Right. Because academics fly 18+ hours to present their work on findings that have been published all over the media.
What is your point? The media is a side. Publications in peer reviewed journals are what matter to someone in his role. In actual fact, people are more likely to present their work after it has already been published (in a science journal, after which the unscientific media might pick it up) to reduce the likelihood of their more recent work being scooped by a competing group.
12-15-2014 08:16 PM
It's2014ComeOnAlready
Quote:
Originally Posted by walrus
What is your point? The media is a side. Publications in peer reviewed journals are what matter to someone in his role. In actual fact, people are more likely to present their work after it has already been published (in a science journal, after which the unscientific media might pick it up) to reduce the likelihood of their more recent work being scooped by a competing group.
Well, what is your point? The findings on PGD2 have been discussed, examined, and he's given interviews on it over the past two years. It's been all over the media. He also has patents on all the work. I'm asking the question - why is it important to him to fly all that way to give a presentation on work that has been shown a LOT? What is the incentive?
12-15-2014 08:47 PM
walrus
Quote:
Originally Posted by It's2014ComeOnAlready
Well, what is your point? The findings on PGD2 have been discussed, examined, and he's given interviews on it over the past two years. It's been all over the media. He also has patents on all the work. I'm asking the question - why is it important to him to fly all that way to give a presentation on work that has been shown a LOT? What is the incentive?
My points are quite clear, read them again. Scientists use conferences as a place to discuss their work, bounce ideas, and make contacts for future collaborations. Presentation of scientific work to peers can lead to valuable feedback. This is very different to for e.g. conducting a phone interview with a journalist who does not fully understand the technical language for a dumbed-down news piece. The role of PGD2 in hair loss in far from fully understood and there are likely many avenues left for future research.
12-18-2014 02:12 PM
It's2014ComeOnAlready
If Follica doesn't come out with a topical soon, they run the risk of other applications getting to the market, getting some popularity and brand loyalty. If CB-03-01 or SM-04554 or DA-4001 make it through their trials and to market before Follica has the chance to, then they are running a risk that they won't make as much money.
It's just mind-boggling to me that they haven't done anything with their PGD2 discovery except patent it. Ridiculous, and hard to believe.
12-18-2014 02:27 PM
It's2014ComeOnAlready
Sorry to go on about this, but if they were to release a PGD2 inhibitor, whilst a PGF2 analog (Bimatoprost) is on the market, they stand to make so much money. Cots has mentioned bim many times, and with these two on the market, they would be prescribed together (and boost the sales of each) because they would provide the type of reversal of hair loss in the mid to early stages that would work for most people.
Cots: "Sure, take CB with bim and reverse your hair loss. Forget about a pgd2 inhibiting topical, we were only half-interested in making billions. Let that money go to someone else. I'm not in it for the money, just the research."
Basically says that PGD2 inhibits the process of follicle neogenesis through the gpr44 receptor. Which means that in order to even get this process off the ground, one of the first things they need to do is block that receptor. This is easy to deduce since balding areas have 3x as much pgd2, and they are trying to allow new hairs to grow in balding areas. It would of course would need to be done topically, which means they already have a topical to inhibit pgd2.
My guess is that they are using a number of compounds in these trials, and also means that this compound is being trialled as well, instead of an additional trial to test it alone. It would make a lot sense, because it would save both time and money and they can get on with their wounding method, while testing a topical compound that blocks the gpr44 receptor.
The whole $2 million for a treatment, $20 million for follicular neogenesis thing also makes sense, because yes, they will need more time and money to give a bald man a full head of hair. The gpr44 blocker is part of the process, and could be released sooner as a treatment than regrowing all your hair.
I think this is great news for anyone looking for a new treatment.
12-22-2014 10:28 AM
inbrugge
Thank you for your messages, man. It's always good to have new information streaming in. So do you think the focus is on blocking gpr-44 receptors or pgd2 inhibition? Correct me if I'm wrong, it's kind of along the lines of RU/CB vs Fin, where RU/CB binds to the receptor where Fin limits DHT production.
Also, any hopes of obtaining GPR-44 receptor binding or PGD2 inhibition from off-the-shelf products while we wait for this thing to come through? I was reading that Vitamin C and E inhibit PGD2 and promote PGE2, but I don't know if those would be effective as topical serums?
12-22-2014 10:37 AM
It's2014ComeOnAlready
pgd2 binds to the gpr44 receptor, so a pgd2 inhibitor or gpr44 blocker is the same thing. As for off the shelf products, I have no idea. We'll just have to wait.
12-23-2014 11:47 AM
noisette
New publication on the Web with Cotsarelis G.
Here the abstract :
" Direct reprogramming provides a fundamentally new approach for the generation of patient-specific cells. Here, by screening a pool of candidate transcription factors, we identify that a combination of the three factors, MITF, SOX10 and PAX3, directly converts mouse and human fibroblasts to functional melanocytes. Induced melanocytes (iMels) activate melanocyte-specific networks, express components of pigment production and delivery system and produce melanosomes. Human iMels properly integrate into the dermal-epidermal junction and produce and deliver melanin pigment to surrounding keratinocytes in a 3D organotypic skin reconstruct. Human iMels generate pigmented epidermis and hair follicles in skin reconstitution assays in vivo. The generation of iMels has important implications for studies of melanocyte lineage commitment, pigmentation disorders and cell replacement therapies. "
Atopix site says it is a CRTH2 antagonist. Not a PGD2 inhibitor, the only thing it says about PGD2 is that PGD2 is the natural lignand of CRTH2. CRTH2 is the primary receptor for PGD2, HOWEVER, it is not the receptor Cotsarelis in his presentation says is in the follicle responding to the PGD2....he shows 3 receptors they tested and it was GPR44 which was responding and inhibiting hair growth. They made mice with each of the 3 types of receptors knocked out. So I do not think A) it is a true PGD2 inhibitor for all receptor types - it does not block the enzyme which makes PGD2 (right when we talk about a DHT inhibitor, like Fin they block the creation of DHT by 5AR), and b) although it is an antagonist of the CRTH2 receptor...this is the wrong receptor for the hair follicle impacts.
