Right now there are two “base” PG treatments available. When I use the term “base” treatment I’m refering to the part of the PG treatment where we inhibit PGD2. I call this the “base” treatment because I think that we all agree that this is probably the most important part of a PG therapy. Look how all the people using OC or cox-inhibitors are reporting that they stopped hair loss. This is a major historical accomplishment if the same thing were to happen in larger populations. At any rate, in my view the PGD2 inhibition part of PG therapy is the “base” treatment and the part of the treatment where we increase PGE2 and/or PGF2a is the secondary part of the treatment.
I can’t make up my mind which base treatment is best: OC000459 or the Cox inhibitor that alecbaldone is using. I see advantages and disadvantages to both. I need help figuring out which way to go.
Either way is probably going to arrest hair loss, but with cox-inhibitors you have to add at least PGE2 and perhaps PGF2a and maybe other things as well. Although I am not sure about that. We might just have to add PGE2. A PGE2 solution is coming to market soon. On the other hand, if we use OC000459 we only need to add PGE2 but the OC000459 is a solubility nightmare plus we would have to count on Kain. I honestly don’t know which is the smarter play but right now I’m leaning towards trying to use the cox-inhibitor with PGE2 and perhaps PGF2a. That way I don’t have to worry about the solubility mess.
The guys over at HLHF have been mixing there OC now with good results, seems there OC-salt dissolves pretty well from what there all saying.
both approches seem pretty good, keep us updated on which you take. im still reading up on all this so im not sure which direction i will take but the fact almost all the people on OC are saying there hairloss has either halted or slowed dramatically has got me interested.
Also with the Kane issue, i had the same worry but i have not heard one issue with his OC and as stated above his OC was tested independently and came back great.
» I don’t think Kane is a huge concern. The OC was tested independently.
what about the solubility fiasco?
Almost everyone using OC is reporting solubility problems. They are also saying that they are still getting enough OC into the follicles to stop hair loss but this solubility issue may prevent enough OC from getting into the follicles to achieve the next step of making hair grow.
» Right now there are two “base” PG treatments available. When I use the term
» “base” treatment I’m refering to the part of the PG treatment where we
» inhibit PGD2. I call this the “base” treatment because I think that we all
» agree that this is probably the most important part of a PG therapy. Look
» how all the people using OC or cox-inhibitors are reporting that they
» stopped hair loss. This is a major historical accomplishment if the same
» thing were to happen in larger populations. At any rate, in my view the
» PGD2 inhibition part of PG therapy is the “base” treatment and the part of
» the treatment where we increase PGE2 and/or PGF2a is the secondary part of
» the treatment.
»
» I can’t make up my mind which base treatment is best: OC000459 or the Cox
» inhibitor that alecbaldone is using. I see advantages and disadvantages to
» both. I need help figuring out which way to go.
»
» Either way is probably going to arrest hair loss, but with cox-inhibitors
» you have to add at least PGE2 and perhaps PGF2a and maybe other things as
» well. Although I am not sure about that. We might just have to add PGE2. A
» PGE2 solution is coming to market soon. On the other hand, if we use
» OC000459 we only need to add PGE2 but the OC000459 is a solubility
» nightmare plus we would have to count on Kain. I honestly don’t know which
» is the smarter play but right now I’m leaning towards trying to use the
» cox-inhibitor with PGE2 and perhaps PGF2a. That way I don’t have to worry
» about the solubility mess.
»
» What does everyone else think?
OC plus PGE2. I posted a study on the other thread which claims that PGE2 inhibited the production of PGD2 maybe that study is wrong, but so far thats the only thing i can find with regards to pumping pge2 into a pgd2 rich environment.
They do however mention that PGe2 has a very very short half life.
“PGE2 has been shown to affect airway physiology, inhibit-
ing both the early and late asthmatic response, without result-
ing in significant bronchodilation (6). The early asthmatic re-
sponse begins almost immediately after exposure to allergen,
reaches its peak at 15 to 20 min, and is followed by resolution
over the next 1 to 2 h. This process, involving the actions of
histamine, PGD2, and cysteinyl leukotrienes (LTC4, LTD4,
LTE4) is thought to be largely mast cell dependent (25). Be-
cause PGD2 is thought to be derived principally from the mast
cell, our finding of a decrease in PGD2 and its metabolite
PGF2b, supports the idea that PGE2 is acting by inhibiting
mast cell activation”
“There are obvious problems with such a study model. PGE2
has a very short half-life, and the time between delivery and
endobronchial allergen challenge likely decreases the efficacy
of the drug. In our study, there was a nearly 40% decrease in
PGE2 concentrations during the 4 min between baseline la-
vage and post-allergen lavage in those receiving PGE2…”
» Right now there are two “base” PG treatments available. When I use the term
» “base” treatment I’m refering to the part of the PG treatment where we
» inhibit PGD2. I call this the “base” treatment because I think that we all
» agree that this is probably the most important part of a PG therapy. Look
» how all the people using OC or cox-inhibitors are reporting that they
» stopped hair loss. This is a major historical accomplishment if the same
» thing were to happen in larger populations. At any rate, in my view the
» PGD2 inhibition part of PG therapy is the “base” treatment and the part of
» the treatment where we increase PGE2 and/or PGF2a is the secondary part of
» the treatment.
»
» I can’t make up my mind which base treatment is best: OC000459 or the Cox
» inhibitor that alecbaldone is using. I see advantages and disadvantages to
» both. I need help figuring out which way to go.
»
» Either way is probably going to arrest hair loss, but with cox-inhibitors
» you have to add at least PGE2 and perhaps PGF2a and maybe other things as
» well. Although I am not sure about that. We might just have to add PGE2. A
» PGE2 solution is coming to market soon. On the other hand, if we use
» OC000459 we only need to add PGE2 but the OC000459 is a solubility
» nightmare plus we would have to count on Kain. I honestly don’t know which
» is the smarter play but right now I’m leaning towards trying to use the
» cox-inhibitor with PGE2 and perhaps PGF2a. That way I don’t have to worry
» about the solubility mess.
»
» What does everyone else think?
PGE2 solution from where? How will they tackle the short half life?
»
» PGE2 solution from where? How will they tackle the short half life?
Right now you have one study indicating PGE2 has a short half life.
It’s evidence but it’s not a ton of evidence. If it turns out that PGE2 always has this terribly short half life then that could render a pure PGE2 solution useless. More likely there are ways to increase the half life of PGE2 and if that is the case then we need to learn what those ways are and relay that info to IDragon.
And how is it possible that PGE2 could ALWAYS have such a short half life when PGE2 is used for other medical indications that would require a long-lasting treatment such as the topical PGE2 applied in cases of open wounds, taken orally to reduce the side effects of chemotherapy, and taken orally to induce labor? What do you think the doctors are doing: applying PGE2 to open wounds every 5 minutes LOL??? And what about making pregnant women taking oral PGE2 every 5 minutes LOL!!! And what about topical PGE2 being used for the treatment of vitiligo - which is a dermatological skin condition???
» »
» » PGE2 solution from where? How will they tackle the short half life?
»
»
» Right now you have one study indicating PGE2 has a short half life.
» It’s evidence but it’s not a ton of evidence. If it turns out that PGE2
» always has this terribly short half life then that could render a pure PGE2
» solution useless. More likely there are ways to increase the half life of
» PGE2 and if that is the case then we need to learn what those ways are and
» relay that info to IDragon.
»
» And how is it possible that PGE2 could ALWAYS have such a short half life
» when PGE2 is used for other medical indications that would require a
» long-lasting treatment such as the topical PGE2 applied in cases of open
» wounds, taken orally to reduce the side effects of chemotherapy, and taken
» orally to induce labor? What do you think the doctors are doing: applying
» PGE2 to open wounds every 5 minutes LOL??? And what about making pregnant
» women taking oral PGE2 every 5 minutes LOL!!! And what about topical
» PGE2 being used for the treatment of vitiligo - which is a dermatological
» skin condition???
»
» Topical prostaglandin analog (PGE2) in vitiligo--a preliminary study - PubMed
Nice! Surely the Idragon alchemists are more knowledgable about these matters? IF the study I posted is right, pge2 might inhibit pgd2 at the right doses. Their conclusion however was a logical one. Though pgd2 decreased, the study didn’t show the mode of action in which pge2 prevented mast cells producing pgd2.
I wonder if dr cots is looking into this as we type? It seems the next logical step in the study. Im far from being a scientist, but given his pgd2 study, i would think it would now be alot easier to investigate the effect of pge2 on pgd2. Keep us posted on the idragon solution news please…
Im sat here with a cup of PG tea. My whole life seems to be PG at the moment
» »
» » PGE2 solution from where? How will they tackle the short half life?
»
»
» Right now you have one study indicating PGE2 has a short half life.
» It’s evidence but it’s not a ton of evidence. If it turns out that PGE2
» always has this terribly short half life then that could render a pure PGE2
» solution useless. More likely there are ways to increase the half life of
» PGE2 and if that is the case then we need to learn what those ways are and
» relay that info to IDragon.
»
» And how is it possible that PGE2 could ALWAYS have such a short half life
» when PGE2 is used for other medical indications that would require a
» long-lasting treatment such as the topical PGE2 applied in cases of open
» wounds, taken orally to reduce the side effects of chemotherapy, and taken
» orally to induce labor? What do you think the doctors are doing: applying
» PGE2 to open wounds every 5 minutes LOL??? And what about making pregnant
» women taking oral PGE2 every 5 minutes LOL!!! And what about topical
» PGE2 being used for the treatment of vitiligo - which is a dermatological
» skin condition???
»
I think its generally accepted that Prostaglandins have a very short half life, no evidence needed for that. It obviously comes down to the vechicle, and method of administration.
Also the PGE2 topical mentioned in that study is of course an analog. Again im no scientist but maybe the analog (being synthetic) have a longer half life. I’ll shut up now.
» » I don’t think Kane is a huge concern. The OC was tested independently.
»
» where? gangsterboy pasted some nmr pdf but i cant find it anymore.
»
» i didnt even check the peaks correlate with pgd2
What about the solubility issue? You can’t even be sure enough of the active ingredient is getting into the skin to do the job with the solubility being so piss poor
» » »
» » » PGE2 solution from where? How will they tackle the short half life?
» »
» »
» » Right now you have one study indicating PGE2 has a short half life.
» » It’s evidence but it’s not a ton of evidence. If it turns out that PGE2
» » always has this terribly short half life then that could render a pure
» PGE2
» » solution useless. More likely there are ways to increase the half life
» of
» » PGE2 and if that is the case then we need to learn what those ways are
» and
» » relay that info to IDragon.
» »
» » And how is it possible that PGE2 could ALWAYS have such a short half
» life
» » when PGE2 is used for other medical indications that would require a
» » long-lasting treatment such as the topical PGE2 applied in cases of open
» » wounds, taken orally to reduce the side effects of chemotherapy, and
» taken
» » orally to induce labor? What do you think the doctors are doing:
» applying
» » PGE2 to open wounds every 5 minutes LOL??? And what about making
» pregnant
» » women taking oral PGE2 every 5 minutes LOL!!! And what about topical
» » PGE2 being used for the treatment of vitiligo - which is a
» dermatological
» » skin condition???
» »
»
» I think its generally accepted that Prostaglandins have a very short half
» life, no evidence needed for that. It obviously comes down to the vechicle,
» and method of administration.
»
» Also the PGE2 topical mentioned in that study is of course an analog. Again
» im no scientist but maybe the analog (being synthetic) have a longer half
» life. I’ll shut up now.
»
» Keep us updated!
“Speculating that activation of prostaglandin-H synthase (PGHS)-1 might be the mechanism by which minoxidil stimulates hair growth in vivo, Michelet et al. demonstrated that minoxidil is indeed a potent activator of purified PGHS-1, by assaying oxygen consumption and prostaglandin (PG)E2 production.[21] This activation was also evidenced by increased PGE2 production by BALB/c 3T3 fibroblasts and by human dermal papilla fibroblasts in culture. These findings suggest that the mechanism behind the hair-growth-stimulating effect of minoxidil is stimulation of PGE2 synthesis. If this conclusion were the case, it would stand to reason that other, more specific, PG activators (PG analogs) might show even better results”
» Nice! Surely the Idragon alchemists are more knowledgable about these
» matters? IF the study I posted is right, pge2 might inhibit pgd2 at the
» right doses. Their conclusion however was a logical one. Though pgd2
» decreased, the study didn’t show the mode of action in which pge2 prevented
» mast cells producing pgd2.
this sounds useless if you ask me… I would imagine that IF PGE2 has an inhibiting effect on PGD2 then the effect would be very marginal…
» » Nice! Surely the Idragon alchemists are more knowledgable about these
» » matters? IF the study I posted is right, pge2 might inhibit pgd2 at the
» » right doses. Their conclusion however was a logical one. Though pgd2
» » decreased, the study didn’t show the mode of action in which pge2
» prevented
» » mast cells producing pgd2.
»
» this sounds useless if you ask me… I would imagine that IF PGE2 has
» an inhibiting effect on PGD2 then the effect would be very marginal…
I do not accept that PGE2 stimulates hair growth ONLY by decreasing PGD2.
I think that PGE2 causes a substantial increase in hair growth:
a) minoxidil grows a little hair
b) latanoprost = hair by about 20%
c) Based on eyelash results I would say that bimatoprost is more powerful at growing hair than either minoxidil or latanoprost.
e) macaque studies establish substantially more hair growth when minoxidil is applied with RU58841 than RU58841 alone.
Nobody is going to convince me that adding PGE2 won’t be more beneficial than a PGD2 blocker alone.
» Nobody is going to convince me that adding PGE2 won’t be more beneficial
» than a PGD2 blocker alone.
I agree that adding PGE2 seems promising but our options are severely limited. Minoxidil may be the best option. Wounding (e.g., dermaroller) could be very interesting as well once you’ve added a PGD2 blocker…
Inhibition of wound-induced hair neogenesis by prostaglandin D2
Prostaglandins (PGs) are key inflammatory mediators involved in wound healing. Recent evidence also illustrated a role for PGs in skin homeostasis with a specific role in regulating hair growth; however, no study to date has examined their role in skin regeneration after injury. Using the wound-induced hair follicle neogenesis (WIHN) assay, we hypothesized that PGs would impact hair follicle neogenesis, a marker for skin regeneration. We found that in C57Bl/6J mice, the levels of prostaglandin synthases and their products (PGD2, PGE2, PGF2a) were reciprocally expressed during wound healing. PGE2 and PGF2a levels increased during the early phases of wound healing while PGD2 increased during the later stages of wound healing (n>3; p<0.05). The level of hair follicle neogenesis after wounding varied significantly among C57Bl/6J, FVB/N and mixed background strains of mice (n>33; p<0.01). Levels of lipocalin-type prostaglandin D2 synthase (Ptgds) mRNA (n>4; p<0.01) and its product PGD2 (n=6; p<0.05) inversely correlated with regeneration ability. C57Bl/6 mice had the highest level of Ptgds mRNA expression, PGD2 levels and the least follicle neogenesis. Additionally, an alternatively spliced transcript variant of Ptgds missing exon 3 correlated with the regeneration phenotype among strains of mice (n=9; p<0.05). Exogenous application of PGD2 decreased WIHN in wild type mice (n=8; p=0.06). Of the two canonical PGD2 receptor null mice, only Gpr44 showed increased WIHN compared to strain-matched control mice (n=31; p<0.05). In all, these findings demonstrate that PGD2 inversely correlates with hair follicle regeneration implying that inhibition of PGD2 production or Gpr44 signaling pathways may promote skin regeneration.
Here is a good paper with all the PGE2 analogues (although they only tested activation of the EP1 receptor). Maybe we can find something stable & reasonably-priced.
» » Nobody is going to convince me that adding PGE2 won’t be more beneficial
» » than a PGD2 blocker alone.
I agree that adding PGE2 seems promising but our options are severely limited. Minoxidil may be the best option. Wounding (e.g., dermaroller)could be very interesting as well once you’ve added a PGD2 blocker. Sucralfate may further increase PGE2 upon wounding.
Inhibition of wound-induced hair neogenesis by prostaglandin D2
Prostaglandins (PGs) are key inflammatory mediators involved in wound
healing. Recent evidence also illustrated a role for PGs in skin
homeostasis with a specific role in regulating hair growth; however, no
study to date has examined their role in skin regeneration after injury.
Using the wound-induced hair follicle neogenesis (WIHN) assay, we
hypothesized that PGs would impact hair follicle neogenesis, a marker for
skin regeneration. We found that in C57Bl/6J mice, the levels of
prostaglandin synthases and their products (PGD2, PGE2, PGF2a) were
reciprocally expressed during wound healing. PGE2 and PGF2a levels
increased during the early phases of wound healing while PGD2 increased
during the later stages of wound healing (n>3; p<0.05). The level of hair
follicle neogenesis after wounding varied significantly among C57Bl/6J,
FVB/N and mixed background strains of mice (n>33; p<0.01). Levels of
lipocalin-type prostaglandin D2 synthase (Ptgds) mRNA (n>4; p<0.01) and its
product PGD2 (n=6; p<0.05) inversely correlated with regeneration ability.
C57Bl/6 mice had the highest level of Ptgds mRNA expression, PGD2 levels
and the least follicle neogenesis. Additionally, an alternatively
spliced transcript variant of Ptgds missing exon 3 correlated with the
regeneration phenotype among strains of mice (n=9; p<0.05). Exogenous
application of PGD2 decreased WIHN in wild type mice (n=8; p=0.06). Of the
two canonical PGD2 receptor null mice, only Gpr44 showed increased WIHN
compared to strain-matched control mice (n=31; p<0.05). In all, these
findings demonstrate that PGD2 inversely correlates with hair follicle
regeneration implying that inhibition of PGD2 production or Gpr44 signaling
pathways may promote skin regeneration.
Here is a good paper with all the PGE2 analogues (although they only tested
activation of the EP1 receptor). Maybe we can find something stable &
reasonably-priced.
» » Nobody is going to convince me that adding PGE2 won’t be more beneficial
» » than a PGD2 blocker alone.
»
» I agree that adding PGE2 seems promising but our options are severely
» limited. Minoxidil may be the best option. Wounding (e.g., dermaroller)
» could be very interesting as well once you’ve added a PGD2 blocker…
»
» Inhibition of wound-induced hair neogenesis by prostaglandin D2
»
» Prostaglandins (PGs) are key inflammatory mediators involved in wound
» healing. Recent evidence also illustrated a role for PGs in skin
» homeostasis with a specific role in regulating hair growth; however, no
» study to date has examined their role in skin regeneration after injury.
» Using the wound-induced hair follicle neogenesis (WIHN) assay, we
» hypothesized that PGs would impact hair follicle neogenesis, a marker for
» skin regeneration. We found that in C57Bl/6J mice, the levels of
» prostaglandin synthases and their products (PGD2, PGE2, PGF2a) were
» reciprocally expressed during wound healing. PGE2 and PGF2a levels
» increased during the early phases of wound healing while PGD2 increased
» during the later stages of wound healing (n>3; p<0.05). The level of hair
» follicle neogenesis after wounding varied significantly among C57Bl/6J,
» FVB/N and mixed background strains of mice (n>33; p<0.01). Levels of
» lipocalin-type prostaglandin D2 synthase (Ptgds) mRNA (n>4; p<0.01) and its
» product PGD2 (n=6; p<0.05) inversely correlated with regeneration ability.
» C57Bl/6 mice had the highest level of Ptgds mRNA expression, PGD2 levels
» and the least follicle neogenesis. Additionally, an alternatively
» spliced transcript variant of Ptgds missing exon 3 correlated with the
» regeneration phenotype among strains of mice (n=9; p<0.05). Exogenous
» application of PGD2 decreased WIHN in wild type mice (n=8; p=0.06). Of the
» two canonical PGD2 receptor null mice, only Gpr44 showed increased WIHN
» compared to strain-matched control mice (n=31; p<0.05). In all, these
» findings demonstrate that PGD2 inversely correlates with hair follicle
» regeneration implying that inhibition of PGD2 production or Gpr44 signaling
» pathways may promote skin regeneration.
»
»
»
» Here is a good paper with all the PGE2 analogues (although they only tested
» activation of the EP1 receptor). Maybe we can find something stable &
» reasonably-priced.
»
» Key Structural Features of Prostaglandin E2 and Prostanoid Analogs Involved in Binding and Activation of the Human EP1 Prostanoid Receptor | Molecular Pharmacology
A PGE2 solution will be coming soon.
The thing is that we need to be sure the half life is sufficient.
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