Winlevi ( Cb 03 01 ) For Acne, Fda Approval

[nameless2]

It really no, It is extremly important since, it fact, is the first medication ever that was created to be use it to treat acne and Androgenetic Alopecia. None finasteride or minoxidil were created for Androgenetic Alopecia .
Why is important ? Because it was even done by small lab, which show to big labs, if is a success, that they should actually invert money in new molecules to treat Androgenetic Alopecia .

Besides, there will be , soon, tons of new studies and tons of new studies done every year about this drug on Androgenetic Alopecia . How many studies can you find of, for example, topical spironolactone in Androgenetic Alopecia ? one , may be ?
And ketoconazole topical ( not shampoo ) ? Only 1 ! the Japanese one.

Now, you see what is the BIG difference that this antiandrogen is actually approve to be use it as topical ?!

That's part of the difference between oral anti-androgens and a topical anti-androgens but the biggest difference is that the local topical anti-androgen works locally & topically without getting into the body enough to cause systemic side effects whereas an oral anti-androgen is taken by mouth and travels all throughout the body.

Some oral antiandrogens will grow hair when turned into a topical and applied topically, but too much of the drug can sink deeper into the body and causes systemic side effects. Some oral anti-androgens turned into a topical solution grow hair but they often do this by sinking deeper into the body and circulating throughout the body...including the hair follicles.

 

[John Difool]

@nameless2 and @jamesbooker1975 congrats for your very instructive posts on this incredible news. Without you we may have missed it so thank you for Investing your time posting some lengthy information on this achievement. Such a valuable information.

 

[Badbald]

It really no, It is extremly important since, it fact, is the first medication ever that was created to be use it to treat acne and Androgenetic Alopecia. None finasteride or minoxidil were created for Androgenetic Alopecia .
Why is important ? Because it was even done by small lab, which show to big labs, if is a success, that they should actually invert money in new molecules to treat Androgenetic Alopecia .

Besides, there will be , soon, tons of new studies and tons of new studies done every year about this drug on Androgenetic Alopecia . How many studies can you find of, for example, topical spironolactone in Androgenetic Alopecia ? one , may be ?
And ketoconazole topical ( not shampoo ) ? Only 1 ! the Japanese one.

Now, you see what is the BIG difference that this antiandrogen is actually approve to be use it as topical ?!

Again false. There have been mutliple studies on Ketoconazole and its effects on hairloss, look it up.

 

[nameless2]

@nameless2 and @jamesbooker1975 congrats for your very instructive posts on this incredible news. Without you we may have missed it so thank you for Investing your time posting some lengthy information on this achievement. Such a valuable information.

This post feels like its' sarcastic and triggered both at the same time. Is that the intent?

 

[jamesbooker1975]

@nameless2 and @jamesbooker1975 congrats for your very instructive posts on this incredible news. Without you we may have missed it so thank you for Investing your time posting some lengthy information on this achievement. Such a valuable information.

For nothing, it is wonderfull to help an average Joe.

 

[jamesbooker1975]

Again false. There have been mutliple studies on Ketoconazole and its effects on hairloss, look it up.

As topical ?lol . Only as shampoo. Or may be I am wrong and you can post that many topicals. For example, what happen if you apply ketoconazoles topical , like a cream, every day for 6 month, it will go systemic ? Yes, no ? why ? Can you post that study ?

There is only one study, done in Japan, about using topical ketoconazole ( cream ) daily . Nothing more. In all the other studies, they use shampoo for a couple of minutes a couple of times per week. And even with the shampoo, there are just s couple of studies vs hundreds done with Finasteride or Minoxidil .

Guys, saying that have not value that a medicine is approve for a certain disease, have none sense at all. It is reall a none sense, is like try to argue with someone that say that the Earth is plane. Want to believe it ? go for it.

 

[John Difool]

Okay so are we done now? Can we please move on?

 

[nameless2]

Okay so are we done now? Can we please move on?

Why ask if "we" can move on? If you want to move on then why don't you just stop posting in this thread for awhile? Why should the rest of us have to move on just because you do?

 

[Jim lahey]

Cause you guys are talking about some technicality that's derailing the thread.

 

[John Difool]

I just chose to ignore these two penguins posts. Their contributions to this forum has never been useful anyway. They are just a couple of detractors.

 

[jamesbooker1975]

Okay so are we done now? Can we please move on?

If you ask please, sure . Nothing more pleasant than an average joe using good manners.

 

[nameless2]

Cause you guys are talking about some technicality that's derailing the thread.

This thread is about Winlevi and the "technicality" I'm discussing is a characteristic of Winlevi. That means I'm talking about Winlevi, which is what this thread is about. How can I derail this thread when what I'm talking about is what this thread is about?

And I only posted about this "technicality" after other posters posted incorrect info on the matter.

 

[nameless2]

Again false. There have been mutliple studies on Ketoconazole and its effects on hairloss, look it up.

Ketoconazole is not FDA-approved as a topical anti-androgen. Ketoconazole is FDA-approved for topical use as an anti-fungal.

When its' used topically for hair growth it may work locally or it may work systemically by sinking deeper into the body. I honestly don't know the answer to that question and I don't think you do ether because that information isn't easy to find. The info is out there but one would have to do a long deep dive to find it. You might have to read every word of every study involving Ketoconazole to get the answer to that question.

In any case, Ketoconazole is a WEAK anti-androgen and that would limit it's efficacy even if it works locally when topically applied. You see, since it's anti-androgenic activity is weak, the benefit from using it ONCE OR TWICE PER DAY in the shower wouldn't satisfy most of us. Hence, we need a STRONGER locally-active topical anti-androgen.

Winlevi is the first FDA-approved drug of this type, which means that even if every other anti-androgen has failed you, Winlevi might still help you because Winlevi is the first FDA-approved anti-androgen of its' kind. And Breezula is even stronger so if Winlevi doesn't help you, Breezula might.

 

[Dimitri001]

Instead of this utterly silly and unproductive discussion, let's talk about something actually relevant. So, what about this:

Hypothalamic-pituitary-adrenal (HPA) axis suppression may occur during or after treatment with WINLEVI. In the PK trial, HPA axis suppression was observed in 1/20 (5%) of adult subjects and 2/22 (9%) of adolescent subjects at Day 14.

Now, my understanding is that the way you test for this is by measuring cortisole levels, which is why they had this bit in the dosing study:

Since the chemical structure of Clascoterone is similar to that of a steroid while its function is not, cortisol levels were tested in a sub-group of patients to verify that Clascoterone is free from systemic steroid activity. The mean absolute changes of cortisol values throughout the study were similar among groups, proving that Clascoterone has no systemic effect on cortisol.

So, with Winlevi, you got (counting only adults) a 20 subject study with 1 person getting HPA and then in this 300+ study they claim no one got it. There are other Winlevi studies where they specifically studied sides and there was no mention of HPA.

They have two trials registered on ClinicalTrials.gov to test specifically for HPA with Winlevi and even though the trials (one with adults, one children) were posted in 2013 and 2016, no results were posted.

https://clinicaltrials.gov/ct2/show/NCT02720627?term=CB-03-01&draw=1&rank=2
https://clinicaltrials.gov/ct2/show/NCT01831960?term=CB-03-01&draw=1&rank=5

So, what to make of this? I think someone mentioned somewhere that HPA is more likely among women (if I'm not making that up, I THINK I read that), could that be why they found it in the Winlevi study and not the Breezula dosing study? The W study featured women, B didn't? Could that mean this potential side effect can't happen in men?

 

[nameless2]

Instead of this utterly silly and unproductive discussion, let's talk about something actually relevant. So, what about this:

Hypothalamic-pituitary-adrenal (HPA) axis suppression may occur during or after treatment with WINLEVI. In the PK trial, HPA axis suppression was observed in 1/20 (5%) of adult subjects and 2/22 (9%) of adolescent subjects at Day 14.

Now, my understanding is that the way you test for this is by measuring cortisole levels, which is why they had this bit in the dosing study:

Since the chemical structure of Clascoterone is similar to that of a steroid while its function is not, cortisol levels were tested in a sub-group of patients to verify that Clascoterone is free from systemic steroid activity. The mean absolute changes of cortisol values throughout the study were similar among groups, proving that Clascoterone has no systemic effect on cortisol.

So, with Winlevi, you got (counting only adults) a 20 subject study with 1 person getting HPA and then in this 300+ study they claim no one got it. There are other Winlevi studies where they specifically studied sides and there was no mention of HPA.

They have two trials registered on ClinicalTrials.gov to test specifically for HPA with Winlevi and even though the trials (one with adults, one children) were posted in 2013 and 2016, no results were posted.

https://clinicaltrials.gov/ct2/show/NCT02720627?term=CB-03-01&draw=1&rank=2
https://clinicaltrials.gov/ct2/show/NCT01831960?term=CB-03-01&draw=1&rank=5

So, what to make of this? I think someone mentioned somewhere that HPA is more likely among women (if I'm not making that up, I THINK I read that), could that be why they found it in the Winlevi study and not the Breezula dosing study? The W study featured women, B didn't? Could that mean this potential side effect can't happen in men?

This issue is irrelevant and silly because most of us would need Breezula rather than Winlevi since Winlevi is a cream so it would be messy if you applied it to your hair. Also, Breezula is much more potent.

 

[Dimitri001]

This issue is irrelevant and silly because most of us would need Breezula rather than Winlevi since Winlevi is a cream so it would be messy if you applied it to your hair. Also, Breezula is much more potent.

Presumably, this effect is caused by CB, so if it's happening with 1% CB in Winlevi it's certainly a risk in 7.5% Breezula, so we're discussing the safety profile of Breezula.

 

[Dimitri001]

So you're discussing if it has systemic safety effects and I was discussing if it has systemic hormonal effects. It sounds to me like there are some key similarities in the two discussions.

I have no idea what you're talking about here. If you're referring to my saying that what you guys were talking about was a pointless discussion, I was referring to the matter of what was the first topical AA and what qualifies as such and what doesn't etc.

Plus, just because it happens with Winlevi does not establish that it will happen with Breezula. I think your discussion is silly and irrelevant. Come back after it's proven that it also happens with Breezula. Until then zip it.

This is such a stupid point and even you must be aware of it, so at this point you're just arguing to argue or you're trolling, which is maybe why you have half as many dislikes as likes. The active ingredient in W is CB, same as B, if a side effect happens with 1% CB it's more likely it will happen with 7,5%, there's no way you're stupid enough to not understand this, so stop being argumentative for the sake of it, let's not spam this thread with any more fighting.

 

[nameless2]

I have no idea what you're talking about here. If you're referring to my saying that what you guys were talking about was a pointless discussion, I was referring to the matter of what was the first topical AA and what qualifies as such and what doesn't etc.

This is such a stupid point and even you must be aware of it, so at this point you're just arguing to argue. The active ingredient in W is CB, same as B, if a side effect happens with 1% CB it's more likely it will happen with 7,5%, there's no way you're stupid enough to not understand this, so stop being argumentative for the sake of it, let's not spam this thread with any more fighting.

1. You picked out one sliver of what I was talking about and act is if that was all I was talking about. There were numerous points in my posts whether you picked up on all of them or not.

2. You're the one who started the fighting by calling my issues irrelevant, silly, and pointless. I don't think my posts were irrelevant, silly, and pointless anymore than you think yours are. You're raising issues about systemic safety effects and I raised issues about systemic hormonal effects. That's not a gigantic difference IMO.

3. Just because a safety issue happens with Winlevi does not mean it will happen with Breezula. You yourself alluded to a small 20-person Winlevi study with a low incidence of HPA and you yourself also said no HPA was reported in the dosing study for Breezula. And you yourself also alluded to a 300-person study involving Winlevi with no reported incidence of HPA. Two different Winlevi studies with two different results regarding HPA. At this point, any opinion we offered would be a guess so your issue is pointless here. Perhaps you should contact the manufacturer for more information.

 

[nameless2]

You are acting deranged @nameless2 going back asks disliking and worrying my old posts just because I liked Dimitri's post. Dislike all you want. I'm not going to argue this nonsense with you. Go get a life

I did no such thing. I can't get to sleep tonight so I'm browsing through the Winlevi posts and I came across a post by you that I thought was mistaken so I disliked it. I'll remove the dislike. What page is it on?

UPDATE: I found the post and I removed the dislike.

 

[Dimitri001]

This HPA thing really is strange. You got this tiny study where of about 40 subjects, 3 get it, but then you have this:

The 3 Phase II studies, n=477, revealed minimal systemic absorption; the active ingredient works locally within hair follicle. Subjects did not show clinical evidence of adrenal suppression under maximal use conditions. (this is also Winlevi, not Breezula)

How the hell do you account for this?

There's a further issue with CB, which is that the story about it metabolizing quickly and being entirely absent from plasma isn't true.

This is from a paper summarizing phase I and II studies:

Phase I study: Clascoterone reached the blood stream after a single dose and repeated BID
application to the alopecic areas. Quantifiable plasma clascoterone concentrations
were found in all treated subjects, from 4 hours after the first application and
increasing during the treatment period. Day 28 pre-dose clascoterone concentration
was similar to the 12-hour postdose concentration—indicating steady state.

Now, they don't give what the concentration is and perhaps it's something negligible and irrelevant, but... I haven't been able to find the phase I study paper to find that info.