Sm04554 Update To Follow! Encouraging. News Release

KO1

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Yes, the addition of things like Samumed and Seti are going to be a major help because SM is a far more potent WNT promoter than minoxidil or LiGlu and plus PGD2 is known to inhibit the creation of neogenic follicles. There is a lot of potential in this platform that can be tapped into with more topical treatments that come out. But it's going to take a while for the the process to mature for that same reason.

Whether this is compoundable is anybody's guess at this point.
 

KO1

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Cool, but that wasn't what you were claiming; you were claiming that the 25% data point was meaningless, as there was no published research to support it. I pointed out that Follica wouldn't claim it if there wasn't substantiating research, because to do so in a prospectus which is relied upon by potential investors would be securities fraud. Now you're not claiming there's no data to support it, only that 25% represents "a few sparse hairs." Stop moving the goal posts.

I stand by my statement that the 25% number is BS. There is no data that substantiates it. If you have that data, I'll be happy to change my opinion. Do you?
 
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Swoop

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^Upregulating bC in DP cells

No, our knowledge on minoxidil in relation to the hair growth activity is still limited even after extensive research. What about the studies that Dench posted? Even the study in question literally says:

"Minoxidil activates β-catenin pathway in human dermal papilla cells: a possible explanation for its anagen prolongation effect".
 

KO1

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Because it fits in with the body of literature we have about Wnt's role in prolonging anagen, inducing anagen, creating new follicles and maintaining DP inductivity. It also explains why other vasodilators don't result in hair growth and why the effect of AR activition is reduced. Stabilizing bC levels in DP cells leads to hair growth, whether it is exogenous application on mature HFs (Ohsang Kwon), or transgenic activation (M Ito). It's also the reason why this thread exists.
 

KO1

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^ I don't believe this would be a material misstatement nor do I believe it would be enough for the SEC to act. Also, thats dumb, why derail them?
 

Takeela370

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As with like most other threads this has turned to pages of back and forth bickering. Someone said they are releasing data November 30th-Dec 1st at a conference? Just 1 month guys. Wait it out and stop getting pissed at each other arguing, it doesn't solve anything.
 

Noisette

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As with like most other threads this has turned to pages of back and forth bickering. Someone said they are releasing data November 30th-Dec 1st at a conference? Just 1 month guys. Wait it out and stop getting pissed at each other arguing, it doesn't solve anything.

Yes this is me ;) I think Osman Kibar will present the results at this conference : Forbes Healthcare Summit.
Forbes.jpg
 

Stupidon

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357583Untitled.png


Funny thing, the presentation has been updated since a while.
https://www.samumed.com/medium/image/american-academy-of-dermatology-aad-washington-dc_19/view.aspx

They did not present the results @90 days but already @135 days. However if you look more in detail in the clinical trial description:

Scalp biopsies obtained prior to initiating therapy, after 90 days of therapy, and after an additional 45 days off therapy will be compared to determine the change in the number of terminal hair follicles over the treatment and off-treatment periods.

https://clinicaltrials.gov/ct2/show/record/NCT02503137?term=SM04554&rank=1


I am definitely more excited than 6 months ago.
 

Noisette

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Samumed wont be presenting results from biopsy trial until spring 2017 :/

http://finance.yahoo.com/news/samumed-selected-seven-presentations-five-130000000.html

I found this link too from Samumed website : https://www.samumed.com/medium/imag...t-american-college-of-rheumatolo_45/view.aspx

I don't understand why they want to present their phase 2 for the next summer. Very strange because this is not the "next medical conference". And why on the paper it's writing " The company expects to report results from an Androgenic Alopecia trial at a medical conference in spring 2017".
It's writing "an AA trial" and not the phase 2 :) so I think it could be an another trial like a phase 3.

However, I found an another interesting article published this October, 25th.
Source: http://magazine.pomona.edu/2016/fall/how-to-build-a-fountain-of-youth-piece-by-piece/

We can see this

They’re in diagnostics and they never shared their data, so their whole approach was: ‘Trust us, we got this,’” he says. “Being in the therapeutic field, we’re coming up with drugs; we don’t have that luxury. We cannot say, ‘Trust us, we got it.’ First and foremost, we have the FDA. The FDA is not going to take our word for it.”


The FDA is the gatekeeper, and though less than 10% of proposed new drugs ultimately earn FDA approval, the likelihood increases with each step forward in the lengthy process. The next step for Samumed’s most advanced projects, the hair loss and osteoarthritis drugs, is large Phase III studies with thousands of participants. Some 64% of drugs that begin Phase III studies are submitted for FDA approval and 90% of those are successful, according to a study cited by the independent site fdareview.org "
.

So, the next step is the phase 3 for their Hair loss product :) :) :) And maybe, they would present the phase 3 at the medical conference in spring 2017.

What do you think bro ?
 

InBeforeTheCure

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Because it fits in with the body of literature we have about Wnt's role in prolonging anagen, inducing anagen, creating new follicles and maintaining DP inductivity. It also explains why other vasodilators don't result in hair growth and why the effect of AR activition is reduced. Stabilizing bC levels in DP cells leads to hair growth, whether it is exogenous application on mature HFs (Ohsang Kwon), or transgenic activation (M Ito). It's also the reason why this thread exists.

On that note, this is one of the studies Dench posted...

Minoxidil activates β-catenin pathway in human dermal papilla cells: a possible explanation for its anagen prolongation effect.

RESULTS:
Modest extension of anagen phase thereby delay of catagen progression was observed by application of minoxidil in mice. Minoxidil stimulated the transcriptional activity of pTopflash but not pFopflash. Nuclear accumulation of β-catenin was also observed after minoxidil treatment. Immunoblot further showed that minoxidil treatment increases the phosphorylation of GSK3β, PKA and PKB. Moreover, minoxidil induced Axin2, Lef-1, and EP2 expression.

They mention another study they had previously done...

kwack1.png


In that previous study, they found that:

- Wnt3a upregulated EP2
- PGE2 activated cAMP and its target PKA
- Neither Wnt3a or PGE2 alone increased cAMP. Therefore, it seems Wnt-induced EP2 expression and PGE2 act synergistically to increase cAMP/PKA activity.

shin1.png


So minoxidil's effects are probably not just from beta-catenin stabilization alone, but that along with other pathways might work together to induce certain effects.
 
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Beowulf

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On that note, this is one of the studies Dench posted...

Minoxidil activates β-catenin pathway in human dermal papilla cells: a possible explanation for its anagen prolongation effect.



They mention another study they had previously done...

kwack1.png


In that previous study, they found that:

- Wnt3a upregulated EP2
- PGE2 activated cAMP and its target PKA
- Neither Wnt3a or PGE2 alone increased cAMP. Therefore, it seems Wnt-induced EP2 expression and PGE2 act synergistically to increase cAMP/PKA activity.

shin1.png


So minoxidil's effects are probably not just from beta-catenin stabilization alone, but that along with other pathways might work together to induce certain effects.

So then Samumed's new treatment will be very similar to minoxidil. But then again can't SM04554 create new hair follices, while minoxodil can only increase the anagen stage of preexisting hair? Samumed must be keeping secrets as all private companies seem to do.

I just hope that Samumed's hair density base cases included preexisting vellus hairs.
 

hairblues

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@Noisette American Academy of Dermatology has a conference in March 2017..You think its this?
 

KO1

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So minoxidil's effects are probably not just from beta-catenin stabilization alone, but that along with other pathways might work together to induce certain effects.

Yes and no. While you're right that the PGE2 and Wnt pathways likely act in concert, they're also linked. bC stabilization is one link in a major cascade involving other pathways including the PGE2, Wnt, VEGF, FGF, and AR cascades. For example. The PGE2/Wnt interaction is also what allows minoxidil to blunt the effect of ARs.

I pointed out bC stabilization as it is consistently marked as a driver for hair growth making it a treatment candidate. Are there other things going on that we don't understand? Of course. Does that mean minoxidil is a mysterious drug? Maybe 10 years ago when we didn't have this information and knew minoxidil only as a vasodilator. What we do not understand are all the signals that promote hair growth, that's what's mysterious.
 
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Noisette

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@Noisette American Academy of Dermatology has a conference in March 2017..You think its this?

Not sure because "The company expects to report results at a medical conference in spring 2017 ". I think a medical conference will take place between June and September 2017 :)
 

Tomtom21

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My intuition tells me that they will present the biopsy results at the 2017 AAD conference like last year when they presented the first phase 2 there.

https://www.aad.org/meetings/annual-meeting/for-abstracts

Hopefully they start a phase III in the meantime. My best guess for sm04554 if it pans out to be anything will be released late 2018-2019. Real question is though... what is taking histogen so long... id love it if someone reached out and found out something regarding a project update in china mexico or even US. sh*t.
 
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