Kintor new AR degrader w/o side effects

[scientist_0005]

people in this forum are raping the scientific method. nobody gives a sh*t what results some bald men on a hair loss forum got, for all we know they might have impurities or whatever. clinical data is important. if CB is weak, why where the results better after 6 months rhan after 12? fact is the drug group was significantly above the vehicle group by P<0.0001. so clearly there is an effect even after 12 months. the increase in sensitivity suggesting an overexpression of AR is another assfuck for science as there is no evidence to suggest this AR antagonists makes your cells more susceptible to the hormone

 

[scientist_0005]

the question is why was there such deterioration with CB after 6 months?? if the 6 months resukts could be extrapolated like finasteride we would have been cured period.

 

[scientist_0005]

Increase in the AR sensetivty is actually a thing that AR degrader was meant to solve .(mostly in prostate cancer which really heavly on the activity of the AR)

but there is only one company doing the degrader, if they fail for any reason, 20 more years for betzer treatmenr

 

[scientist_0005]

Actually no ARV-110 is ar degrader that work the same as kintor ar degrader and its been tested these days on cancer .
Google ARV 110.

actually ppl on this fourm already test this on themself . If its work you wont need to wait for kintor . An AR degrader that works is the best treatment to stop hairloss you can get

but this will not get researched for hair loss. we dont want to use research powder from china, thats ridiculous

 

[Dimitri001]

people in this forum are raping the scientific method. nobody gives a sh*t what results some bald men on a hair loss forum got, for all we know they might have impurities or whatever. clinical data is important. if CB is weak, why where the results better after 6 months rhan after 12? fact is the drug group was significantly above the vehicle group by P<0.0001. so clearly there is an effect even after 12 months. the increase in sensitivity suggesting an overexpression of AR is another assfuck for science as there is no evidence to suggest this AR antagonists makes your cells more susceptible to the hormone

I haven't looked at the graph for a long time, but IIRC, yes, the treatment group is above baseline, but after 6 months they deteriorate faster than the control group. They are above baseline because they started at a higher place.

What do you think could explain that if not AR upregulation?

 

[scientist_0005]

I haven't looked at the graph for a long time, but IIRC, yes, the treatment group is above baseline, but after 6 months they deteriorate faster than the control group. They are above baseline because they started at a higher place.

What do you think could explain that if not AR upregulation?

and you have no idea what happens afterwards. they could just maintain for years later. if androgen receptor antagonists cause upregulation, what will happen to people with prostate cancer? they get more cancer with their anti androgens? i domt think so

 

[scientist_0005]

but id love to understand why it happens. modern AA not only antagonise but reduce expression as well

 

[ElToso]

@StayPositive https://www.sitri.it/document/idrocortisone-in-tricologia/

 

[Dimitri001]

and you have no idea what happens afterwards. they could just maintain for years later. if androgen receptor antagonists cause upregulation, what will happen to people with prostate cancer? they get more cancer with their anti androgens? i domt think so

The reasonable assumption is that they continue losing at least at the same rate as control. The notion that they might suddenly start maintaining after falling off a cliff between 6 months and 12 is completely unmotivated.

I've always wanted the answer to your question - why do people assume it's AR upregulation. Is this a phenomenon that is well known in medicine and that's why it is assumed to be happening here? That once you block a receptor continuously it upregulates?

As for prostate cancer, IDK, because I don't know what kinda AA is used for that. Maybe they use something with higher binding affinity than DHT, so upregulation makes no difference. Again, IDK.

 

[scientist_0005]

The reasonable assumption is that they continue losing at least at the same rate as control. The notion that they might suddenly start maintaining after falling off a cliff between 6 months and 12 is completely unmotivated.

I've always wanted the answer to your question - why do people assume it's AR upregulation. Is this a phenomenon that is well known in medicine and that's why it is assumed to be happening here? That once you block a receptor continuously it upregulates?

As for prostate cancer, IDK, because I don't know what kinda AA is used for that. Maybe they use something with higher binding affinity than DHT, so upregulation makes no difference. Again, IDK.

honestly it is completely ridiculous and cannot be explained by molecular biology. it frankly makes no sense. it is pretty sad for cassiopea because breezula will be such an utter fsilure i am honestly suprised that they have not decided to drop it and not do the third trial. even their female trial was so painful to watch, it just did not pan out at all. it is pretty sad for us who were banking on it and for the company who will probably not exist anymore in 5-10 years. certainly not gonna make much money with the rug breezula. really sad bc it was such a promising drug, an anti androgen that inactivates upon entering the blood stream. i hope they get to the bottom of this and i hope this does not reflect on other topical anti androgens as a while

 

[FollicleGuardian]

Kintor’s GT20029

 

[FollicleGuardian]

Their doses tested in mice were 0.4, 0.8, 1.6 and 3.2%. It performed equal to minoxidil 5%.

For acne (sebum/gland reduction) it was actually outperformed by Breezula on hamsters xD

 

[Ralph Wiggum]

So GT20029, which is supposed to be more advanced and superior to pyrilutamide, was only as effective as standard minoxidil?

 

[FollicleGuardian]

So GT20029, which is supposed to be more advanced and superior to pyrilutamide, was only as effective as standard minoxidil?

A46= GT20029

In this experiment, 6 groups were used, namely, a Vehicle group, a DHT (30mg/kg) concentration group, a DHT (30mg/kg) + minoxidil 5% concentration group, a DHT (30mg/kg) + A460.5% concentration group, a DHT (30mg/kg) + A461% concentration group and a DHT (30mg/kg) + A463% concentration group. The results of hair regrowth in the androgen alopecia model in C57 mice are shown in table 9 below:

table 9 hair regrowth effect on C57 mouse androgen alopecia model (AVER, n ═ 6)
As can be seen from the results, the DHT (30mg/kg) concentration group scored 0.5 for hair development 17 days after the administration, and had almost no hair development, which was significantly lower than that of the Vehicle group, indicating successful molding. The average value of the score of the DHT (30mg/kg) + minoxidil 5% concentration group is 2.33, which is obviously higher than that of the DHT (30mg/kg) model group, and the DHT/minoxidil composition shows good hair growth effect. The DHT (30mg/kg) + A46 0.5% concentration group scored slightly higher than the building block DHT (dihydrotestosterone) group, but there was no statistical difference. The scores at Day17 for the A46 1% and 3% concentration dose groups were approximately equivalent to the 5% minoxidil group, and the scores were significantly different from the DHT (dihydrotestosterone) group (p < 0.05; p < 0.01).

 

[FollicleGuardian]

As for sebaceous gland reduction it was compared to CB and Flutamide. Right is % of inhibition/reduction of size:

 

[Kagaho]

Good news. A prevention drug working almost as good as the best growth stim we have is encouraging.

Its a shame they cant test it on macaques though.

 

[scientist_0005]

Their doses tested in mice were 0.4, 0.8, 1.6 and 3.2%. It performed equal to minoxidil 5%.

For acne (sebum/gland reduction) it was actually outperformed by Breezula on hamsters xD

extremely discouraging as CB is hot garbage and so is minoxidil

 

[scientist_0005]

As for sebaceous gland reduction it was compared to CB and Flutamide. Right is % of inhibition/reduction of size:

the fact that CB which has flat out failed in clinical trials to remotely challenge the 40 year old finasteride outperforms kintors drug a supposedly innovate breakthrough decades later by 40% should be discouraging to everyone yet people still frame this as if it would be good news. kintor suggested this was the strongest in animal models which is not true. whydid they not compare it with RU or finasteride? isnt its binding affinity and ICD 50 much higher than RU? again, CB is weak as fuuck, both as an anti androgen and a hair loss drug, very ineffective. if this approach does not work.. peopleare gettinf hypes about how it will outperform breezula by a mile when rhe reality is, this might not even get throigh trials due to lack of efficacy.

my prediction? finasteride will be rhe golden standard, not just that but without alternatives, until 2040 or some sh*t. this industry is hot garbage

 

[kuba197]

It will outperform Breezula by a mile

Damn

 

[Redgate]

It was probably a bad vehicle. Can't trust mouse testing.

Spoiler