Is finasteride bonds reversable

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

An irreversible antagonist is a type of antagonist that binds permanently to a receptor, either by forming a covalent bond to the active site, or alternatively just by binding so tightly that the rate of dissociation is effectively zero at relevant time scales.

This concept is real thing.

Please post your source that Fin is an irreversible antagonist to which ever receptor you are suggesting that it is

Are my onto something or not?

Go to the library and get on a PC. Since you’ve done all the research and have screenshots to prove it, none of us are going to waste our time recreating your amazing work.

1 Like

Finasteride is an irreversible inhibitor. However this doesn’t explain the permanent side effects because the enzymes are constantly being regenerated.

1 Like

We could be. If you find any good sources on what you are proposing post them here. Don’t stress over it though it’s not a big deal.

troll detected

2 Likes

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.

The enzymes can regenerate but if they try to react with their substrate that’s bonded with
“dihydrofinasteride” this could still be a problem seeing that according to the source I posted above in order for the 5AR enzyme to convert T-DHT it needs its substrate.

I think the question you want to ask is does the substrate regenerate it self resulting in new substrate not covalently bonded with this dihydrofinasteride? Or does the dihydrofinasteride “stick around” and continue to bond to the new regenerated substrate? When you see people talking about Fin preventing it’s own metabolism I think this is what they are talking about. We would need a bio chemist to chime in haha …

Either way I don’t think Lack of 5ar, t or DHT is the problem so I don’t think we need to worry about it. It’s about making the T and DHT we still have work again.

https://bio.libretexts.org/Bookshelves/Cell_and_Molecular_Biology/Books%3A_Cells__Molecules_and_Mechanism_(Wong)/3%3A_Bioenergetics__Thermodynamincs_and_Enzymes/3.4%3A_Regulation_of_Enzyme_Activity

Not sure if above link is working just copy and paste into search engine duckduckgo. Having to write these word for word as phone won’t connect to site

http://www.hairlosstalk.com/interact/threads/lets-talk-about-competitive-enzymes-inhibitions-both-finasteride-dutasteride.100785/y

The above gives detailed info as to what’s going on inside the receptor sites and the studies that say finasteride is a competitive inhibitor are only feeding off what Merck has published it’s all just recycled misinformation. It would explain why we can’t get better because the chemical bonds are nailed into the receptor sites stopping them from activating even if people go on HRT they won’t see any significant difference as the hormones are just circulating in the body doing nothing or abeit attaching to a small number of sites that haven’t been nuked yet depending how long you took it. There’s another 5alpha inhibitor but less potent in terms of reducing DHT it’s only legalised in China (someone look up the name please) it is heavily documented as a non competitive compound even though finasteride holds almost indentical properties and it’s interesting that it’s use is banned in America and elsewhere this would hold weight as to why they would lie to bypass the FDA as there’s no way this would have got the go ahead or maybe it would just to get the money rolling. American corporations work in unison which is why you’ll not find too much info on Google. If people on this forum want to put it down to a conspiracy that’s fine but there’s countless evidence if you look hard enough you’re doing youselves an injustice otherwise. Merck and Co knew of the sides a long time ago and the truth is they probably had a small team working on a fix as it would save them millions in lawsuits but this is irreversible coming from a chemistry point of view some might see improvements years down the line if the body produces new receptors which I’m not sure it does. This would also go hand in hand as to why epignetic changes are being picked up using genetic diagnostics.

1 Like

Have a look at my latest post please, I was only able to post a few links as I’m having to type everything manually but the evidence is out there especially on duckduckgo. If people want to know what’s happening to them then I beg them to read into what I’m saying.

I just wanted to add this info that I found online about Fin.

Is it possible that the drug is still in our system and our body has hard time getting read of it? because it is insoluble in water.

what do you guys think any comments?

could alcohol consumption help body get read of this drug.
In fact anaerobic exercise have helped some people recover from this condition.
Just an idea.

The empirical formula of finasteride is C23H36N2O!

1 Like

But wouldn´t everyone be damaged, not just a small group experiencing a crash and getting PFS. Also how do crashes come into play here?

1 Like

Looking at the PFS study the researchers believed that finasteride was still in our systems via cerebral spinal fluid and could take years to expell but I think what I’m saying holds very credible merit and I can put my life on it that I’m right.

It’s damaging them one way or another whether they believe it or not there’s also a possibility that hypotoxicity plays a role then trigging autoimmune in more sensitive people. I’m not sure about the crashes but a trade off between estrogen dominance at play and body can’t a find a state of stable equilibrium so crashes.

Dude I ran 5 miles a day plus while wearing a trash bag under my clothes…I lost massive amounts of fluids and the only th in ng that happened is my mileage got less and less as the months went by and my weight kept increasing fir no reason until eventually now I can’t run at all or do anything…

Finasteride slowly denatures the receptor sites which is why I’m progressively getting worse. Reminds me of that scene from limitless were they all start getting sick after withdrawel.

I myself took SSRI, which I believe isn’t an irreversible non competitive inhibitor and experience the exact same ongoing symptoms as u guys. Penis shrinkage, zero libido, gyno etc. How could this happen and be so similair to the state u guys are in, without SSRI having these non competitive qualities. I think ur putting too much weight on finasteride supposedly being an irreversible non competitive inhibitor because as I said, for other drugs, this isn’t needed to create these ongoing effects.

1 Like

The brain should never be fucked around with peroid sounds like you have serotonin syndrome that’s sent your hormones out of whack. I had a nasty reaction to them once almost similair to finasteride but they finally subsided months after.

Nah wasn’t serotonine syndrome tbh. I know the signs of that and I wasn’t experiencing that at all throughout the use. Also my shit really started when quitting, not while using. With serotonine syndrome it happens while using the SSRI. Also my symptoms really became worse during the withdrawal. And yeah I agree we should never fuck with our endocrine systems, it’s a very risky business.

Since there seems to be some false information being posted here about finasteride being found in cerebrospinal fluid of PFS patients in a PFS study (this never happened), and some confusing statements made about the denaturing of the 5-ar “receptor”, this topic will now be locked. Perhaps this will give other members time to “research” that information being dispensated by someone who has been “researching” PFS for months .

@Blueryan123 , as the forum guidelines that you have repeatedly violated in your couple-day stint here explicitly state:

Theories

We welcome theoretical discussion or speculation, and simply request that it is clear from your post that you are presenting your opinion and the basis for that opinion. Contributors should refrain from making declarative statements regarding the etiology of PFS without significant and specific evidence. Take care not to present your ideas and experiences as definitive medical advice or diagnosis. Instead, try to provide information of what has worked for you, or others on this site.

As examples, instead of using definitive statements about the condition that can appear as factual claims such as “PFS is this”, “This will work every time” or “Do this and it will cure you”, consider using language such as “I believe…”, “You could try…”, or “This has worked for me”.

2 Likes