South Korean Scientists Has Developed A New Type Of Biochemical Material To Prevent Hair Loss

[kuba197]

Ok.
I used this email KYCHOI@YONSEI.AC.KR

Dear Sir,
I would like to ask about your last hair discovery. Could you tell me if you are going to test it in humans and when?

Response
'We hope to do that as soon as possible. But first need to prepare fund for the tests. Kang-Yell'
So maybe one of native English speakers could send him a few questions from HairLossTalk.com community?

 

[inmyhead]

Ok.
I used this email KYCHOI@YONSEI.AC.KR

Dear Sir,
I would like to ask about your last hair discovery. Could you tell me if you are going to test it in humans and when?

Response
'We hope to do that as soon as possible. But first need to prepare fund for the tests. Kang-Yell'
So maybe one of native English speakers could send him a few questions from HairLossTalk.com community?

What else do you want to ask? they are collecting funds and trying to test it. That's all we need to know.

 

[kuba197]

What else do you want to ask? they are collecting funds and trying to test it. That's all we need to know.

I'm sure that there are guys who want to know more specific and advance information.

 

[mecevik]

Someone should tell him create a social media account. He can keep us informed through it.

 

[bboy]

It wasn't tested on human cells, according to the article. The same binding of proteins and resulting inhibition of follicle growth was observed in human hair.

Good god of course it was tested on human cells.... Please don't just make things up and then go around acting like some kind of authority when you haven't even bothered to do even a minimum level of research.

From page 8 of the study.

CXXC5 attenuates ALP activity and proliferation in human hair follicle dermal
papilla cells via interaction with Dvl-1

The role of CXXC5 in modulating ALP activity and cell proliferation was investigated using
human hair follicle dermal papilla cells (HFDPCs). Transfection with CXXC5 significantly
inhibited expression of β-catenin, ALP, and PCNA (Figure 2a). Analyses using
immunocytochemical and ALP staining also showed that the levels of both β-catenin and
were diminished by CXXC5 transfection (Figure 2b). In contrast, CXXC5 knockdown
induced the expression of β-catenin, ALP and PCNA (see Supplementary Figure S3). CXXC5
possesses a Dvl-binding motif (DBM) at its C terminus that is essential for CXXC5 function
as a negative regulator of the Wnt/β-catenin pathway (London et al., 2004). Transfection with
CXXC5∆DBM, which lacks the DBM (London et al., 2004), did not inhibit the expression of
β-catenin and ALP, as well as PCNA in HFDPCs (Figure 2c). Overexpression of CXXC5
markedly reduced the transcriptional activity of a Wnt/β-catenin reporter gene (Figure 2d).
Furthermore, ALPL promoter activity and ALP activity were significantly lowered by
CXXC5 overexpression (Figures 2e and f). Cell proliferation was also decreased in HFDPCs
by 66% at 72 hours after transfection with CXXC5 (Figure 2g). To further clarify the role of
the Wnt/β-catenin pathway in CXXC5 function, we confirmed the effect of Wnt3a in
HFDPCs. Interestingly, β-catenin and CXXC5 were concomitantly increased in human
dermal papilla cells treated with Wnt3a as shown by western blot and immunocytochemical
analyses (see Supplementary Figure S4). Based on in vivo results, we expected Wnt3a-
dependent induction of CXXC5 to be a negative feedback mechanism. We also found that
CXXC5 interacted with Dvl-1 in human hair follicle cells, but only detected this interaction
when HFDPCs were treated with Wnt3a (Figure 2h). However, CXXC5∆DBM failed to
interact with Dvl-1 in HFDPCs, even when the cells were treated with Wnt3a (Figure 2h).
Endogenous CXXC5 also bound to Dvl-1 in Wnt3a-treated HFDPCs as shown by western
blot analyses of immunoprecipitates (see Supplementary Figure S5). To confirm the
possibility of further Wnt/β-catenin pathway activation after disrupting the negative feedback
regulation of CXXC5, we co-treated HFDPCs with both CXXC5 siRNA and Wnt3a.
Expression of β-catenin, ALP, and PCNA were synergistically increased by co-treatment with
CXXC5 siRNA and Wnt3a (Figures 2i and j). In summary, our data indicate that CXXC5
interacts with Dvl in a Wnt3a-dependent manner to negatively regulate the Wnt/β-catenin
pathway in HFDPCs.

 

[spring15]

Ok.
I used this email KYCHOI@YONSEI.AC.KR

Dear Sir,
I would like to ask about your last hair discovery. Could you tell me if you are going to test it in humans and when?

Response
'We hope to do that as soon as possible. But first need to prepare fund for the tests. Kang-Yell'
So maybe one of native English speakers could send him a few questions from HairLossTalk.com community?

Tell them there are also plenty of humans on this site willing to f*** themselves up as guinea pigs for the cause. It's not life or death, it's hair or death b**ch

 

[ElTioLaBota]

Ok.
I used this email KYCHOI@YONSEI.AC.KR

Dear Sir,
I would like to ask about your last hair discovery. Could you tell me if you are going to test it in humans and when?

Response
'We hope to do that as soon as possible. But first need to prepare fund for the tests. Kang-Yell'
So maybe one of native English speakers could send him a few questions from HairLossTalk.com community?

Can we f*****g present ourselves as testing subjects for free? Like this the funding proces for trials will be shorter

 

[Trichosan]

Ok.
I used this email KYCHOI@YONSEI.AC.KR

Dear Sir,
I would like to ask about your last hair discovery. Could you tell me if you are going to test it in humans and when?

Response
'We hope to do that as soon as possible. But first need to prepare fund for the tests. Kang-Yell'
So maybe one of native English speakers could send him a few questions from HairLossTalk.com community?

Money is always the biggest impediment to a project, especially bio research. Without big pharma or government, it could take quite awhile.

 

[thecure]

Why they don't test it on a single damn human? What funds do you need with that? Give proof of concept by making a nw7 to nw1 and you will have the funds and media coverage of the entire planet earth. I understand that this way they may have a chance to fail and not earn any money while securing some funds first they earn even if they fail in the future.

I have read the study several times and connecting the dots with other studies I think the follicles are still there in the bald scalp but don't recieve signals to grow because too much CXXC5 disrupts the cycle completely and you don't see any hair anymore. I don't know, maybe this could work better in humans than in mice because there is no scar in the scalp or dead follicles like previosly thought. In mice they destroy the follicles and create new follicles by wound-induced follicle neogenesis, may not be the case here.

In my opinion things should be tested immediately and prove results and not fund reasearch that maybe will work and after 5 to 10 years we find out it doesn't work.

 

[Dat5Years]

Why they don't test it on a single damn human? What funds do you need with that? Give proof of concept by making a nw7 to nw1 and you will have the funds and media coverage of the entire planet earth. I understand that this way they may have a chance to fail and not earn any money while securing some funds first they earn even if they fail in the future.

I have read the study several times and connecting the dots with other studies I think the follicles are still there in the bald scalp but don't recieve signals to grow because too much CXXC5 disrupts the cycle completely and you don't see any hair anymore. I don't know, maybe this could work better in humans than in mice because there is no scar in the scalp or dead follicles like previosly thought. In mice they destroy the follicles and create new follicles by wound-induced follicle neogenesis, may not be the case here.

In my opinion things should be tested immediately and prove results and not fund reasearch that maybe will work and after 5 to 10 years we find out it doesn't work.

Its frustrating for sure, but what if someone dies in human testing? they have to establish the safety first. It's sh*t and i would volunteer myself tbh but it is what it is. I think there is fat less red tape over there so heres hoping

 

[thecure]

Its frustrating for sure, but what if someone dies in human testing? they have to establish the safety first. It's sh*t and i would volunteer myself tbh but it is what it is. I think there is fat less red tape over there so heres hoping

Yes after safety is proved of course but after that it works or not. I don't like this dragging 5 years.

 

[Jonnyyy]

Its frustrating for sure, but what if someone dies in human testing? they have to establish the safety first. It's sh*t and i would volunteer myself tbh but it is what it is. I think there is fat less red tape over there so heres hoping

Pay someone a sh*t ton of money to test it out, I'd f*****g take the risk regardless. I'm sure that's against the law though.

 

[Balding curse]

If there any drug inhibits CXXC5 we can just use it!

 

[Jonnyyy]

If there any drug inhibits CXXC5 we can just use it!

Doubt it, I'm sure someone would've reported extreme hair growth as a side effect.

 

[bboy]

Doubt it, I'm sure someone would've reported extreme hair growth as a side effect.

Not unless they've found a way to get the drug to the site where it needs to work somehow. I don't think systemically inhibiting cxxc5 across your entire body through oral consumption is probably a desirable or effective thing to do.

 

[That Guy]

Good god of course it was tested on human cells.... Please don't just make things up and then go around acting like some kind of authority when you haven't even bothered to do even a minimum level of research.

From page 8 of the study.

CXXC5 attenuates ALP activity and proliferation in human hair follicle dermal
papilla cells via interaction with Dvl-1

The role of CXXC5 in modulating ALP activity and cell proliferation was investigated using
human hair follicle dermal papilla cells (HFDPCs). Transfection with CXXC5 significantly
inhibited expression of β-catenin, ALP, and PCNA (Figure 2a). Analyses using
immunocytochemical and ALP staining also showed that the levels of both β-catenin and
were diminished by CXXC5 transfection (Figure 2b). In contrast, CXXC5 knockdown
induced the expression of β-catenin, ALP and PCNA (see Supplementary Figure S3). CXXC5
possesses a Dvl-binding motif (DBM) at its C terminus that is essential for CXXC5 function
as a negative regulator of the Wnt/β-catenin pathway (London et al., 2004). Transfection with
CXXC5∆DBM, which lacks the DBM (London et al., 2004), did not inhibit the expression of
β-catenin and ALP, as well as PCNA in HFDPCs (Figure 2c). Overexpression of CXXC5
markedly reduced the transcriptional activity of a Wnt/β-catenin reporter gene (Figure 2d).
Furthermore, ALPL promoter activity and ALP activity were significantly lowered by
CXXC5 overexpression (Figures 2e and f). Cell proliferation was also decreased in HFDPCs
by 66% at 72 hours after transfection with CXXC5 (Figure 2g). To further clarify the role of
the Wnt/β-catenin pathway in CXXC5 function, we confirmed the effect of Wnt3a in
HFDPCs. Interestingly, β-catenin and CXXC5 were concomitantly increased in human
dermal papilla cells treated with Wnt3a as shown by western blot and immunocytochemical
analyses (see Supplementary Figure S4). Based on in vivo results, we expected Wnt3a-
dependent induction of CXXC5 to be a negative feedback mechanism. We also found that
CXXC5 interacted with Dvl-1 in human hair follicle cells, but only detected this interaction
when HFDPCs were treated with Wnt3a (Figure 2h). However, CXXC5∆DBM failed to
interact with Dvl-1 in HFDPCs, even when the cells were treated with Wnt3a (Figure 2h).
Endogenous CXXC5 also bound to Dvl-1 in Wnt3a-treated HFDPCs as shown by western
blot analyses of immunoprecipitates (see Supplementary Figure S5). To confirm the
possibility of further Wnt/β-catenin pathway activation after disrupting the negative feedback
regulation of CXXC5, we co-treated HFDPCs with both CXXC5 siRNA and Wnt3a.
Expression of β-catenin, ALP, and PCNA were synergistically increased by co-treatment with
CXXC5 siRNA and Wnt3a (Figures 2i and j). In summary, our data indicate that CXXC5
interacts with Dvl in a Wnt3a-dependent manner to negatively regulate the Wnt/β-catenin
pathway in HFDPCs.

Nope, point still stands. And I'm not going to read all the papers on something that isn't likely to lead to a practical treatment before I'm like 35 anyway. The article did not say this or I missed it.

My wording my have been incorrect, but the rest remains the same.

This is not done in a person with Androgenetic Alopecia; it's simply an observation that a similar phenomena occurs in vitro. We don't know what will happen (if anything) when the compound is subjected to a living person with the condition. The other underlying causes of Androgenetic Alopecia may render it useless.

A very good and promising find, but not a smoking gun yet.

 

[bboy]

Nope, point still stands. And I'm not going to read all the papers on something that isn't likely to lead to a practical treatment before I'm like 35 anyway. The article did not say this or I missed it.

My wording my have been incorrect, but the rest remains the same.

This is not done in a person with Androgenetic Alopecia; it's simply an observation that a similar phenomena occurs in vitro. We don't know what will happen (if anything) when the compound is subjected to a living person with the condition. The other underlying causes of Androgenetic Alopecia may render it useless.

A very good and promising find, but not a smoking gun yet.

No, it doesn't stand at all. You didn't misspeak you literally said "It wasn't tested on human cells". It was. My point stands that you are speaking with an air of authority of which you have no justification. Of course we don't technically know exactly what is going to happen when this is tried on a human scalp, but that's a far cry from saying it's just a random shot in the dark. We have a very good understanding of how we expect this to work in relation to our current model of Androgenetic Alopecia. A model that also just been expanded by this study, which is extremely important in and of itself.

From our current understanding the two focal points of the pathology of Androgenetic Alopecia is the Androgen Receptor, and the Wnt pathway. This study showed us a new suppressor of the Wnt pathway and how we easily and safely can nullify it. Now there are other suppressors that we know of like DKK1, but guess what? DKK1 expression is elevated by DHT and they found swamping the cells in DHT had no effect as long CXXC5 was suppressed. Do you have any other objection apart from just pure pessimism? I don't think you do.

The problem is you're posting completely factual wrong information with an air of authority and certainty that seems to be backed up by nothing but ignorance and ego. Even when I've called you out and show how completely wrong and ignorant you are you still don't back down and insist your point stands.

Now in terms of time frames, this study was submitted a year ago, so there may well be safety data already out there. If not there may well be some kind of analogue that has already been through safety trials that we can use.

Now I'm not an expert, but to me it looks as though CXXC5 could be well be the limiting factor to all other methods of attack we've had, if so this study is the most important study of Androgenetic Alopecia ever released and a treatment could well be implemented by the collective resources on this forum in a matter of months, if not weeks. And your dismissive hand waving, based on little to no knowledge of what you're talking about, coupled with your self proclaimed sense of certainty, is not helpful.

 

[Spanishboy97]

No, it doesn't stand at all. You didn't misspeak you literally said "it wasn't treated on human cells". It was. My point stands that you are speaking with an air of authority of which you have no justification. Of course we don't technically know exactly what is going to happen when this is tried on a human scalp, but that's a far cry from saying it's just a random shot in the dark. We have a very good understanding of how we expect this to work in relation to our current model of Androgenetic Alopecia. A model that also just been expanded by this study, which is extremely important in and of itself.

From our current understanding the two focal points of the pathology of Androgenetic Alopecia is the Androgen Receptor, and the Wnt pathway. This study showed us a new suppressor of the Wnt pathway and how we easily and safely can nullify it. Now there are other suppressors that we know of like DKK1, but guess what? DKK1 expression is elevated by DHT and they found swamping the cells in DHT had no effect as long CXXC5 was suppressed. Do you have any other objection apart from just pure pessimism? I don't think you do.

The problem is you're posting completely factual wrong information with an air of authority and certainty that seems to be backed up by nothing but ignorance and ego. Even when I've called you out and show how completely wrong and ignorant you are you still don't back down and insist your point stands.

Now in terms of time frames, this study was submitted a year ago, so there may well be safety data already out there. If not there may well be some kind of analogue that has already been through safety trials that we can use.

Now I'm not an expert, but to me it looks as though CXXC5 could be well be the limiting factor to all other methods of attack we've had, if so this study is most important study of Androgenetic Alopecia ever released and a treatment could well be implemented by the collective resources on this forum in a matter of months, if not weeks. And your dismissive hand waving, based on little to no knowledge of what you're talking about, coupled with your self proclaimed sense of certainty, is not helpful.

@That Guy my nigga you just got roasted

 

[itsAlright]

About a year and a half ago,prior to creating an account, I used to enjoy @That Guy 's posts, but it seems he's grown increasingly pessimistic. Now it seems he only shows up to attack and belittle others. I feel for you @That Guy , healthy skepticism is necessary, but what's the point of purposefully trying to dash little glimmers of hope that people hold? Not everyone can tolerate finasteride.

 

[dermrafok]

About a year and a half ago,prior to creating an account, I used to enjoy @That Guy 's posts, but it seems he's grown increasingly pessimistic. Now it seems he only shows up to attack and belittle others. I feel for you @That Guy , healthy skepticism is necessary, but what's the point of purposefully trying to dash little glimmers of hope that people hold? Not everyone can tolerate finasteride.

@That Guy More and more people know the truth about Finasteride. The post-finasteride syndrome is real. And people know it. It is for this reason. New treatment alternatives are needed.