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The Truth About Hair Loss - • Hair Loss Industry Exposed! - How I regrew... There’s few topics that raise as much excitement in the hair loss community as Breezula. Aka clascoterone. We’ll often do a video on an unrelated topic, and in the comments people will be asking us about Breezula. “Tell us about Breezula, we want Breezula” Well, today we’ll be doing just that. We’re gonna dive into the science and take a look at exactly how clascoterone works, what sets it apart from other hair loss medications, and what you can realistically expect it to do for your hair. So stay tuned. Timestamps 📌0:00 - Intro 📌0:55 - What's Clascoterone? 📌1:58 - Mechanism of action 📌3:45 - Side effects and metabolism 📌5:00 - Efficacy Full Transcript And without any further delay let’s get straight into it. So clascoterone… …is a topical medication developed for two conditions: acne and androgenetic alopecia. This past August it made history when it was FDA-approved for the treatment of acne. Which made it the first medication with a novel mechanism of action to gain this distinction in nearly 4 decades. It will be sold as an acne cream under the brand name Winlevi, and it’s expected to be available in early 2021. The company behind clascoterone, Cassiopea, are about to start phase 3 trials on clascoterone for male pattern hair loss. They are also conducting phase 2 research for female pattern hair loss. If the drug gets approved for hair loss it will be sold as a liquid, and the proposed brand name is Breezula. So it will be something very similar to minoxidil, though at this point we don’t know if it will be once daily or twice daily. But we do know that it will be at a 7.5% concentration. More on that later. We have no further details of on this scheduled phase 3 trial, but as soon as these become available you can be sure you will be the first to learn them, right here on this channel. Mechanism of action So let’s see how clascoterone works to combat hair loss. As I mentioned it’s a topical anti-androgen, and in particular an androgen receptor blocker. So the androgen receptor is the structure in the hair follicle and sebaceous gland cells onto which DHT binds. After the DHT binds onto this receptor, it sends a signal to the cell nucleus, modifying the expression of androgen-related genes. And it’s this biochemical chain triggered by DHT that leads to the gradual miniaturization of the hair follicle. Or at least that’s the theory. Now finasteride and dutasteride are oral medications that systemically inhibit the synthesis of DHT. So they prevent your body from producing DHT in the first place. DHT is described by some as a more or less a useless hormone in adulthood. But whatever the case, it is a hormone - and completely blocking its production is not really a good idea. Well, clascoterone doesn’t inhibit DHT production one bit. It works downstream, topically blocking the androgen receptors in the hair follicles and sebaceous glands. Thereby preventing the cells from being activated by the DHT molecule. The way this works is, clascoterone has the same general backbone structure as DHT, with 4 rings: So it’s sufficiently similar with DHT to bind to the androgen receptor. But not similar enough to actually activate it. Which means that there’s then no possibility for the actual DHT that’s floating around in your scalp to bind to the androgen receptor and activate the cells. The end result is exactly what you get with finasteride or dutasteride. Reference Links https://onlinelibrary.wiley.com/doi/f... https://www.accessdata.fda.gov/drugsa... https://link.springer.com/content/pdf...