Kintor new AR degrader w/o side effects

[scientist_0005]

Seriously? This and minoxidil are polar opposite treatments. If you get legitimate growth from an AR degrader, it's permanent and will probably last decades with 90%+ of the AR degraded.

This doesn't even factor in that every other growth treatment including minoxidil (and future ones) will work significantly better with almost 0 androgens attacking the follicle.

you realize that the cell produces new AR every day right? just like with finasteride you will havr to takr this regularily or the results will fade. its not permanent. also the 90% figure is made up

 

[Micky_007]

Why? From what i understood AR degrader do not completely destroy the AR forever, the human body regenerate that sh*t better than it regenerates hair lmao, still need continued use.

The only thing that could allow you to buy some years before having to obsess over your scalp again is HMI, and the fact that people from the GB reports shedding after cessation of SMI treatment doesn't look particularly good for that part, tho it's hard to tell with that.

Regarding the AR Degrader like Kintors GT20029, we know it's effect on the AR is not going to last forever, hence regular use will be required, however, it was be a lot less often than taking for example Finasteride daily.

 

[Dimitri001]

CB doesn't even have enough strength to compete with DHT. If it had decent results and lost them it's because whatever temporary boost your hair gets from removing a slight amount of DHT and T isn't sustainable.

This compound degrades/removes the AR completely, it's not the same thing, and you are wasting everyone's time by scoping in on one line about sebaceous glands on hamsters.

This doesn't make sense, why would it be able to outcompete DHT and T for 6 months, but not thereafter?

 

[trialAcc]

This doesn't make sense, why would it be able to outcompete DHT and T for 6 months, but not thereafter?

I never said it out competed DHT/T for a 6 months, or at all. I'm saying that whatever benefit it's competition provided (at whatever level) doesn't last as the results show.

 

[trialAcc]

you realize that the cell produces new AR every day right? just like with finasteride you will havr to takr this regularily or the results will fade. its not permanent. also the 90% figure is made up

Oh look, another thing you don't understand in the slightest but feel the need to lecture on. The drug is designed to degrade the AR in cycles, and I clearly said that the results would be permanent "so long as you take the drug". The compound binds to the AR and degrades it on a constant basis, which is what allows this drug to be dosed in long intervals of a week or more.

The 90% figure is not made up, it's from similar dosing concentrations that were achieved in the prostate for cancer on real humans. Whether or not that is achievable on the scalp is dependent on how accurate the drug is and how well it hits its intended target. That's where the success or failure of this drug will be found, in the safety of hitting the intended target and in the efficacy for being able to degrade it at the safe topical concentrations.

 

[trialAcc]

i think the drop in CB is simply bc its not strong of an anti androgen. upregulation of AR is not common with anti androgens, if it was thrn this mechanism would have been discovered becsuse it would be VERY bad for conditions like prostate cancer where sou rely on continuous suppression of androgenic activity. no literature would suggest this kind of reaction. however that poses the questioj if it was strong enough to give better results than finasteride its clearly getting to the follicle so why would it suddenly drop? it is quite strange and unusual for anti androgens in hair loss

Actually, the existence of the theory for AR upregulation comes from the fact that it has been observed in the prostate of cancer patients. It's actually never been observed anywhere else, which is why we don't know if things like finasteride or topical AAs can cause it.

Androgenic up-regulation of androgen receptor cDNA expression in androgen-independent prostate cancer cells - PubMed

The expression of the androgen receptor (AR) gene is regulated by androgens. Although androgens down-regulate AR mRNA in most cell lines and tissues, including the prostate, up-regulation occurs in some tissues. Androgen-mediated reduction in AR mRNA is reproduced in COS1 cells and in the...

pubmed.ncbi.nlm.nih.gov

 

[jan_miezda]

Why? From what i understood AR degrader do not completely destroy the AR forever, the human body regenerate that sh*t better than it regenerates hair lmao, still need continued use.

The only thing that could allow you to buy some years before having to obsess over your scalp again is HMI, and the fact that people from the GB reports shedding after cessation of SMI treatment doesn't look particularly good for that part, tho it's hard to tell with that.

Smi does not equal hmi

 

[trialAcc]

The upregulation is the only thing that explain how in 6 month cb stop working , how in 2 years finasteride hair count start to go down (based on FDA) .
And by stop working i mean the body found a way to overcome its effect

I don't think that's true about finasteride, but I have no idea about CB (although I doubt upregulation is a thing from 6 months of use). The increase of hair from CB at the start could have been due to something else, like a temporary spike in E from T (the more common thing CB can compete with) not binding to the receptor. Without more data we don't know how long it maintained, all we know is that the gains disappeared. If AR were that easy to upregulate, how would any prostate cancer treatment ever work?

The DHT inhibition of finasteride on the scalp never goes beyond 30-40% as far as I'm aware. The more likely scenario is that the initial lesser DHT amount if able to hold off the loss for a certain period of time for each person, but damage still happens on a more slow pace. Eventually your cells just become more prone to damage, just as any cell does as you age.

Why would we expect 30% inhibition of DHT to prevent 100% of damage?

 

[trialAcc]

In both cases either the body create more AR , or the AR become more sensetive

If it were that simple it would have been more easily observed. The fact that it hasn't should probably tell us there is something else going on.

 

[poopfeast420]

Janey chill with thw long *** comments

Please stop making these posts. If there's one person who's posts are worse than Janey its you.

 

[Dimitri001]

I don't think that's true about finasteride, but I have no idea about CB (although I doubt upregulation is a thing from 6 months of use). The increase of hair from CB at the start could have been due to something else, like a temporary spike in E from T (the more common thing CB can compete with) not binding to the receptor. Without more data we don't know how long it maintained, all we know is that the gains disappeared. If AR were that easy to upregulate, how would any prostate cancer treatment ever work?

The DHT inhibition of finasteride on the scalp never goes beyond 30-40% as far as I'm aware. The more likely scenario is that the initial lesser DHT amount if able to hold off the loss for a certain period of time for each person, but damage still happens on a more slow pace. Eventually your cells just become more prone to damage, just as any cell does as you age.

Why would we expect 30% inhibition of DHT to prevent 100% of damage?

Do you know how long upregulation typically takes?

Why would CB cause a temporary spike in T and why only temporary? If you're thinking it takes up T's place in the receptor, thus causing more free T, which then leads to more E, it's DHT that binds to the receptor in absence of CB, not T. And, again, if that's the reason, why would the increase in E from T be temporary?

What sort of AAs are used in prostate cancer?

If it were that simple it would have been more easily observed. The fact that it hasn't should probably tell us there is something else going on.

You mean more easily observed in medical studies generally or in CB studies? Because if you mean the latter, I'm not sure anyone was looking for it.

 

[trialAcc]

Do you know how long upregulation typically takes?

Why would CB cause a temporary spike in T and why only temporary? If you're thinking it takes up T's place in the receptor, thus causing more free T, which then leads to more E, it's DHT that binds to the receptor in absence of CB, not T. And, again, if that's the reason, why would the increase in E from T be temporary?

What sort of AAs are used in prostate cancer?



You mean more easily observed in medical studies generally or in CB studies? Because if you mean the latter, I'm not sure anyone was looking for it.

You don't think people would be looking for AR upregulation in other tissues other then the prostate?

 

[Micky_007]

Janey chill with thw long *** comments

Thank you! Yet another person who figured out scientist_0005 is Janey Elizabeth.

 

[Dimitri001]

You don't think people would be looking for AR upregulation in other tissues other then the prostate?

You didn't answer the CB T->E question. I don't know what point you're making with the question.

 

[scientist_0005]

"Although androgens down-regulate AR mRNA in most cell lines and tissues, including the prostate, up-regulation occurs in some tissues."

normally increased levels of androgens do not increase AR expression thus this theory is wuite unlikely. also what do people referr to when they talk about receptor sensitivity? what does that even mean? from my understanding sensitivity of a single receptor is not a thing, you can talk about an entire cell line being sensitive to something based on how much receptor they express, increased sensitivity sould then merely be an upregulation of the transcription of those receptors, not that a sinlge binding xomplex produces different biological results.

biologically it makes sense for androgens to dosnregulate the AR unless the cells are fucked up and want to stay in a stage of hyper growth like prostate cancer. when you have an excess of androgens, you do not need that many receptors to fulfill the same effect on downstream genes, when you have very few androgens you want to have more receptors so you can get the most out of the few you have and

if there us upregulation such processes can take place within hours, as fast as it takes for the androgen to reach the promoter region or whatever it attaches to and then to make the proteins i think.

you will indeed have more androgens in the scalp because they cannot attsch to their receptors. these floatinf androgens could out compete CB if CB is not present in large enough quantities. remember if yiu bring CB directly to the follicle it is very potent in fact.

so no doubt there will be more DHT present in the follicle but this would be the case from day one not just after 6 months so they anomaly in their data i think cannot be explained this way

 

[trialAcc]

You didn't answer the CB T->E question. I don't know what point you're making with the question.

Because I don't even know what you're asking. CB is going to displace a lot more T then DHT due to it's low binding affinity.

Look at finasteride. The majority of the excess growth you get when you start finasteride is due to T spiking E when it can't be converted to DHT, yet that growth doesn't continue past that initial 6~ months. The difference is that the lower androgen environment actually lets you maintain. With CB, it isn't strong enough to maintain and you probably lose whatever benefit you get as a result.

Just a guess, because I think AR upregulation is a stupid theory to explain a complex process.

 

[scientist_0005]

Because I don't even know what you're asking. CB is going to displace a lot more T then DHT due to it's low binding affinity.

Look at finasteride. The majority of the excess growth you get when you start finasteride is due to T spiking E when it can't be converted to DHT, yet that growth doesn't continue past that initial 6~ months. The difference is that the lower androgen environment actually lets you maintain. With CB, it isn't strong enough to maintain and you probably lose whatever benefit you get as a result.

Just a guess, because I think AR upregulation is a stupid theory to explain a complex process.

thats not true about finasteride

 

[scientist_0005]

as for regrowth the mere absence of androgens gives the regrowth dzring treatment as well

 

[Dimitri001]

Because I don't even know what you're asking. CB is going to displace a lot more T then DHT due to it's low binding affinity.

Look at finasteride. The majority of the excess growth you get when you start finasteride is due to T spiking E when it can't be converted to DHT, yet that growth doesn't continue past that initial 6~ months. The difference is that the lower androgen environment actually lets you maintain. With CB, it isn't strong enough to maintain and you probably lose whatever benefit you get as a result.

Just a guess, because I think AR upregulation is a stupid theory to explain a complex process.

How is it going to displace more T than DHT??? If it binds to the receptor then DHT, which normally binds to it, can't. If it's gonna cause more free hormone of any kind it's going to be DHT.

 

[trialAcc]

How is it going to displace more T than DHT??? If it binds to the receptor then DHT, which normally binds to it, can't. If it's gonna cause more free hormone of any kind it's going to be DHT.

CB can't out compete DHT for the receptor. It can out compete T. It's binding affinity is too weak.