Is finasteride bonds reversable

General Discussion
#1

I have an important question is there any science heads out there that can tell me if finasteride is
A) a competitive inhibitor or
B) a none competitive inhibitor

If it’s B then wouldn’t this explain the epignetic changes and why we don’t see any improvements? And is it theortically possible to undo those bonds that finasteride has made to the the receptor sites. I have did countless research and this theory would explain everything that’s going on with us. My God this drug should never have been approved!!!

#2

Finasteride is an irreversible or non competitive inhibitor…Instead of competition for room with the 5ar enzyme it destroys it…Similar cyanide…However the body regenerates the enzymes but there hav ed been speculation that they may not be regenerating correctly as before finasteride…As for altering the receptor sites idk…Someone else would have to answer…But Merck has always advertised finastride as an irreversible type 2 5ar inhibitor…

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#3

What I read from the FDA report filed by Merck and co was that it was a competitive inhibitor, there’s just no way it would have gotten approval if it was a non competitive compound which is what finasteride is. The research that I did is that finasteride binds to the receptor site permanently and denatures it effectively stopping it from working and there’s no way to undo it because the bond is basically like super glue effectively inactivating key hormones or releasing them in a critically low level.

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#4

Please present the research that led you to this conclusion.

#5

I will once my phone is fixed as I’m currently writing from my xbox. Why is it so hard for you to believe, I’m not throwing around wreckless statements like I said a simple Google search will tell you all you need to know. Can anyone else please confirm what I’m saying so I don’t look like a raving baffoon? I did my own research, it took alot of digging but 100% I’m right and shouldn’t be shot down until someone else confirms what I’m saying!

#6

Maybe you don’t want to believe me but I urge you to research it like I did and you’ll find the conclusion to this whole mess very fast.

#7

Just present the research. If you dont have any evidence/ research to back up your claim just admit it. Believe me we had many people on here before you claiming they know what PFS is. At least your theory doesnt come with a herb list attached. :slightly_smiling_face:

Btw: Nobody is censoring you. I am just asking you to present the research you have done. If it is all clear, and no more studies are needed, you should be able to back up your claims with evidence.

#8

Trust me when I get my phone fixed I’ll blow the lid right off this thing, I’m urging everyone to please look into this ASAP. PFS is caused by finasteride binding to receptor sites (denaturing them) so they can no longer function properly. I seriously can’t believe this hasn’t been talked about it blows my mind!

#9

Do you have a smartphone or laptop if so can you not verify what I’m saying? I can’t do it from an xbox.

#10

Btw to anyone reading this I literally had a mental breakdown when I read into finasteride being a non steroidal effectively a none competitive inhibitor once you know what that means you’ll come to your own conclusions as to how finasteride permanently fucks up the receptor sites. I’d also ask anyone is there a way for the brain to make new receptor sites?

#11

Absolute nonsense. 95%+ of people have no issues with taking Finasteride. Once it’s out of their system enzymes are simply regenerated by the body. To assume that Finasteride in some way permanently inhibits the enzymes even after it’s no longer taken can be considered to be false until proven otherwise.

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#12

I’d say that 95% is way, way off the mark especially younger men you’re almost agreeing with mercks orginal stats on those that suffered sides which everyone knows was fabricated in order to pass FDA approval. There’s a difference between enzymes and receptor sites and we’re not talking about those who don’t suffer. I’m not a scientist and don’t pretend to know all the pieces to the puzzle but what I am saying shouldn’t be thrown down the toilet either until everyone here gets a chance to review it and has their say. This matter should be open for debate and if not I think you and the moderators would be doing a disservice. I know I’m right that is why I refuse to back down until it’s proven otherwise either by you or someone else I’m not bothered who it is.

#13

What the mods have proposed here linking these substances is that any reduction of androgens can cause the syndrome…Even some that don’t effect the 5ar enzyme…Any substance that lowers androgen levels through various mechanisms can cause pfs…Some even ed n argued the fact that dht returns after cessation of finastride is what causes the syndrome…So it is possible the receptors no longer function correctly but claims here indicate it is due to an up regulation of them…Many think lowering androgen levels causes this but I have wonderd if it is the change gene in the brain that actually happens first and that is what causes the upregulated reaction instead of the lowering of dht…

#14

Being totally confident about a theory without any evidence to prove it to be the case drastically diminishes your credibility.

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#15

I know from my own personal experience that before I took finasteride I could get a paper towel rub it on my face and you’d see the oil (disgusting) I know but that has completely disappeared which would be a strong indication that DHT levels have yet to turn back to baseline and my face is severely dry now with zero oil. The epignetic gene change is finasteride bonding to receptor sites inactivating them holyhead you seem like someone with an open mind please look into what I’m saying.

#16

Plenty of evidence do you need reminding that my phone is broke?

#17

I think this is all wrong. Here is what it’s really doing:

In biochemistry enzyme substrate is the material upon which an enzymeacts

“In the presence of nicotinamide adenine dinucleotide phosphate (NADPH), steroid 5 alpha-reductase converts testosterone to dihydrotestosterone (DHT)”

“Knowing that finasteride is a mechanism-based inactivator of 5α-reductase type 2 and that the mechanism of inactivation has an obligatory requirement for NADPH”

“Finasteride was originally thought to act as a competitive inhibitor with nanomolar affinity for 5α-reductase type 2 (12). More recently, it was found that finasteride acts as a mechanism-based inactivator of this enzyme (13). Subsequent to inhibitor binding, there is hydride transfer from the NADPH cofactor to the Δ1-2-ene double bond of finasteride.”

“The intermediate enolate tautomerizes at the enzyme active site to form a bisubstrate analogue in which dihydrofinasteride is covalently bound to NADP+”

Here is my understanding of what this means.

NADPH is the substrate required for 5AR to convert T-DHT (material upon which enzyme acts) Fin is fucking with the substrate. More specifically “forms an analogue of itself called dihydrofinasteride which is covalently bound to NADP+”

It’s forming dihydrofinasteride and than “covalently bonding” with the substrate that the enzyme needs to convert T-DHT. In other words it’s creating a permanent alteration of the substrate so that it can’t interact with the enzyme like it normally would.

Source:

If you look up what the strongest bond in bio chemistry is you get this definition:

The strongest bondsthat are present in biochemicals are covalent bonds, such as the bondsthat hold the atoms together within the individual bases shown in Figure 1.3. A covalent bondis formed by the sharing of a pair of electrons between adjacent atoms.

In my opinion what this means is dihydrofinasteride has been covalently bonded to 5AR’s substrate. But we still produce enough DHT and I don’t think our symptoms are due to lack of DHT. I’m sure it does not help but probable is not the cause.

I think we need to look harder at 3B-HSD. I have evidence that 3B-HSD is not working right in me. I also think when you fuck with that substrate you are making 3B-HSD not work as good.

I think that T-DHT conversation occurs in such a large systematic level in our bodies that just because some substrate gets “dihydrofinasterided” haha we are still ok because enough DHT is still getting made.

If you look at the functions of 3B-HSD it’s more specific in scope. For example the 3B-HSD enzyme makes 3b-adiol a very specific steroid metabolite that you are less likely to see getting made up in different places. I’m low in 3b-a diol. At least according to some old labs from 2014. I wonder if messing with the substrate NADPH is responsible for possible issues with the 3B-HSD enzyme

#18

Thank you for digging into the subject I really appreciate it but if you do more searching you’ll find out that finasteride once binded to the receptor changes the structure thus even if the key and lock fit it won’t activate the receptor sites it permanently “denatures” them which would absolutely explain why there is epignetic changes being registered. What about other key neurosteroids being inhibted by the same mechanisms is this plausible?

#19

I genuinely believe this is what’s going on there are only a handful of these drugs that make covolant bonds to the receptors and it would explain why our bodies can’t find a state of equilibrium because it hasn’t got a f’n clue what’s happening and trust me our bodies want to get better, it’s probably caught in the middle of wanting to be a man or women lol but that’s the truth it doesn’t know how to balance itself. Why Merck and Co would use this method is completely insane!

#20

I’m going to bed now hopefully I die in my sleep or wake up in paradise somewhere from this God awful nightmare.