OC and setipip news

[Swooping]

LOL..and you're basing this information off of what?

Why don't you go tell cots and kythera that their product and theory is bs..im sure they will want to know your scientific opinion based off years of your own research and expertise.

Someone asked me for my opinion so I did give my opinion. Furthermore you can see that I say myself that my opinion is based on speculation.

You asked my why I form this opinion about the PGD2 angle. I'll tell you. I follow the masses generally. Currently Cotsarelis & Garza are sitting on an island. The discovery of PGD2 is almost 5 years old. In the meantime several researchers attain the fact of other important factors in androgenetic alopecia. Nobody followed up Cotsarelis & Garza his work or even showed a interest.

They are showing that other factors in androgenetic alopecia are involved which we didn't touch upon yet even in modern medicine. That the problem evolves around the cells adopting a other cell fate. Furthermore COX-2 is mediated by MAPK/JNK, Nf-Kb and 20 other transcriptional regulators so it may very well lay downstream and not be an important factor after all. If I have to chose between the consensus of multiple researchers/teams or only Dr. Cotsarelis. I'm going to go with the former, sorry. I can link all those studies for you and discuss them with you if you like.

That aside Garza works closely together with Cotsarelis and concurs with the idea that the PGD2 angle is 50/50 and may be an unimportant factor after all. So they both know damn well that they also have a hypothesis and nothing more at the moment. That's why they probably picked up this compound after all. They still believe in it, but that doesn't mean that they are right.

Also as I said multiple CRTH2 compounds are in clinical trials and medicines have been used and still are which evolve around manipulation of prostaglandins. This strengthens my opinion that the PGD2 has a very low probability of working as good as finasteride.

I'm sorry furthermore if I hurt your feelings with my opinion. Perhaps the thought of it not going to succeed is really hard for you to imagine? Reality is a bitch sometimes I guess.

Do you know how much funding goes into cancer and atherosclerosis on a side note? There are 100's of hypotheses released each year for those diseases. 100's of academics, extremely talented researchers are on the quest of curing these diseases. Literally with 100x the magnitude and effort of androgenetic alopecia. Pharmaceutical companies are throwing billions around in these sectors like it's nothing. Do you know how many of these hypotheses and compounds fail? I guess you don't. Welcome to the real world.

[It's2014ComeOnAlready]

Someone asked me for my opinion so I did give my opinion. Furthermore you can see that I say myself that my opinion is based on speculation.

You asked my why I form this opinion about the PGD2 angle. I'll tell you. I follow the masses generally. Currently Cotsarelis & Garza are sitting on an island. The discovery of PGD2 is almost 5 years old. In the meantime several researchers attain the fact of other important factors in androgenetic alopecia. Nobody followed up Cotsarelis & Garza his work or even showed a interest.

They are showing that other factors in androgenetic alopecia are involved which we didn't touch upon yet even in modern medicine. That the problem evolves around the cells adopting a other cell fate. Furthermore COX-2 is mediated by MAPK/JNK, Nf-Kb and 20 other transcriptional regulators so it may very well lay downstream and not be an important factor after all. If I have to chose between the consensus of multiple researchers/teams or only Dr. Cotsarelis. I'm going to go with the former, sorry. I can link all those studies for you and discuss them with you if you like.

That aside Garza works closely together with Cotsarelis and concurs with the idea that the PGD2 angle is 50/50 and may be an unimportant factor after all. So they both know damn well that they also have a hypothesis and nothing more at the moment. That's why they probably picked up this compound after all. They still believe in it, but that doesn't mean that they are right.

Also as I said multiple CRTH2 compounds are in clinical trials and medicines have been used and still are which evolve around manipulation of prostaglandins. This strengthens my opinion that the PGD2 has a very low probability of working as good as finasteride.

I'm sorry furthermore if I hurt your feelings with my opinion. Perhaps the thought of it not going to succeed is really hard for you to imagine? Reality is a bitch sometimes I guess.

Do you know how much funding goes into cancer and atherosclerosis on a side note? There are 100's of hypotheses released each year for those diseases. 100's of academics, extremely talented researchers are on the quest of curing these diseases. Literally with 100x the magnitude and effort of androgenetic alopecia. Pharmaceutical companies are throwing billions around in these sectors like it's nothing. Do you know how many of these hypotheses and compounds fail? I guess you don't. Welcome to the real world.

Armchair scientist ^

[Swooping]

Armchair scientist ^

You call Philpott, Bahta, Y. Yang, Christiano, Upton, among others armchair scientists? LOL. I rest my case. Anyway we'll see. Just know that every second counts in AGA. Luckily I'm not the one who is hoping .

[It's2014ComeOnAlready]

You call Philpott, Bahta, Y. Yang, Christiano, Upton, among others armchair scientists? LOL. I rest my case. Anyway we'll see. Just know that every second counts in AGA. Luckily I'm not the one who is hoping .

No, no, no. I'm calling YOU an armchair scientist. You have no affiliation or in-depth knowledge of their work, and also proclaim to know more than Cotsarelis, the world's foremost authority on hair biology. Quite arrogant to do so.

[Swooping]

First of all I never claimed to know more than him. Stop calling him an authority because he isn't an authority and will never be. Other researchers/people who work in the field are just equally important as him. I just happen to base my opinion rather on the consensus, what's wrong with that can you tell me? If 15+ researchers say Y and 2 researchers says X, I happen to go for option Y. Especially if it's more logical to me. Cause that is what happens lately in AGA research.

Furthermore I refer you to Garza his work who is implicated with Cotsarelis in the PGD2 findings; http://www.ncbi.nlm.nih.gov/pubmed/24521203. He HIMSELF concurs with the fact that PGD2 may be very well be an irrelevant small player in AGA. He concurs with the fact that perhaps it won't work at all.

So the hypothese still stands, it can only be validated by in vivo validation through double placebo controlled trials. That's how science works, whether you like it or not. There is 0% proof for it yet.

I just happen to have an opinion that it most likely isn't going to work good at all and furthermore concur with other researchers. I have all rights too form an opinion as do you. Sorry if that hurts you again. I'm straightforward and honest to my own opinion, hate it or love it babe <3.

[Swooping]

Here you go straight from Garza his mouth. He works alongside Cotsarelis;

[FearTheLoss]

I agree there is reason to be skeptical, swooping, but with anecdotal results people have had using pgd2 inhibitors, and myself experiencing results with cetrizine..I think we will see that pgd2 inhibitors could be as effective or more effective then AA's.

We will have a definite answer to this by the end of 2016. Ken Washinek also supports the theory and believes its part of the future of treatments. It's not just cots.

[Swooping]

I agree there is reason to be skeptical, swooping, but with anecdotal results people have had using pgd2 inhibitors, and myself experiencing results with cetrizine..I think we will see that pgd2 inhibitors could be as effective or more effective then AA's.

We will have a definite answer to this by the end of 2016. Ken Washinek also supports the theory and believes its part of the future of treatments. It's not just cots.

__________________________________________________ __________________________________________________ __________________________________________________ ________________

Nov. 4, 2004 -- Balding men and women take note. Hair cloning -- the next hair restoration remedy -- is on the way.

OK, it's not exactly cloning, although that's what it's come to be called. Researchers working to perfect the new technique prefer the term "hair multiplication."

And no, it's not ready for prime time. Not yet, says Ken Washenik, MD, PhD. Washenik is medical director for Bosley, the giant hair restoration company that's one of several firms racing to bring hair multiplication to market. He's also clinical assistant professor of dermatology at New York University Medical Center.

"There is no doubt it will be a tremendous breakthrough," Washenik tells WebMD. "It is the thing people have been waiting for. There have been so many remedies for hair loss that didn't pan out. This is one that really looks like it is going to happen -- and happen in the next few years." It's not just hype, says hair researcher George Cotsarelis, professor of dermatology and director of the hair and scalp clinic, at the University of Pennsylvania School of Medicine in Philadelphia. Cotsarelis consults for Bosley, but is not involved in the company's research program.

"It is hard to predict whether they will be successful, but there is good evidence that will happen," Cotsarelis tells WebMD. "It is not quackery -- they are not charlatans. It is based on real scientific knowledge. But there are a lot of hurdles still to overcome."

The promise of early research often evaporates in the harsh light of clinical testing. Yet Washenik predicts that hair multiplication will be available for hair restoration in three or four years.

That was in 2004, FearTheloss, 11 years ago. Just a small reality check.

On a positive note I do think that we are finally heading in the right direction and research goes faster than ever. I just think there is too much evidence to think that PGD2 is a minor contribution of AGA and definitely not a big one. I just concur with the consensus of other researchers in the AGA pathology recently. That's all. But we'll see mate, indeed 2016 will bring us the answers!

[KO1]

Swooping is right, even Cots and Garza have been clear that they don't know if it will work. Even in the original PGD2 study they didn't do the all important step of applying a PGD2 inhibitor on one of those bald mice, which I found odd.

My expectation is that it will probably work, not as well as fin, but without the sides, but no real regrowth. Hopefully I'm wrong.

[It's2014ComeOnAlready]

First of all I never claimed to know more than him. Stop calling him an authority because he isn't an authority and will never be. Other researchers/people who work in the field are just equally important as him. I just happen to base my opinion rather on the consensus, what's wrong with that can you tell me? If 15+ researchers say Y and 2 researchers says X, I happen to go for option Y. Especially if it's more logical to me. Cause that is what happens lately in AGA research.

Furthermore I refer you to Garza his work who is implicated with Cotsarelis in the PGD2 findings; http://www.ncbi.nlm.nih.gov/pubmed/24521203. He HIMSELF concurs with the fact that PGD2 may be very well be an irrelevant small player in AGA. He concurs with the fact that perhaps it won't work at all.

So the hypothese still stands, it can only be validated by in vivo validation through double placebo controlled trials. That's how science works, whether you like it or not. There is 0% proof for it yet.

I just happen to have an opinion that it most likely isn't going to work good at all and furthermore concur with other researchers. I have all rights too form an opinion as do you. Sorry if that hurts you again. I'm straightforward and honest to my own opinion, hate it or love it babe <3.

You are entitled to your own opinion, but your arguments are mostly negative speculation based on old information.

Prostaglandin technology is a new school of thought when it comes to battling male pattern baldness. A PGD2 inhibitor (setipiprant) and a prostaglandin analogue (bimatoprost) have always been linked. One claims it can halt hair loss, the other claims it can make existing hair thicker, and with more pigmentation. When the phase 2b study for bimatoprost in AGA was completed, Allergan was acquired by Actavis for a record-breaking sum in the pharma industry, with the stock going through the roof (and continues to climb). If the drug had failed in the trial, then it would've been stopped, and we'd hear nothing more about prostaglandins and hair.

Quite the opposite has happened. Not only did we see the acquisition, the stock grew exponentially, but we also saw that Kythera wants to trial a drug that blocks the GPR44 receptor. This is now the ONLY drug in their trials, and after two years of working with Cotsarelis at his lab, they are trialling it. They wouldn't put their eggs in one basket, or take the risk of trialling a drug for hair loss (after there have been so many misses by others) unless they had some assurance that this works.

It works, the science is real, and the pharma industry's actions prove that they firmly believe this will work. Kythera is not the sort of company who can afford a failure or a gamble on a drug their not certain will stop hair loss. Like I said before, it's the ONLY drug in their pipeline, it is their future. They have decided on it. Sorry you don't agree with PGD2 causing hair loss or whatever, but Cotsarelis is the head of Dermatology at UPenn and has done years of research on this. A company has decided to take up his work, and spend MILLIONS of dollars to try and produce it. They would need to be damn sure it works, if they were going to take that risk.

You just need to look for the right signals or bits of information. I think you are missing them.

[KO1]

PGD2 is definitely a good and interesting angle as it directly causes miniaturization and sebaceous gland hyperplasia. However, if it is downstream of the AR....I'm afraid it may just be a maintenance med. However for those who can't take fin, or don't want to take fin, it may be a big asset.


I think PGD2 will be useful in building a mouse model of AGA though.

[Swooping]

@It's2014ComeOnAlready, We just happen to look at things differently. That's cool, it's healthy after all.

Thing is I care for evidence. That's how science works. Not by some company claiming anything or a researcher claiming anything. I also don't get convinced by in vitro models or rat models. Prove is what I want through validation by a proper in vivo trial/experiment. That's how science works. By your philosophy we would have cured cancer and be living for 500 years now. Hell, AGA would have been cured 15 years ago.

On a side note, bimatoprost also got outperformed by minoxidil in the clinical trial of allergan 13% vs 22%. Almost double as good results by minoxidil. That is actual evidence. . Anyway I'll get back to you in a while when we know more . Maybe you are right!

[It's2014ComeOnAlready]

@It's2014ComeOnAlready, We just happen to look at things differently. That's cool, it's healthy after all.

Thing is I care for evidence. That's how science works. Not by some company claiming anything or a researcher claiming anything. I also don't get convinced by in vitro models or rat models. Prove is what I want through validation by a proper in vivo trial/experiment. That's how science works. By your philosophy we would have cured cancer and be living for 500 years now. Hell, AGA would have been cured 15 years ago.

On a side note, bimatoprost also got outperformed by minoxidil in the clinical trial of allergan 13% vs 22%. Almost double as good results by minoxidil. That is actual evidence. . Anyway I'll get back to you in a while when we know more . Maybe you are right!

That is evidence, but it is OLD evidence based on an earlier trial. The trial that followed was 10X the concentration. We don't know yet what those results are, but if all the big pharma activity is any indication, it outperforms minoxidil.

[Swooping]

That is evidence, but it is OLD evidence based on an earlier trial. The trial that followed was 10X the concentration. We don't know yet what those results are, but if all the big pharma activity is any indication, it outperforms minoxidil.

Still wishful thinking, I bet you would say the same thing a year ago when these results weren't known and we would have this discussion. Can you link me to a valid source where it states that they are using 10x the concentration? Anyway by all means I do actually hope you are right.

[It's2014ComeOnAlready]

Not wishful thinking. Here's the article: http://www.bloomberg.com/news/articl...ill-be-delayed

Now, what was the effect of this trial? Shares fell. After the most recent trial - 66 billion dollar acquisition, stock prices soar, kythera announces they will begin trials with setipiprant. You seem to behind in the news, they ran a 2a trial which didn't show much, then they ran 2b trial at 10X the concentration. That trial ended in November, when Allergan was acquired by Actavis.

Cause and effect.

By the way, the results of the phase 2a were known a few months after the trial was completed. You're just biased about all of this. I don't need to prove anything to you, because I've done my homework. I suggest you do yours.