» I can’t see it getting tested by any amateurs at that price.
»
» For all we know it might easily take $100+ per day to get anywhere with it.
» That would be $3000 a month right there, and we would still have no idea
» if that was too much or not enough. And you might not learn anything
» worthwhile from staying on it any less than 3-6 months.
no need to get it tested. It’s most likely legit. And if it’s not, is $100 really that big of a deal? There is a very high chance that this would work why not give it a try?
» no need to get it tested. It’s most likely legit. And if it’s not, is $100
» really that big of a deal? There is a very high chance that this would work
» why not give it a try?
you are dangerously stupid.
If its such a clear cut case why are you sitting here convincing others when you could be smearing these potentially carcinogenic substances on your head yourself?
» » no need to get it tested. It’s most likely legit. And if it’s not,
» is $100
» » really that big of a deal? There is a very high chance that this would
» work
» » why not give it a try?
»
» you are dangerously stupid.
»
» If its such a clear cut case why are you sitting here convincing others
» when you could be smearing these potentially carcinogenic substances on
» your head yourself?
» TM30089 works in the same way as Ramatroban and OC000459 by blocking the
» CRTH2 (DP2) receptor. According to the study in may have longer lasting
» effects than Ramatroban and is more selective to target the right
» receptor.
»
» On the Mechanism of Interaction of Potent Surmountable and Insurmountable
» Antagonists with the Prostaglandin D2 Receptor CRTH2
» http://molpharm.aspetjournals.org/content/69/4/1441
»
» The other “bad” PGs are derivatives of PGD2, in other words they come from
» further degredation of PGD2. Cots refers to 15-dPGJ2 as one such derivative
» which completely halts hair growth. Google 15-dPGJ2 and you will find many
» papers which show 15-dPGJ2 leading to cell death.
Is OC000459 a surmountable or insurmountable blocker?
I thought we were trying to get a GPR44 receptor blocker but I see where some folks are talking about a CRTH2 blocker instead. Which is it? Cotseralis wrote in his paper that we need to block the GPR44 receptor but guys at this site are talking about CRTH2. I don’t get it. Why is it that the scientist told us to block GPR44 and we are instead going to block CRTH2? WTF?
» » PGD2 is not the only postaglandin that is taking our hair. Cotseralis
» says
» » that at least one other postaglandin also causes hair loss and that
» other
» » one is way more powerful at taking our hair than PGD2 is. That’s why we
» » need to block the applicable receptor rather than blocking just PGD2.
» If
» » we block the receptor instead then we block all of the postaglandins
» that
» » are taking our hair.
»
» I disagree with you on this, jarjar, because different prostaglandins will
» have DIFFERENT RECEPTORS.
»
» If they all had one generic receptor, every time ANY of the
» prostaglandins bound to it, it they would activate it and messages would be
» completely scrambled.
roger_that, we do not need to block ALL postaglandins. We only need to block the postaglandins that shrink hair. Some postaglandins cause hair to grow. We need to increase the postaglandins that cause hair to grow.
It’s my understanding that there is only ONE receptor that the postaglandins that cause hair to stop growing bind to and that receptor is GPR44.
Why is it that Cotseralis told us one thing and we are doing something totally different? Are posters here deluding themselves into believing that they are more skilled and aware about hair loss than Cotseralis, who is one of the leading hair loss researchers in the world?
It’s my understanding that Cotseralis told us we need to block the receptor that the hair-stealing postaglandins bind to and he told us that receptor is GPR44. He also told us that we need to add the postaglandins that cause hair to grow and there are things available that will allow us to do this - latanoprost, bimatoprost, and minoxidil. According to Cotseralis we only need to block one receptor - GPR44.
» TM30089 works in the same way as Ramatroban and OC000459 by blocking the
» CRTH2 (DP2) receptor. According to the study in may have longer lasting
» effects than Ramatroban and is more selective to target the right
» receptor.
»
» On the Mechanism of Interaction of Potent Surmountable and Insurmountable
» Antagonists with the Prostaglandin D2 Receptor CRTH2
» http://molpharm.aspetjournals.org/content/69/4/1441
»
» The other “bad” PGs are derivatives of PGD2, in other words they come from
» further degredation of PGD2. Cots refers to 15-dPGJ2 as one such derivative
» which completely halts hair growth. Google 15-dPGJ2 and you will find many
» papers which show 15-dPGJ2 leading to cell death.
It’s my understanding that we are supposed to block GPR44. I’m pretty sure that’s what Cotseralis said so why are we talking about CRTH2 instead?
So what if these other postaglandins bind to CRTH2? Cotseralis did not say we need to worry about the CRTH2 receptor. Cotseralis told us we need to focus on the GPR44 receptor. Why are you changing the target zone to the CRTH2 receptor when Cotseralis told us the target zone is the GPR44 receptor?
Keep in mind that Cotseralis tested all abnormalities in balding scalp tissue.
He determined that only PGD2 and its’ derivatives were in excess amounts in balding skin. These other postaglandins you are talking about were only in the balding scalp skin in normal amounts so wtf are you even talking about them for? Why are you trying to eliminate postaglandins that is not shown to be involved in hair loss? Also, why are you focusing on the CRTH2 receptor even though Cotseralis told us the problem is the GPR44 receptor?
Again, there is nothing out of the ordinary about the PHG1, PGH2, and PGD1 in balding scalp or else Cotseralis would have discovered that abnormality. He did not report an excess amount of these items in balding scalp over what is found inside of non-balding scalp so why are we getting side-tracked with these postaglandins that are not implicated in hair loss and again why are we talking about a receptor that is not the receptor that Cotseralis said to focus on?
There is no difference in the quantity or quality of PHG1, PGH2, and PGD1 found in balding scalp skin vs non-balding scalp skin which means there is NO EVIDENCE that PHG1, PGH2, and PGD1 are involved in hair loss.
» » Actually I stand to be corrected, i cant recall if the Cots study only
» » included testing PGD2 and its derivative. According to this study PGD2
» and
» » its derivatives may not be the only enemy.
» »
» » PGH1, the Precursor for the Anti-Inflammatory Prostaglandins of the 1-series, Is a Potent Activator of the Pro-Inflammatory Receptor CRTH2/DP2 - PMC
» » PGH1, PGH2 and PGD1 might also exhibit the same effect on the CRTH2
» » receptor as PGD2.
»
»
»
» This is likely why drug companies are focusing on CRTH2 inhibitors rather
» than PGD2 inhibitors. For example Oxagen and Actelion.
It’s my understanding that these two drug companies are focused on GPR44 blockers. If I’m not correctly informed please advise with an explanation. It’s my recollection that Cotseralis was talking about blocking the GPR44 receptor rather than CRTH2 blocker. Are you changing the target zone that Cotseralis said to focus on???
It seems to me that the mechanism that is of confusion for some users is that there is a gateway for the signal that is received via the GPR-44 to PGD2 chemical communication. The TM-30089 inhibits the PGD2 from communicating, presumably with the follicle, not mesaging to essentially go bald (shrink). This action is very likely a succesful action towards stopping the Androgenic Aplopecia expression, although the message is still being sent, and the receptor, namely the hair follicle, is still able to receive the message if the TM-30089 is not in the channel for the communication.
This raises the concern that this chemical alone would NOT likely work without some mechanism for specifically achieving a proper delivery. This begs for the possible use a nanoparticle (nano-lipid) delivery. I tend to agree that based on what I’ve seen posted by some, that there are no studies that have been used for a topical application, at least yet? It seems that this may be a self-limiting mechanism, but I still fear that there could be a catabolic expression that no one has experienced yet. It seems that at least a nano-particle animal study on the skin of lab animals is needed to determine if there is enough safety for testing it’s efficacy on human baldness? I wonder if anyone has really tried this out yet, and if they are using a nano-particle delivery mechanism? I would love to find out more, and if the patent holder is planning to move on at least that level, soon?
Any additional information would be appreciated, or an update?
[quote]It seems that this may be a self-limiting mechanism, but I still fear that there could be a catabolic expression that no one has experienced yet.
Any additional information would be appreciated, or an update?[/quote]
Hoopa’s comment makes no sense scientifically. It appears that he misunderstands the mechanism of action of TM-30089, although his comment isn’t expressed clearly, so I can’t even be sure if what he’s trying to say.
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