fluridil

[Petchsky]

I'm going to test that out sometime soon. Hey Bryan, what do you think about the long term use of finasteride? I know the 10 year study is still not complete, but your opinion? whether backed by studies or not.

 

[SoThatsLife]

It would be really nice if dr P sponsored 5-10 men at some hair site with Proxiphen for 6-10months and made them take pictures each month. Im not really confident in Nano shampoo, but I really think Nano conditioner is a good conditioner. (If he added lavender/l-argine it would even more effective). Prox-n is good for scalp health, but cant really say I have seen any regrowth own head. But Proxiphen have a nice mix of ingredients that have been shown in studies to be effective, so just to bad about the price.

Petchsky, couldn't hairlosstalk talk to Interpharma and ask if they want to let 5-10 users test Eucapil for 5-10months for free. The only problem with Eucapil is something el dutrino have pointed out many times, there are no regrowth stories about Eucapil.

 

[Petchsky]

I doubt that they would be up for it STL, and finding posters who are willing to be guinea pigs who then then stick with it is very hard.

 

[el_duterino]

We know for a fact that stopping the androgenic effects will not regrow lost hair. This was well documented by the Hamilton research on castrated men a few decades ago.

For fluridil to "work" you need healthy follicles. this is clearly written on their documentation.
The same requirement applies to finasteride, dutasteride, Flutamide and RU58841...etc
In some rare cases..a few "new" hair can re-appear at totally bald areas if the loss is recent but these are exceptions and will be in very small scale anyway.

What fluridil does is inhibit androgen receptors.
That's all it does and this is not sufficient to halt aggressive hairloss on its own because no drug in the world can currently inhibit ALL the androgen receptors ALL THE TIME, which would be ideally needed to halt aggressive hairloss.

Therefore, testing fluridil on its own will be somehow misleading. Its like testing cooking ingredients separetly.
Hairloss is a lot like cooking food..you need a good combo of ingredients to work together and produce an "new" effect.

Therefore, if you add Fluridil to finasteride or even better, to dutasteride, you will obtain a combo very effective at stopping aggressive hairloss.
Even better, you might add a topical drug that blocks the androgen receptors like Ru58841 or Flutamide..and you have an extremely strong combo which covers the androgenic effects at close to 100% just like a castrated man.

Fluridil is really needed in the combo for steady, long term results.

Using only RU58841 or flutamide will not guarantee long-term success.
This is because the body will upregulate the number of androgen recpetors and/or their sensitivty to androgens, when subjected to a lot of androgen-antagonist stimulation over a long term.
Also, it has been proven that over time, the androgen receptors can mutate to react to the anti-androgen simulation and trigger hairloss like it was DHT.

So you really need to knock down as much androgen receptors as possible in the process, hence the need for a drug that does what fluridil does.

A lot of people have reported a diminished effectiveness of RU58841 or flutamide over time, such after few weeks or months.
I also did notice diminishing results after a while on flutamide & dutasteride alone, or RU58841 & dutasteride alone. Adding fluridil to the combo gave much better results overall in terms of thickness, reduced shedding and a much better consistency of those results over time.

 

[Bryan]

Using only RU58841 or flutamide will not guarantee long-term success.

I really don't know of any particular reason to believe that. Topical RU58841 was effective in stumptailed macaques for a couple of years or so, and there was no indication that its effects faded over time.

This is because the body will upregulate the number of androgen recpetors and/or their sensitivty to androgens, when subjected to a lot of androgen-antagonist stimulation over a long term.
Also, it has been proven that over time, the androgen receptors can mutate to react to the anti-androgen simulation and trigger hairloss like it was DHT.

But castration was shown to be effective for male pattern baldness for as long as 20-30 years.

 

[el_duterino]

If i remember well, the macaques test was only 1 year and besides, it is scientifically proven that animal studies are not exactly the same as the outcome in humans.
If everything that works in animals would work in humans, we would have no bald people by now.

Bryan, you should really try this RU58841 yourself one day..after all the numerous posts you wrote about it ! that will give you a "new" human perspective to talk about.

As for the castrated men, yes agreed this is effective forever because there is no androgenic or androgenic-antagonist simulation at all..
AR mutations due to the anti-androgen drugs have been well documented in androgenic-sensitive prostate cancer.

 

[waynakyo]

But any thoughts on the safety of fluridil ?
Surely it sounds the safest thing and that's why I am tempted to take it twice or more daily.
However the mechanism in which it operates or the ingredients ... any of this could be harmful in the long run for the scalp or follicules?

B.t.w. I have been losing my hair for 5 years now and It's not as advanced as many others here, so fluridil should be optimal for someone at my stage.

 

[el_duterino]

i don't see any reports that it is not safe. the drug has been approved for hairloss in Europe and used since 2004, if there were safety issues we would know by now.
people are often confused with flutamide, which has some potential liver issues, although i did not have those myself as far as i know.

i "tested" 4 times the recommeded fluridil amount of 1 amplues a day for 2 months when I was on oral dutasteride EOD. i used 2 ampules each time, twice a day at 12 hours interval. I did not observe any androgenic side effects or adverse effects at all.

 

[CCS]

Fluridil is safe. I just don't know if it works. No placebo after 3 months. That is very unscientific and smells like a sales pitch to me. "after just 3 months we saw such an improvement over the placebo group that it was unethical not to give the wonderful fluridil to the placebo group too." That was their reasoning in their paper, for a cosmetic. Do you really think they are that dumb, or do you think they are scamming us?

 

[el_duterino]

Some fluridil related info:

See last post:
http://hair-restoration-info.com/eve/fo ... 6431062273

BP-766= fluridil, patent:
http://www.patentstorm.us/patents/68284 ... ption.html

A user report i found interesting:
http://hairlosshelp.com/FORUMS/messagev ... adid=78658

A US firm has aquired the rights for fluridil:
http://www.reuters.com/article/pressRel ... NW20080428

Inhibiting andorgen receptors is the "holy grail" in male pattern baldness..unfortunetely this is not an easy task. Androgen Receptors are not designed to be "inhibitied"..they are designed to bind to another molecule that takes the shape of an androgen.
That's why Androscience and their ASC-j9 is struggling now.

That's why a molecule that binds to the AR and blocks it, like RU58841 or flutamide is going to be more effective.

The real question is: in addition to a proven anti-androgenic regimen, if you had the option to inhibit a certain number of androgen receptors without adding side effects, would you do it ?
For me the answer is yes.

Some of the posters here choosed the Hair Transplant route to solve their hair issue;
I rely on drugs only. And this since 1997. If this fluridil was not doing anything I would be the first one to dump it. Fortunately it is a valuable addition to a serious anti-androgenic regimen.

 

[Bryan]

If i remember well, the macaques test was only 1 year...

Actually, in one of the macaque studies by Uno, the monkeys were treated with topical RU58841 for at least 17 months, and the implication in the text is that it continued for some time after that.

As for the castrated men, yes agreed this is effective forever because there is no androgenic or androgenic-antagonist simulation at all..

There is still _some_ androgenic stimulation, it's just sharply reduced. According to one study I have, serum testosterone is reduced by around 90%-95%, and serum DHT is reduced by around 70% or so. If there were an increase in the number and/or sensitivity of androgen receptors like you're claiming happens with the use of antiandrogens, the same thing would happen after castration, yet clearly it does NOT happen. At least, not enough to alter the favorable effects of castration on hair growth.

AR mutations due to the anti-androgen drugs have been well documented in androgenic-sensitive prostate cancer.

Yes, but those are in CANCER cells. There is no indication that I know of that it happens in normal, non-cancerous hair follicle cells.

 

[goata007]

AR mutations due to the anti-androgen drugs have been well documented in androgenic-sensitive prostate cancer.

Yes, but those are in CANCER cells. There is no indication that I know of that it happens in normal, non-cancerous hair follicle cells.

That's what I noticed too, that studies usually said CANCER cells. However, looking at the number of people who come back after a few years saying that finas isn't working for them anymore. What do you think is the cause for that? To me it sounds like body developing some sort of resistance to finas by either increasing sensitivity of ARs or increasing testosterone to compensate for the missing DHT.

 

[SoThatsLife]

El_duto, what do they mean by Phase 2? I have read several places that the makers of Eucapil claimed that they was putting it to FDA trials, but if one looks at the clinical trials site, one can not see anything. http://clinicaltrials.gov/search/condit ... ting=false . I even searched for several of the patent names.



It's seems like you are on a really heavy regime, so all props to you to keep it up.

 

[Petchsky]

It's good having some big brains on the forum. I'm thinking of using proixphen when i get off finasteride, but i've not considered Fluridill, or even flutamide, think i'm a little scared of flut, unless there is a way to take it without getting the sides, is twice a week worthwhile El dutasteride?

 

[Bryan]

That's what I noticed too, that studies usually said CANCER cells. However, looking at the number of people who come back after a few years saying that finas isn't working for them anymore. What do you think is the cause for that?

My basic assumption is that it's a progression of the fundamental balding process. An increasingly negative response of hair follicle cells to androgens.

BTW, I don't even believe people when they claim that finasteride "isn't working for them anymore". I think it's still working, although it may not be working WELL ENOUGH to completely stop further balding. In other words, they'd be even WORSE, without the finasteride.

To me it sounds like body developing some sort of resistance to finas by either increasing sensitivity of ARs or increasing testosterone to compensate for the missing DHT.

Sure...those things happen, but they happen RIGHT AWAY, like in days or weeks. It doesn't take YEARS to happen.

But in any event, I don't even think those specific things you mentioned (increased receptor sensitivity and increased testosterone) really have that much to do with it, since those things almost certainly happen to everybody who uses finasteride. I think it's a gradual increase in tissue (cellular) sensitivity to androgens over a period years which causes the slow deterioration: as the years go by, the same amount of androgenic stimulation (what's left over even while taking finasteride) gradually becomes sufficient to cause further balding in some people.

 

[el_duterino]

Actually, in one of the macaque studies by Uno, the monkeys were treated with topical RU58841 for at least 17 months, and the implication in the text is that it continued for some time after that.

There is still _some_ androgenic stimulation, it's just sharply reduced. According to one study I have, serum testosterone is reduced by around 90%-95%, and serum DHT is reduced by around 70% or so.

The problem I have with those monkeys is that they don't seem to suffer the type of young age, aggressive balding that some humans do. The monkeys go bald with old age but are there many monkeys that go NW6 by the time they reached a third of their life ? And if yes, were they included in those RU58841 tests ?

People with aggressive/advanced balding like we have on those forums, including myself, will have a lot more going on in terms of AR sensitivity increase, follicular DHT or variations of the number of AR to be on pace with the aggressive genetic plan to go bald in young age.

Regarding the castrated men, you would agree that the key here is the sharp decrease in testosterone. With only 5% of the Test level , how much follicular DHT can be converted ? it has to be very little orclose to none since these guys never go bald.
Topical Androgen antagonists compete with DHT at the follicular level.
Bryan, you are the one who always claimed that follicular DHT is the most improtant factor here.

In any case, we can all agree that inhibiting as many androgen receptors as possible is the smartest thing we can do, and fluridil is the only drug that can do that currently.

If this ASC-J9 ever makes it to the market then we will have more choices, but I am not going to wait for all these years. "Dead" follicles will not be revived by ASC-j9.

 

[Bryan]

The problem I have with those monkeys is that they don't seem to suffer the type of young age, aggressive balding that some humans do.

I don't really know if that's true or not, but the ONLY point I'm making here is that I don't know of any scientific evidence to support this idea that 5a-reductase inhibitors and antiandrogens eventually fail after a few years because of these alleged increases in androgen receptors, androgen receptor sensitivities, etc. etc. I think that's pure speculation, and not based on science.

Regarding the castrated men, you would agree that the key here is the sharp decrease in testosterone. With only 5% of the Test level , how much follicular DHT can be converted ? it has to be very little orclose to none since these guys never go bald.

But keep in mind that serum DHT dropped by only a more modest 70%, which is similar to what happens when you take finasteride.

In any case, we can all agree that inhibiting as many androgen receptors as possible is the smartest thing we can do, and fluridil is the only drug that can do that currently.

Maybe. Frankly, I just don't trust ANY of the claims made by the fluridil people. Not until it's tested by independent researchers!

 

[CCS]

AR mutations due to the anti-androgen drugs have been well documented in androgenic-sensitive prostate cancer.

Yes, but those are in CANCER cells. There is no indication that I know of that it happens in normal, non-cancerous hair follicle cells.

That's what I noticed too, that studies usually said CANCER cells. However, looking at the number of people who come back after a few years saying that finas isn't working for them anymore. What do you think is the cause for that? To me it sounds like body developing some sort of resistance to finas by either increasing sensitivity of ARs or increasing testosterone to compensate for the missing DHT.

male pattern baldness is a progressive condition. It eventually overpowers finasteride. Finasteride does not make it stronger. Basically when the placebo group is dropping really fast, or has no hair left, that is when the finasteride group would find that even they are starting to lose hair. If finasteride stopped working, you'd have a FAST, MASSIVE shed, not a gradual decline.

 

[CCS]

With only 5% of the Test level , how much follicular DHT can be converted ? it has to be very little orclose to none since these guys never go bald.

5% is the serum testosterone measured after castration. I'm sure body makes more, but 5% is what is left over after some is turned into DHT. DHT is only reduced by 70%. Pretty close to what propecia does, but less testosterone too.

In any case, we can all agree that inhibiting as many androgen receptors as possible is the smartest thing we can do, and fluridil is the only drug that can do that currently.

What makes you so sure Fluridil works when there was no placebo group? And the study was only 9 months? Are you aware that hair numbers go up and down with the seasons, I think denser in winter or something? It is enough to make a 6% increase in a well timed study look like good results. And the people who tested fluridil are the same ones selling it. And get ready to stop showering your head. They say you must use dry shampoo.

 

[CCS]

Fluridil is really needed in the combo for steady, long term results.
Using only RU58841 or flutamide will not guarantee long-term success.
This is because the body will upregulate the number of androgen recpetors and/or their sensitivty to androgens, when subjected to a lot of androgen-antagonist stimulation over a long term.
Also, it has been proven that over time, the androgen receptors can mutate to react to the anti-androgen simulation and trigger hairloss like it was DHT.
So you really need to knock down as much androgen receptors as possible in the process, hence the need for a drug that does what fluridil does.

Why do you think fluridil is better than other androgen receptor blockers? Where did you read this, and what specifically do you mean?

A lot of people have reported a diminished effectiveness of RU58841 or flutamide over time, such after few weeks or months.I also did notice diminishing results after a while on flutamide & dutasteride alone, or RU58841 & dutasteride alone. Adding fluridil to the combo gave much better results overall in terms of thickness, reduced shedding and a much better consistency of those results over time.

It takes 6 months to see a change. If you are just going by shedding rates, it depends how slippery your scalp is when the 15% of hairs in telogen fall out. That is why most hair falls out in the shower. I doubt this can measure the effectiveness of a drug.