Androgen receptor overexpression and sensitivity to hormones reversed by epigenetic therapy that restores Pur-α to a transcriptional repressor complex of AR deregulated in HRPC

good luck my man, let me know how it goes. I read somewhere else on here that different tissues may have responded to what fin did in different ways- for example, I myself have had crazy hairloss, much much worse than before fin, for several months now, as well as super increased sweat (signs of reflex hyperandrogenicity). BUT I have no libido and weak erections- so maybe different body parts have a different response, which just muddles the waters further.

This is super interesting…it’s a huge thread and I had trouble following it- did the people who tried the protocol get better after the second week? I can’t read the whole thing rn but I can go back later and update you too if you haven’t read it yet. If this works it could be huge, no? I do feel like there’s some cure brought up every other week. I don’t doubt people are getting better but this seems like a drastic measure.

Also, he supplemented proviron so he kinda worked on this from the “other side” of the receptor. I wonder if it matters if you high dose tribulus vs high dosing proviron. I’m not sure of the exact method of action of tribulus…


Just read the first 100 posts, u will underastand whole matter, no need of entire thread. He says once u come off fin, the receptors get overexpressed and when the androgens come back, the overexpressed receptors ain’t able to dock our androgens properly. I believe this theory.

I am a firm believer of what he tried, could really gain some insights f how to cure this, it’s just my opinion
though. Yeah many people tried his protocol here and later they got significant impeovements once they completed the cycle of 200 mg for 7 weeks. I never tried it but i guess such experiments condicted in mice can help us.

No tribulus can never reach the strength of proviron, proviron is pure dht and acts most powerfully than any other thing, nowadays some trestolone trials are going on here so i guess trestolone is even more powerful on receptors than proviron.


Gotcha, I’ll read those posts then. Hmm “significant improvements” are good but I was hoping everyone would get way better after it…

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Maybe others need few more cycles like that !

We need to hear of more people’s results too!

Just a point I would like to make.

If the receptors got messed up due to “reflux hyperandrogenicity”, or DHT rebound post ceasing fin, why would high dose proviron which would essentially mimic this hyperandrogenic phase post finasteride be the solution to reset the receptors?

I suppose everyones case is different, not expecting an answer, just a point I would like to make.

U can just try some small dose of proviron like 25 mg or 50 mg to see how u react to it. U will get the answer if u have receptor problems or not. @JustTrynaMakeIt Same.

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The term “overexpression” can confuse indeed. As i learned, overexpressed receptors mean = much higher amount of androgen receptors, which means even with high amount of androgens, we just havent enough to have an effect on the increased receptor count wich makes androgen signaling weak.

Note that its tissue specific

Is metformin an AR antagonist? If so, you are doing the opposite of what you should do. AR antagonists actually upregulate the AR’s.

You have to take androgens to lower your AR overexpression. I don’t know why you think it didn’t work on other people, it actually worked on many people. Those who didn’t experience benefits probably needed higher doses of Androgens. Dosed wrongly, needed an AI due to overactive aromatizing genes. Or God knows what else, everyone is different.

The damage we are talking here is huge, you are not going to fix that with lowe dose HCG or Proviron. Take into account of Moonman1, Ifoundacure and JoeKool’s story.

First two, were on TRT, i mean TRT, the real deal, strong, but didn’t see any benefits until they introduced the one of the strongest AR agonist out there, Trestolone, and within just a few days, latter guy recovered fully. Moonman had permanent benefits after 15 years of PFS after a week of Trestolone. JoeKool, did lots of TRT and high doses of Proviron before his HCG monotheraphy, downregulated the receptors. Still felt bad but somewhat improved. Then added HCG as a PCT and for his crashed neurosteroids from strong Androgenic usage+ PFS, then fully healed. There are many similar cases like this on different forums.

Hope this helps.

PS, IMPORTANT: Don’t take my message too seriously, i did a mistake on jumping to conclusion out of excitement. I am discussing this topic with two medical stundents, one pharmacologist, one guy who expertised, although amateurly on epigenetics, and some first hand experiences from PFS guys in a chat app, which fixed themselves with androgens. And offical studies confirmed PFS people having Overexpressed (Upregulated) androgens. Im going to edit this message if i can find the true answer. I have 4 conflicting studies about androgens and AR’s but the topic is too deep. Sorry.


This study puts it differently.

The effects of novel anti-androgens on androgen receptor action and expression.

Androgens play an important role in prostate cancer (PC) development and progression through activation of the androgen receptor (AR). Alterations in the AR, including increased expression, mutation, and amplification have been highlighted as potential mechanisms for PC progression and resistance to treatment with androgen antagonists. Recent studies increasingly show a continuing role of the AR, even in hormone-refractory PC. Current PC therapies include androgen ablation through chemical or surgical castration, as well as AR blocking agents. Compounds that inhibit androgen biosynthesis, and antagonize/downregulate the AR, may be more effective than current agents. We have previously identified VN/85-1, VN/108-1, VN/124-1, VN/125-1, VNLG/14-1 and VNLG/21-1 as novel inhibitors of 17α-hydroxylyase/C17,20-lyase, a key enzyme in androgen biosynthesis. The purpose of this study was to further evaluate the interactions of these compounds with the AR. Compound-AR interactions were evaluated in vitro using competitive binding, transcriptional activation, and western blot techniques. The human prostatic cancer cell lines LAPC4, LNCaP, and PC3 transiently transfected with a mutated AR (PC3-T575A, kindly provided by Dr. Lamb and Dr. Marcelli, Baylor, TX), were utilized. LAPC4 cells express wild-type AR, while LNCaP and PC3-T575A cells express mutated forms of the AR in the ligand and DNA binding domains, respectively. Competitive binding studies revealed binding to the AR with IC50 values ranging from 248 to 4300nM. The binding affinities of all compounds were similar for the wild-type and T575A receptors, whereas binding to the LNCaP receptor was generally decreased. Inhibitors were further assessed to determine if they were AR antagonists in the presence and absence of the AR ligand dihydrotestosterone (DHT). A luciferase assay system (Promega) was used with the Probasin luciferase reporter construct ARR2-Luc. All compounds showed inhibition of DHT induced transcriptional activation with a potency similar to or greater than the anti-androgen bicalutamide at 1μM or higher. VNLG/21-1 and VNLG/14-1 inhibited >60% at 1μM concentration, and >90% at 10μM. None of the compounds exhibited agonistic properties in the absence of DHT. Western blot analysis of protein expression shows strong down regulation of the AR after 24 hour treatment with 10μM VN/85-1, VN/108-1, VN/124-1, and VN/125-1. The results indicate that these compounds, with activities to reduce androgen synthesis and action, may be useful in the treatment of PC.

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You do understand that everything youre discussing is nothing more than speculation, right? And as @Mcbbould said, why dont you try these things out yourself and report back rather than tell others what they should or shouldnt do?

Man, it is not a ‘‘speculation’’. But it is not a theory either. It is merely a hypothesis. Because everyone is different and there are many other variables.

Now im discussing the study Guitarman posted, it is strange, i will delete all my latest messages if we can’t find the right answer. But it is pretty known how androgens downregulate the AR’s. I experienced this myself.

Uhm, helloooo, don’t you read my threads? I am experimenting on myself since this summer. Proviron, Tamoxifen, HGH, currently on HCG. And many other supplements. You never saw them? LOL.


Okay, my bad. goodluck.

I agree with @Cooper … androgens do downregulate the upregulated receptors, it’s my personal experience. I took a tab of proviron just once and after 3 weeks i started to feel androgens in many parts of body. It’s just that some people may need more time and dose to downregulate it. And sometimes maybe a stronger AR agonist than dht itself.


A second limitation is due to the impossibility to determine DHT levels, especially locally, which could help in interpretation of results. Finasteride is a drug which specifically dampens DHT levels [53]. DHT has a 10-fold higher potency of inducing AR signalling than T, and reduction of DHT and neurosteroids by finasteride may influence sexual behavior [14,54]. In fact, it was demonstrated that in patients with male-pattern baldness treat- ment with finasteride is effective in reducing local DHT/T in scalp hair [5]. Consistently, DHT was formed in negligible amounts in fibroblasts cultured from the genital skin of a patient with 5 alpha- reductase deficiency [55].

From the study.

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