will mean that your scalp will have as little androgens present that is currently possible, and will give your hair the best chance of survival.

Is RU58841 safe for use, since it's a research chemical?
This next part is not my words, it's from a post else where.
I found out about a clinical researcher that worked on the compound.
I wrote him two e-mails, but he didn't answer.
Therefore I tried to call him on the phone. It was quite hard to get to him since his secretaries apparently don't speak English. But the third time I was calling, I was lucky enough to get himself on the phone.
When I mentioned PSK-3841 he knew immediately what I was talking about. Apparently he got at least 10 phone calls in the last 3 years about this subject.
I asked him wether he remembers major safety concerns and he said no. He thinks the research was stopped because of financial issues or bad marketability.
He also said he tried to contact Prostrakan about it, but they are not interested in continuing the research.

He said that PSK-3841 was quite effective when he used it in the 6 month trial. He even suggested crowdfunding to make Prostrakan release the data or continue research.
This corresponds with the following statement, that was released by Prostrakan.

Topical anti-androgen
This is an innovative molecule with a unique mechanism of action for the treatment of androgen-dependent conditions, such as alopecia and acne.
In pre-clinical studies, it has shown promising activity in various models of acne, alopecia and hirsutism. The product has good systemic and dermal tolerance.
In human clinical pharmacology, there was no systemic anti-androgenic activity and again good general and dermal tolerance.
The molecule has completed several Phase I studies and a Proof of Concept Phase II study for alopecia.
It has demonstrated similar efficacy after 6 months treatment as that observed with current oral therapy for alopecia after twelve months, based on the increase in net hair count. Again, no systemic anti-androgenic effect was observed (n=90).
This product is available for licensing.


PS: English is not my native language so I may have not understood everything 100% correctly. But I asked him about the safety concerns 2 times, so I'm quite sure about that.

Edit: I don't want the researcher to get into legal trouble. Therefore I have deleted the name from the post. He has not shared confidential Data with me but I want him to be safe.

How to make an RU58841 solution.
You can either use a premade solution or you can home brew your own, which is much cheaper.
I will outline how to make your own now.

You will need: Precisions measuring scale 0.001g, Propylene Glycol, Ethanol 95%, RU58841 raw powder, glass measuring beakers.

I will outline how to make a 5% solution.
This will contain 50mg RU58841 per mL. And it will be a 50mL solution.
70% Ethanol 30% Propylene Glycol is the best ratio for the solution.
You can use DMSO if you wish instead of Propylene Gylycol, with the same 70% 30% ratio.

Steps
1) Get the precision scale and put a measuring beaker on it, and set the weight to 0
2) Put the RU58841 powder into the beaker, measuring out 2.5g
3) Using the measuring beaker, measure out 35mL of ethanol 95%, and add that to the one with the RU58841 powder in it.
4) Using the measuring beaker and measure out 15mL of Propylene Glycol and add that to the beaker with the RU58841 and ethanol.
5) Stir until the RU dissolves.
Store the ready made solution in the fridge. Store the raw RU58841 powder in the freezer.

Here is a video from Reddit if you wish to follow that instead:


Drug Dosages.
Why 1mg of FInasteride and not 0.1mg or 5mg?

View attachment 3683969
Why 2.5mg Dutasteride and not the standard dosage of 0.5mg?
You are taking supraphysiological amounts of Testosterone, which as a result means you are going to have high DHT levels, and if you are particularly prone to androgens raping your hair follicles, you need to be as nuclear as you can be.
Serum DHT inhibition is not that different (about 4% more with 2.5mg) but the Scalp DHT inhibition is almost 80% at 2.5mg compared to 50% with 0.5mg.
Best RU58841 dosage?
I will clarify, by dosage I mean the amount of ru58841 that is applied to your scalp. You are not drinking it or taking it orally, you will be a Testosteroneless creature.
Apply between 50-100mg of RU58841 to the scalp. I would recommend not exceeding 100mg as it will increase the chances of systematic absorption.
If you still lose hair on the stack mentioned in this thread, you are likely not balding due to AGA.

Also go check out @Jonas2k7 thread about Minoxidil:

TAGS
@Drugsmaxxer @Hexmask @spectrumaesthetics2

@imontheloose (I will respond on dc to you, I just haven't gotten round to it yet)

good threat, tired of niggas saying Fin makes them impotent they were either impotent from the start or are just living a shitty lifestyle been on fin for 3 months not a singular side effect aside from the fact that my hair is way healthier/denser, but the more people fear monger the more gatekept fin is gonna be so maybe its not that bad
 
  • +1
Reactions: attention_spanlet
There is enough evidence that topical dutasteride works if you apply it after microneedling, probably due to more absorption in the skin like you said, without lowering the serum DHT too much. The same way topical finasteride has less sides than oral fin.

That doesn't mean it works better than oral, my advice would be to just use 0.5mg dutasteride every 5 days and add a topical formula of Dutasteride after microneedling on top of it for extra scalp DHT reduction.

Besides, ketoconazole, which is the main compound in nizoral shampoo, is used as the big 3 against hair loss for decades and also has a higher molecular weight, even if it doesn't go systemic it still can work on the scalp to some extend.

Also, that is what I'm doing for 4 years now. I didn't use minox, I just use 1x 0.5mg dut every 5 days + a topical solution with alfatradiol and I regrew most of my hair while my whole male side of the family is balding.
wanna hear a real fix?
a trip to turkey
 
View attachment 3683815

The Cure For Hair Loss - The Truth about 5α-Reductase Inhibitors and Topical Anti-Androgens - Part 2
(excuse the shit formatting, I don't normally write threads, so I can't format for shit)

What does this thread include?
In this thread I will be covering the different treatments depending on your age and situation for hair loss, as well as what impact each of these drugs will have on your development.

1) Introduction
2) Why are you balding in the first place?
3) What can we do about DHT at the scalp?
4) Distinguishing between Type 1 isoenzyme and Type 2 isoenzyme
5) Should I be worried about side effects from FInasteride?
6) Hair loss treatment if you are over 18
7) Hair loss treatment if you are under 18
8) What do do if you still experience hair loss on 5α-Reductase inhibitors
9) Is RU58841 safe for use, since it's a research chemical
10) How to make RU58841 solution
11) Drug dosages


Introduction.
We all know, hair is life, if you have no hair, you have no life.

Once you down the rabbit hole of finding a "cure" for hair loss, you will find that you have only 2 real options in term of halting the actual hair loss itself. Those options would be Finasteride/Dutasteride (5α-Reductase inhibitor) or research produces like ru58841. In this thread I will go into depth about these, and which one people should use depending on their situation, or if they should use one at all.

Why are you balding in the first place?
The vast majority of men go bald because of a hereditary condition called Androgenic Alopecia (AGA). Unfortunately, the number of men that do not have condition are in the minority, so do not assume that you are safe from the norwood reaper, ever. Everyone's hair follicles has a different sensitivity to androgens. The androgens binding to the hair follicles will make the Anagen phase shorter and shorter until a permanent state of anagen phase is present and the hair follicle is deactivated. The strongest hormone that shorten the Anagen phase is DHT (dihydrotestosteron) and Testosterone. Some woman are so sensitive to DHT and Testosterone that the small amount they produce is sufficient enough to cause hair loss.

What can we do about DHT at the scalp?
As I mentioned above, there is a very limited number of things we can do to combat this, however using the protocols I will outline in this thread will leave you having you hair for life. First we have to take care of the main androgen in causing hair loss, which already outlined above, is DHT. There is only one safe way to decrease the amount of DHT in your body, and that is taking a 5α-Reductase inhibitor such as Finasteride or Dutasteride. In taking on of these 5α-Reductase inhibitors, we are systematically decreasing the amount of DHT in out body, and subsequently decreasing the amount of scalp DHT we have, which is what we want to reduce as much as possible. I will outline which is best to take for each individual, since it's dependant on your age, if you use certain compounds to "pubertymaxx" etc.

Will 5α-Reductase inhibitors stunt bone development?
Is taking 5α-Reductase inhibitors going to keep you boneless forever? Lets find out.

Study:
Results: Patients with dihydrotestosterone deficiency present normal bone mineral density, suggesting that dihydrotestosterone is not the main androgen acting in bone.

Study:
Results:
View attachment 3683851

The two guys on the left have 0 DHT (literally) and they still have a normal bone structure and an identical height, bone density and skeletal mass to their healthy siblings, it have a higher binding affinity to the androgen receptor but it doesn't cause the same physiological response.
The pubertal growth spurt (for men) is also induced by testosterone and not DHT.

Also 5AR is not very active in bone tissues and DHT is mainly a paracrine hormone (i.e it acts where it's produced while testosterone acts on the whole body despite being produced in the testes).

So, does that mean we should all just take the strongest 5α-Reductase inhibitor (Dutasteride) and call it a day? Well, no. First we have to distinguish between the two forms of DHT, as these studies to not distinguish between them, so it is not the full picture.

Distinguishing between Type 1 isoenzyme and Type 1 isoenzyme.

Both these studies show that DHT doesn't have an effect on bones, right? So, we should all just take Dutasteride? Wrong.

These studies have not differentiated between type 1 isoenzyme, and type 2 isoenzyme.

So, first we have to see where type 1 DHT and type 2 DHT are expressed in the body.

Type 2 DHT is not expressed in bones at all, it's only expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles, and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys.

However, Type 1 DHT is actually expressed in bones. This matters because the studies I have shown above, are actually only deficient in the type 2 isoenzyme, which is the one that is not present in bones. This is the reason they present with normal bone mineral density, bone structure etc. If they were also deficient in Type 1 DHT, this would likely not be the case at all.

"5α-Reductase type 1 inactivated male mice have reduced bone mass and forelimb muscle grip strength, which has been proposed to be due to lack of 5α-reductase type 1 expression in bone and muscle.[29] In 5 alpha reductase type 2 deficient males, the type 1 isoenzyme is thought to be responsible for their virilization at puberty.[6]"

Bone growth and change will be minimal after 18, I definitely agree, but it still does happen. Facial bones are flat bones. They do not fuse, so they will continue to change forever, obviously to a lesser extent the older you get. Bones development/growth “stops” when resorption becomes greater than formation. As you age, this is more likely to happen, and will happen at a certain age most likely. Taking Dut with inhibits type 1, which is active in bones would likely have a negative impact, and speed up this process. You also won't achieve the slight bone changes that maybe desirable. It's true you don't know if you will have any noticeable change. Even in terms of BMD, doesn't effect aesthetics, it is still somewhat important for health. I would feel more comfortable to take Finasteride over Dutasteride if natural, since enhanced individuals would probably be able to compensate with supraphysiological Test levels and compensate for the lack of Type 1 DHT. The only thing I can really think of that have possibly comparable DHT type 1 levels to men on Dutasteride, would be women, who do actually have lower bone mass and lower BMD than men, and are at a greater risk of developing osteoporosis compared to men. That is not me saying if you take Dut your bones are going to melt and dissolve off your face.

Should I be worried about side effects from Finasteride?
I am not going to say that side effects do not exist, there are going to be the very unfortunate minority that may get side effects, but most of the people that are reporting side effects are schizo, especially if you go to places like r/tressless. They are basically all mentally ill. I’m not saying PFS or side effects in general aren't real, but I am saying that side effects, including PFS, are very much exaggerated in 2025.

Even in long-term studies (10 yr +) in Asians, no evidence of PFS symptoms were ever discovered. Only 1-3% get sexual sides, which wasn't even significantly different from the placebo arm in the original trials.

View attachment 3683840


Only after social media started popping off side effect reports started skyrocketing, and no, it’s not because there were fewer users back in the 2000s, millions of men were already on it back then.

There is some evidence for the existence of PFS and I will link a post here:
Personally, I would take the chance 10/10 times.

Hair loss treatment if you're over 18.
If you are above the age of 18, and are natural, which means you DO NOT take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Finasteride at 1mg ever day.
If you are above the age of 18, and are enhanced, which means you DO take exogenous hormones, such as Testosterone to achieve supraphysiological Testosterone levels in the body, I would recommend taking Dutasteride at 2.5mg a day.

Hair loss treatment if you're under 18.
If you are younger than, you don't want to reduce your serum DHT levels since you are obliviously still growing, and DHT does play an important role in puberty. This means we are going to have to deal with scalp DH and Testosterone through compounds that will not effect your systematic levels. This can be accomplished through the use to the research chemical RU58841. This is a anti androgen which is applied topically to the scalp. To put it simply, it binds to the androgen receptors instead of DHT and Testosterone. Since hormones like DHT and Testosterone will not be able to bind, your hair will be safe from the norwood reaper, at least until you are old enough to get on approved treatments.

What should I do if you still experience hair loss while taking a 5α-Reductase inhibitor?
So you may have taken a 5α-Reductase inhibitor and are still seeing hair loss after a few months on treatment. You are probably very sensitive to androgens at the scalp, since for a large majority, 5α-Reductase inhibitors will be enough. If you still experience loss, it is because 5α-Reductase inhibitors will not completely remove scalp DHT, there is still some present at the scalp. As well as this, 5α-Reductase inhibitors don't decrease scalp Testosterone. The only way to deal with any residual DHT at the scalp, and the scalp Testosterone is by using ru58841. I already mentioned above that it does. Adding this on top of 5α-Reductase inhibitors will mean that your scalp will have as little androgens present that is currently possible, and will give your hair the best chance of survival.

Is RU58841 safe for use, since it's a research chemical?
This next part is not my words, it's from a post else where.
I found out about a clinical researcher that worked on the compound.
I wrote him two e-mails, but he didn't answer.
Therefore I tried to call him on the phone. It was quite hard to get to him since his secretaries apparently don't speak English. But the third time I was calling, I was lucky enough to get himself on the phone.
When I mentioned PSK-3841 he knew immediately what I was talking about. Apparently he got at least 10 phone calls in the last 3 years about this subject.
I asked him wether he remembers major safety concerns and he said no. He thinks the research was stopped because of financial issues or bad marketability.
He also said he tried to contact Prostrakan about it, but they are not interested in continuing the research.

He said that PSK-3841 was quite effective when he used it in the 6 month trial. He even suggested crowdfunding to make Prostrakan release the data or continue research.
This corresponds with the following statement, that was released by Prostrakan.

Topical anti-androgen
This is an innovative molecule with a unique mechanism of action for the treatment of androgen-dependent conditions, such as alopecia and acne.
In pre-clinical studies, it has shown promising activity in various models of acne, alopecia and hirsutism. The product has good systemic and dermal tolerance.
In human clinical pharmacology, there was no systemic anti-androgenic activity and again good general and dermal tolerance.
The molecule has completed several Phase I studies and a Proof of Concept Phase II study for alopecia.
It has demonstrated similar efficacy after 6 months treatment as that observed with current oral therapy for alopecia after twelve months, based on the increase in net hair count. Again, no systemic anti-androgenic effect was observed (n=90).
This product is available for licensing.


PS: English is not my native language so I may have not understood everything 100% correctly. But I asked him about the safety concerns 2 times, so I'm quite sure about that.

Edit: I don't want the researcher to get into legal trouble. Therefore I have deleted the name from the post. He has not shared confidential Data with me but I want him to be safe.

How to make an RU58841 solution.
You can either use a premade solution or you can home brew your own, which is much cheaper.
I will outline how to make your own now.

You will need: Precisions measuring scale 0.001g, Propylene Glycol, Ethanol 95%, RU58841 raw powder, glass measuring beakers.

I will outline how to make a 5% solution.
This will contain 50mg RU58841 per mL. And it will be a 50mL solution.
70% Ethanol 30% Propylene Glycol is the best ratio for the solution.
You can use DMSO if you wish instead of Propylene Gylycol, with the same 70% 30% ratio.

Steps
1) Get the precision scale and put a measuring beaker on it, and set the weight to 0
2) Put the RU58841 powder into the beaker, measuring out 2.5g
3) Using the measuring beaker, measure out 35mL of ethanol 95%, and add that to the one with the RU58841 powder in it.
4) Using the measuring beaker and measure out 15mL of Propylene Glycol and add that to the beaker with the RU58841 and ethanol.
5) Stir until the RU dissolves.
Store the ready made solution in the fridge. Store the raw RU58841 powder in the freezer.

Here is a video from Reddit if you wish to follow that instead:


Drug Dosages.
Why 1mg of FInasteride and not 0.1mg or 5mg?

View attachment 3683969
Why 2.5mg Dutasteride and not the standard dosage of 0.5mg?
You are taking supraphysiological amounts of Testosterone, which as a result means you are going to have high DHT levels, and if you are particularly prone to androgens raping your hair follicles, you need to be as nuclear as you can be.
Serum DHT inhibition is not that different (about 4% more with 2.5mg) but the Scalp DHT inhibition is almost 80% at 2.5mg compared to 50% with 0.5mg.
Best RU58841 dosage?
I will clarify, by dosage I mean the amount of ru58841 that is applied to your scalp. You are not drinking it or taking it orally, you will be a Testosteroneless creature.
Apply between 50-100mg of RU58841 to the scalp. I would recommend not exceeding 100mg as it will increase the chances of systematic absorption.
If you still lose hair on the stack mentioned in this thread, you are likely not balding due to AGA.

Also go check out @Jonas2k7 thread about Minoxidil:

TAGS
@Drugsmaxxer @Hexmask @spectrumaesthetics2

@imontheloose (I will respond on dc to you, I just haven't gotten round to it yet)

Thoughts about topical cyproterone acetate?
 

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