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Yeah, or it's a troll. I'm sure nurses are just throwing this type of information out there to anyone that asks, even though it could be detrimental to the study. I realize it would only take one to mess up, but I'm also not going to ignore a potential treatment because a random user says it isn't working.Comment
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Or Intercytex, or Histogen, etc.
You haven't even been a full year here and look at your post count!
You should curb your enthusiasm a little bit, you keep trying to inject naive optimism to every treatment that has been announced in the last year.
Better read a little bit, there is more than a decade of information available on hair loss forums. You can see how many like you have come and go and we still don't have a treatment availableComment
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Here's a piece of good news that bodes well for SM05445
One thing - can someone please tell me what telogenic mice are?Comment
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Sounds like mice they've altered so their hair is in a telogen state, as opposed to the normal hair growth cycle, so that they may test their hypothesis with a drug, treatment etc.
Remember when Cotsarelis induced AGA into mice by overexpressing Cox-2? That was in part how he developed his PGD2 hypothesis.Comment
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I think we all have to wait for phase 2 to finish before getting too excited.
If results are disclosed or phase 3 confirmed, then i will be happy as hell
Its a good sign they are planning to expand their facilities thoughComment
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Don't trust any mouse study guysComment
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One thing that bothers me about the SM05445 concept is that more and more the dermatological community is saying that growth factors mediate hair growth downstream from the anti-androgen pathway, but if that's true then it seems like SM05445 would have to be continuously applied the same as anti-androgens have to be continuously applied. I mean if they work on the same pathway.
If anti-androgens have to be continuously applied in order to keep the bald genie in check then any treatment that works downstream on the same path should also have to be applied continuously.Comment
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Indeed, sadly MPB is chronic condition and requires lifelong treatment. The ultimate solution would be shutting down our Androgen Receptors. Why we are balding in such a pattern - Fron NW1-NW7? Beacuse of the density of ARs on our scalp
LINK
So, do we have impaired Androgen Receptors? The answer is yes."The higher levels of androgen receptors in cells from balding scalp hair follicles with similar properties to those from non-balding scalp concur with the expectations from their in vivo responses to androgens."
LINK
As stated in the study above, mutation of AR gene is not enough for MPB to come in full glory. DHT binds to the AR receptor, RU58841 binds too - blocking DHT. Shouldnt it be full cure(with Fin and Dut)? Sadly It is not.In summary, our findings represent the first association between a candidate gene and MPB. We suggest that abnormality of the AR gene is necessary, but not sufficient for the phenotype. We envisage a polygenic inheritance, dependent on a combination of a mutation in or around AR affecting the expression of the androgen receptor and genes controlling androgen levels. Interactions between such genes might account for the tissue-specific and developmental stage-specific expression of AR that is necessary to explain the characteristic anatomic and temporal patterns of MPB.
Lets find out other factors. But hey, what about the fact that women dont go bald even with balding gene? Some of them have got all of our AR mutations and even more ARs on scalp.
LINKl
It strongly suggests that DHT is the only one to blame. The onset of AGA, the castration results - everything is connected with DHT!Both women and men with androgenetic alopecia have higher levels of androgen receptors and 5-reductase type 1 and 2 in frontal than in occipital hair follicles, whereas higher levels of aromatase were found in their occipital follicles (Sawaya and Price, 1997). Aromatase content in women's frontal hair follicles was six times greater than in frontal hair follicles in men. Frontal hair follicles in women had 3 and 3.5 times less 5-reductase type 1 and 2, respectively, than frontal hair follicles in men (Sawaya and Price, 1997)."
Now back to the SM04554 topic
LINK
Androgens are inhibiting Wnt/B-catenin pathaway - which is crucial for hair loss cycle
Telogen cell arest - sounds familiar?These results suggest that Wnt signaling in DP cells is regulated by androgen and this regulation plays a pivotal role in androgen’s action on hair growth
This study identified four AGA risk loci with genome-wide significance on chromosomes 2q35, chr3q25, chr5q33.3, and chr12p12.1, and provides biological evidence that WNT10A is the gene responsible for the effect on chr2q35.We ve go impaired Wnt10A genes. It seems that AGA is poligenic disease. We need DHT blocker for sure but we also need Wnt agonist! Thats why I strongly believe in SM04554 there is a lot of science behind it. Wnt pathaway is crucial for Anagen onset. Without this mechanism Antiandrogens are almost useless.In particular, some authors have suggested that WNT signaling constitutes an important regulatory signal for the transition from telogen to anagen in postnatal hair follicles (Reddy et al., 2001; Li et al., 2011). Interestingly, WNT10A expression has been detected at anagen onset in mouse hair follicles (Reddy et al., 2001), suggesting that WNT10A is implicated in
So, SM04554 with DHT inhibiotor would be a cure? In theory, yes.Comment
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Sm04554
Interesting article about Wnt and wounding
Generating New Hair
How stem cells can help hair re-grow after wounding
Look at one of your scars. You'll notice some differences between a scar and the skin around it. For one, the scar isn't as stretchy as the skin. And it doesn't have any hair.
Wouldn't it be great if scientists knew how to make scars less scar-like? Well, they have taken the first step in mice.
What scientists have done is to begin to figure out how to grow hair where a scar forms. And when head scars leave bald spots being able to re-grow hair becomes pretty important. Just ask my sister.
On one of my family vacations as a kid, my sister and I were playing around on a teeter-totter. She fell off and hit her head. There was a pretty nasty gash.
So I carried her as fast as I could back to my mom and dad. They rushed her to the hospital. Luckily she didn't need any stitches.
Looking at her today, you wouldn't even know that she hit her head. Everything looks completely normal at first glance. Unless you know where to look.
As you can imagine, she has a good sized scar on the back of her head. But what you might not imagine is that she doesn't have any hair where the scar is.
The scar didn't re-grow any hair. So she has a small bald spot. She's lucky the cut wasn't any bigger. Girls don't generally look very good with large bald spots.
Hair doesn't grow no matter where a scar forms. Take a look at a couple of the scars on your body. I bet they don't have any hair.
When we get cut, scars replace normal skin so we don't have open wounds on our body. But it would be even better if we could re-grow skin like new.
The new finding helps shed light on how we might be able to re-grow hair in a scar after wounding. This will take us closer to completely healing after an accident.
How to re-grow hair
Recently, scientists stumbled onto the finding that, at least in mice, hair will sometimes re-grow after wounding. They were studying how wounds heal in mice and noticed that sometimes hair grew back. And sometimes not.
This was surprising. Why? Because scientists thought that losing hair because of scarring was permanent.
Hair grows out of hair follicles. Since hair follicles are like "mini organs," scientists thought they only formed when a fetus grows in the womb. Like how your liver or your lungs only form as a fetus.
So hair re-growing in the wounds was completely unexpected. To figure out what was going on, the scientists wounded adult mice by cutting away some of the back skin.
The wounds needed to be at least half the size of the mouse's back to form new hairs. Any smaller and hair follicles didn't form.
They weren't sure why the wound had to be that big. But they wanted to learn more about how the hair grew back in. And if the process was similar to what happens when we're in the womb.
How could the scientists answer these questions? First off, they needed to understand how hair forms in an embryo.
Turns out, we already know a lot of what is going on there. We know some of the key genes and proteins that cause hair growth.
So they looked to see if one of the key players in hair development, KRT17, was involved in growing hair after wounding. And it was.
KRT17 showed up in the new hair follicles at about the same time it would be expressed in embryonic hair follicles. So these hair follicles developed similar to embryonic hair follicles.
But the scientists knew the growth wasn't exactly the same. Why? Because the hairs always came in white. They had no pigment.
So not everything in the hair follicle grew back. The cells that have pigment, the melanocytes, didn't grow along with the rest of the hair follicle. (Like when you age and your hair turns white or gray, it's because all your melanocytes are gone.)
Alright, so can we now grow my sister's hair back after her teeter-totter accident (even if it'll be white)? Not quite. First, we need to know where the hair is coming from. And what helps it grow.
More Information
Wnt-dependent hair follicle regeneration in adult mouse skin after wounding
Gray hair and hair stem cells
Hair follicles are like
mini-organs.
Where the hair came from
So now we can see that the hair grows pretty similarly to what happens in the embryo. But do the hairs come from the same tissue as an embryo? In other words, do they come from hair follicle stem cells?
As adults, we have many different kinds of stem cells. Nerve stem cells. Liver, hair, blood, bone, and immune stem cells.
Each type of adult stem cell makes a specific set of cells. That means hair follicle stem cells can become any cell in a hair follicle. And form a hair follicle from scratch.
The scientists used special mice to look at the hair follicle stem cells. Treated with a chemical, the hair follicle stem cells in these mice turn blue. All the cells that come from these stem cells are also blue.
So, if the mice grow blue hair after wounding, then the hair came from hair follicle stem cells. If not, then it came from somewhere else.
The scientists treated the mice with the chemical before wounding. Just as we'd expect, all the hair follicle stem cells turned blue.
After wounding, they looked at the new hair in the wounded area. None of them were blue. So none of the hair follicles came from hair follicle stem cells.
This was unexpected. If the hair follicles weren't coming from stem cells, where were they coming from?
The scientists used another set of special mice to answer this question. In these mice, the outermost layer of skin cells (the epidermis) turns blue after treatment with the chemical.
If the new hair came from this layer of skin, then the mice would be blue-haired. If the hairs came from somewhere else, then they'd still be white.
After wounding, about half of the hairs were blue. So epidermal not hair follicle stem cells probably formed the new hairs in the wounded area.
This was a big surprise. Why? Because most adult stem cells stick to producing a small group of cells.
Take hair follicle stem cells. They produce all the parts of the hair follicle. But not the epidermis.
So epidermal stem cells should only produce parts of the epidermis. Instead, these epidermal stem cells formed all the different parts of the hair follicle.
Neat, but how does this help my sister's head scar? How can she get her hair to grow back?
Ideally, we'd like to be able to help hairs to form in scar tissue. So the scientists looked at what helps or hurts hair follicle forming in the wounded mice.
If they can figure out what is turning on the process in big wounds in mice, they may be able to mimic it in people. With smaller wounds.
They started by looking at Wnt proteins because Wnt proteins help normal hair follicles develop. They looked to see what happens in mice where they could shut off Wnt. And what happens in mice with extra Wnt protein.
If Wnt is important, we'd expect the mice without it to have hairless wounds. And maybe for the mice that make extra Wnt to have even hairier wounds. That's just what the scientists found.
After wounding, mice without Wnt didn't form hair follicles. But mice with the extra Wnt made even more hair follicles. So Wnt was very important.
We might be able to help hair follicles form in wounded regions by treating the wound with Wnt proteins before the scar forms. But we have to be careful because too much Wnt protein can sometimes lead to cancer.
Now if only we could prevent scars from forming altogether. Scientists are working on that too.
Amy Radermacher
More Information
Different types of stem cells
New hair comes
from stem cells.
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