Replicel news and answers

[sdsurfin]

The following is a conversation I had with replicel. They very kindly answered all my questions, and their reply gives me a lot more hope for their treatment. These trials can't start soon enough. The gist of the info is that it's probably not going to be a treatment that is great for bald areas (at least not in it's current iteration), but will hopefully really help those who are thinning and want to maintain. Here ya go, you're welcome.


******************
I have a question about RCH-01. It has been shown that as follicles miniaturize in balding scalp, they form a fibrotic tissue around the follicle (as early as 30 months from commencement of balding). How does replicel's technique aim to achieve the rehabilitation of these follicles when they are encased in scar tissue (wouldn't it make it impossible for fresh DSC cells to "find" the existing follicles?, and also when other cells besides the DSC are still androgen sensitive, continuing to promote inflammation? Replicel's video states that new DSC cells might form new follicles, but wouldn't this only be possible if non androgen sensitive DP and other cells existed in the area? I understand that replicel might be able to revive follicles that have barely begun to miniaturize, but in recent interviews your CEO mentioned that he aims for this to be a "cure" which could restore bald areas. I find this perplexing given what is known about the balding process, but perhaps I'm wrong? It seems as if you are hesitant to answer any technical questions but any input would be much appreciated. thank you

************************************
"Thank you for your very astute inquiries. As you will appreciate, your questions will likely only be answered with any certainty by data from clinical trials. Clinical evidence will help us determine the extent to which our treatment succeeds, fails, and/or how it may be modified to improve results.

Our current hypotheses is as follows:

1) Fibrotic tissue. This is variable between different people. Some have quite a lot, others very little. In general, fibrosis increases with the progression of AGA. We are proposing that our phase 2 clinical trial will be tested on people with thinning hair --not extensively bald -- so these people generally do not have a significant degree of fibrosis. The main objective of the study is to have the injected cells migrate to, integrate with, and enlarge the resident follicles. Fibrosis could be a challenge for the injected cells, however, the DSC cells do express some matrix metalloproteinases, albeit at a lower level compared to ordinary fibroblasts. We have observed in cell culture studies that the DSCs will migrate through collagen sheets in response to a chemoattraction gradient. The full answer will only be known when we examine the tissue biopsies from people in the phase 2 trials.

2) Androgen sensitive cells. Androgen sensitive cells will be present in the resident hair follicles of people suffering from AGA. However, the DSC cells injected are derived from follicles at the back of the scalp that are androgen insensitive. The objective is to introduce enough DSC cells to the follicle that the properties of the injected cells are dominant. Over time, as the resident androgen sensitive hair follicle cells become senescent/die off, we anticipate the DSC cells will become progressively more dominant. Recent evidence indicates that a subset of cells in the cup region are responsible for repopulating other HF cells including DP (Rahmani et al. Developmental Cell. 2014 Dec; 31: 543-58). In theory, the injected ‘androgen insensitive’ DSC cells can repopulate DS and DP with ‘androgen insensitive’ cells.

In addition, the healthy DSC cells express immunoregulatory factors and so should help to reduce any local inflammation which in turn should help reduce or stop further fibrosis. We published a paper on some of our work on DSC immunoregulation last year. (Wang et al. Hair follicle mesenchyme-associated PD-L1 regulates T-cell activation induced apoptosis: a potential mechanism of immune privilege. J Invest Dermatol. 2014 Mar;134(3):736-45).

3) New follicle formation. In principle, with new follicle formation, the issue of fibrosis around pre-existing follicles is not relevant. The injected DSC cells may directly interact with non-follicular epithelium to make new follicles. In such cases, as the DSC are immunoregulatory and not androgen sensitive, any new follicles would have the same properties. However, it is expected that this will NOT be the mechanism of treatment in the planned phase 2 trial. Due to the methodology employed using our injector device, and because we will be injecting people with thinning hair and not extensively bald people, it is simple migration of cells to resident follicles and their subsequent enlargement which is expected.

We anticipate our treatment may be a cure in that it should produce permanent improvement - once the injections are complete we believe there should be no need for further treatment. For people with extensive baldness of many years duration, we will need to conduct a separate study. It is likely that extensive, long-term duration AGA will need different cell dosages and changes to the parameters of our injection device.

For corporate, competitive reasons we do not always publish our data but research is ongoing at RepliCel and many improvements have been made in response to the data we obtained from the phase I trial and subsequent studies. We are excited to glean the data from our next phase of trials (both ours and that of Shiseido).

We hope these answers helps and appreciate your continued support and engagement.

[Sogeking]

Thank you sdsurfin. You basically proved that they are moving from the immunization perspective. There was some mention about this in 2012. And I spoke about this (although I was speculating) in my posts. Basically Replicel will make Propecia obsolete. It should stop the further hair loss, by stopping fibrosis and it has one of the best safety profiles, meaning no side effects.
There are still some questions remaining:

1. Will they be able to prove this in phase 2 trials?
   
2. Since this is mostly for stopping hair loss, it means we will have to turn to other treatments to generate new hair: HTs would be very viable if someone uses this while being NW3 and lower. However higher Norwoods will have to use something else to generate new hair. My highest hope is for Histogen they showed decent results in their latest trials, after 6 months. They showed increased total terminal hair count after 12 months compared to 6. And they have shown diminishing results after repeated injections at the same treatment site.
   
3. This is the biggest question IMO. Replicel phase 2 trials as reported many times in their investor reports will last 39 months. Will they start Phase 3 before finishing Phase 2? Or will we have to wait? What about Shiseido? Sure they don't need to go for Phase 3 trials but we still don't know if they will go for Phase I, Phase IIa or clean Phase II trials.

[woodnor]

I have a question about this (sorry I'm a noob on the subject so bear with me)...

If this treatment makes androgen sensitive follicles to become insensitive, that means DHT would not affect them (right?). But are androgens the only reason for hairloss? For example in another thread they were talking about the trials for a PGD2 inhibitor. is PGD2 an androgen too? (If it was, it would mean that this treatment would inhibit PGD2 receptor too right?)
In any case, would blocking androgen receptors really be the cure for further hairloss or could there be other factors that could exacerbate AGA?

[lupero83]

The following is a conversation I had with replicel. They very kindly answered all my questions, and their reply gives me a lot more hope for their treatment. These trials can't start soon enough. The gist of the info is that it's probably not going to be a treatment that is great for bald areas (at least not in it's current iteration), but will hopefully really help those who are thinning and want to maintain. Here ya go, you're welcome.


******************
I have a question about RCH-01. It has been shown that as follicles miniaturize in balding scalp, they form a fibrotic tissue around the follicle (as early as 30 months from commencement of balding). How does replicel's technique aim to achieve the rehabilitation of these follicles when they are encased in scar tissue (wouldn't it make it impossible for fresh DSC cells to "find" the existing follicles?, and also when other cells besides the DSC are still androgen sensitive, continuing to promote inflammation? Replicel's video states that new DSC cells might form new follicles, but wouldn't this only be possible if non androgen sensitive DP and other cells existed in the area? I understand that replicel might be able to revive follicles that have barely begun to miniaturize, but in recent interviews your CEO mentioned that he aims for this to be a "cure" which could restore bald areas. I find this perplexing given what is known about the balding process, but perhaps I'm wrong? It seems as if you are hesitant to answer any technical questions but any input would be much appreciated. thank you

************************************
"Thank you for your very astute inquiries. As you will appreciate, your questions will likely only be answered with any certainty by data from clinical trials. Clinical evidence will help us determine the extent to which our treatment succeeds, fails, and/or how it may be modified to improve results.

Our current hypotheses is as follows:

1) Fibrotic tissue. This is variable between different people. Some have quite a lot, others very little. In general, fibrosis increases with the progression of AGA. We are proposing that our phase 2 clinical trial will be tested on people with thinning hair --not extensively bald -- so these people generally do not have a significant degree of fibrosis. The main objective of the study is to have the injected cells migrate to, integrate with, and enlarge the resident follicles. Fibrosis could be a challenge for the injected cells, however, the DSC cells do express some matrix metalloproteinases, albeit at a lower level compared to ordinary fibroblasts. We have observed in cell culture studies that the DSCs will migrate through collagen sheets in response to a chemoattraction gradient. The full answer will only be known when we examine the tissue biopsies from people in the phase 2 trials.

2) Androgen sensitive cells. Androgen sensitive cells will be present in the resident hair follicles of people suffering from AGA. However, the DSC cells injected are derived from follicles at the back of the scalp that are androgen insensitive. The objective is to introduce enough DSC cells to the follicle that the properties of the injected cells are dominant. Over time, as the resident androgen sensitive hair follicle cells become senescent/die off, we anticipate the DSC cells will become progressively more dominant. Recent evidence indicates that a subset of cells in the cup region are responsible for repopulating other HF cells including DP (Rahmani et al. Developmental Cell. 2014 Dec; 31: 543-58). In theory, the injected ‘androgen insensitive’ DSC cells can repopulate DS and DP with ‘androgen insensitive’ cells.

In addition, the healthy DSC cells express immunoregulatory factors and so should help to reduce any local inflammation which in turn should help reduce or stop further fibrosis. We published a paper on some of our work on DSC immunoregulation last year. (Wang et al. Hair follicle mesenchyme-associated PD-L1 regulates T-cell activation induced apoptosis: a potential mechanism of immune privilege. J Invest Dermatol. 2014 Mar;134(3):736-45).

3) New follicle formation. In principle, with new follicle formation, the issue of fibrosis around pre-existing follicles is not relevant. The injected DSC cells may directly interact with non-follicular epithelium to make new follicles. In such cases, as the DSC are immunoregulatory and not androgen sensitive, any new follicles would have the same properties. However, it is expected that this will NOT be the mechanism of treatment in the planned phase 2 trial. Due to the methodology employed using our injector device, and because we will be injecting people with thinning hair and not extensively bald people, it is simple migration of cells to resident follicles and their subsequent enlargement which is expected.

We anticipate our treatment may be a cure in that it should produce permanent improvement - once the injections are complete we believe there should be no need for further treatment. For people with extensive baldness of many years duration, we will need to conduct a separate study. It is likely that extensive, long-term duration AGA will need different cell dosages and changes to the parameters of our injection device.

For corporate, competitive reasons we do not always publish our data but research is ongoing at RepliCel and many improvements have been made in response to the data we obtained from the phase I trial and subsequent studies. We are excited to glean the data from our next phase of trials (both ours and that of Shiseido).

We hope these answers helps and appreciate your continued support and engagement.

Not Believe That A Company in phase 2 studies are answered in such information.
Sdsurfin is lying in 99%

[Sogeking]

Not Believe That A Company in phase 2 studies are answered in such information.
Sdsurfin is lying in 99%

No, he's not.
If he would to lie he would tell it as a potential treatment for great regrowth of hair. So far Replicel is hoping to stop the hair loss progression but they are not too hopeful for regrowth.
I disagree with sdsurfin on some of his opinions but I don't think he is lying.
Besides what does he have to gain?
Everyone will be careful about buying Replicel stocks after the last phase trials. And they can't fudge with trial results, not when it comes to hair loss.

[Slam1523]

Not Believe That A Company in phase 2 studies are answered in such information.
Sdsurfin is lying in 99%

You're an idiot, get off this dudes nuts! Thanks sdsurfin for proactively searching info!

[sdsurfin]

You're an idiot, get off this dudes nuts! Thanks sdsurfin for proactively searching info!

No problem man. Some people on here are braindead, they can believe what they want. I'd be happy to take screenshots from where I asked them the questions, but honestly I couldn't be bothered, and have no desire to reveal my real name. I was honestly stunned that they answered my questions, and so thoroughly, it's probably because I can use my brain and ask about things that are relevant to their line of inquiry. It's funny that someone would think I took the time out of my life to invent all that stuff, I'm just trying to enlighten people on here because I know it sucks not to have info. Maybe from now on I'll keep it to myself, god knows these researchers don't need their names associated online with the morass of imbeciles that seems to lurk on here. Pretty sure Dr. Xu stopped answering my emails because his name started to pop up on here.

[LongWayHome]

You did a great job.
Do yourself a favor and don't listen to anyone.

[Tenma]

Im surprised they took the time to elaborate such detailed response.

Its pretty good info by the way

Sdsurfin, if you have the chance and given the positive feedback with whoever wrote to you, ask him/her about their improved DSCs culturing method.

I read somewhere that it was easier to culture DSCs cells compared to DP cells.

To confirm that info would be great

[brocktherock]

The following is a conversation I had with replicel. They very kindly answered all my questions, and their reply gives me a lot more hope for their treatment. These trials can't start soon enough. The gist of the info is that it's probably not going to be a treatment that is great for bald areas (at least not in it's current iteration), but will hopefully really help those who are thinning and want to maintain. Here ya go, you're welcome.


******************
I have a question about RCH-01. It has been shown that as follicles miniaturize in balding scalp, they form a fibrotic tissue around the follicle (as early as 30 months from commencement of balding). How does replicel's technique aim to achieve the rehabilitation of these follicles when they are encased in scar tissue (wouldn't it make it impossible for fresh DSC cells to "find" the existing follicles?, and also when other cells besides the DSC are still androgen sensitive, continuing to promote inflammation? Replicel's video states that new DSC cells might form new follicles, but wouldn't this only be possible if non androgen sensitive DP and other cells existed in the area? I understand that replicel might be able to revive follicles that have barely begun to miniaturize, but in recent interviews your CEO mentioned that he aims for this to be a "cure" which could restore bald areas. I find this perplexing given what is known about the balding process, but perhaps I'm wrong? It seems as if you are hesitant to answer any technical questions but any input would be much appreciated. thank you

************************************
"Thank you for your very astute inquiries. As you will appreciate, your questions will likely only be answered with any certainty by data from clinical trials. Clinical evidence will help us determine the extent to which our treatment succeeds, fails, and/or how it may be modified to improve results.

Our current hypotheses is as follows:

1) Fibrotic tissue. This is variable between different people. Some have quite a lot, others very little. In general, fibrosis increases with the progression of AGA. We are proposing that our phase 2 clinical trial will be tested on people with thinning hair --not extensively bald -- so these people generally do not have a significant degree of fibrosis. The main objective of the study is to have the injected cells migrate to, integrate with, and enlarge the resident follicles. Fibrosis could be a challenge for the injected cells, however, the DSC cells do express some matrix metalloproteinases, albeit at a lower level compared to ordinary fibroblasts. We have observed in cell culture studies that the DSCs will migrate through collagen sheets in response to a chemoattraction gradient. The full answer will only be known when we examine the tissue biopsies from people in the phase 2 trials.

2) Androgen sensitive cells. Androgen sensitive cells will be present in the resident hair follicles of people suffering from AGA. However, the DSC cells injected are derived from follicles at the back of the scalp that are androgen insensitive. The objective is to introduce enough DSC cells to the follicle that the properties of the injected cells are dominant. Over time, as the resident androgen sensitive hair follicle cells become senescent/die off, we anticipate the DSC cells will become progressively more dominant. Recent evidence indicates that a subset of cells in the cup region are responsible for repopulating other HF cells including DP (Rahmani et al. Developmental Cell. 2014 Dec; 31: 543-58). In theory, the injected ‘androgen insensitive’ DSC cells can repopulate DS and DP with ‘androgen insensitive’ cells.

In addition, the healthy DSC cells express immunoregulatory factors and so should help to reduce any local inflammation which in turn should help reduce or stop further fibrosis. We published a paper on some of our work on DSC immunoregulation last year. (Wang et al. Hair follicle mesenchyme-associated PD-L1 regulates T-cell activation induced apoptosis: a potential mechanism of immune privilege. J Invest Dermatol. 2014 Mar;134(3):736-45).

3) New follicle formation. In principle, with new follicle formation, the issue of fibrosis around pre-existing follicles is not relevant. The injected DSC cells may directly interact with non-follicular epithelium to make new follicles. In such cases, as the DSC are immunoregulatory and not androgen sensitive, any new follicles would have the same properties. However, it is expected that this will NOT be the mechanism of treatment in the planned phase 2 trial. Due to the methodology employed using our injector device, and because we will be injecting people with thinning hair and not extensively bald people, it is simple migration of cells to resident follicles and their subsequent enlargement which is expected.

We anticipate our treatment may be a cure in that it should produce permanent improvement - once the injections are complete we believe there should be no need for further treatment. For people with extensive baldness of many years duration, we will need to conduct a separate study. It is likely that extensive, long-term duration AGA will need different cell dosages and changes to the parameters of our injection device.

For corporate, competitive reasons we do not always publish our data but research is ongoing at RepliCel and many improvements have been made in response to the data we obtained from the phase I trial and subsequent studies. We are excited to glean the data from our next phase of trials (both ours and that of Shiseido).

We hope these answers helps and appreciate your continued support and engagement.

This is hands down one of the most valuable posts Ive seen on these websites, I don't see why all the hate. I really appreciate the info. I have high hopes for them.