Samumed sm04554. Only drug on phase 3

[jan_miezda]

I personally think its both issues as Balding men in autopsies have densly calcified scalps, where as non balding men had significantly less calcium build up. Also, as we grow older our scalp stretches out and thins out (thinning could be due to highly androgenic DHT); our brains demand a crazy amount of blood flow and nutrients as well, taking away from other areas of our body.

However; DHT is the predominant culprit here. There are many compunding factors such as growth of scalp, thinning of skin, blood flow, gene transcription and pathway signaling, Cellular Metabolism, AR density etc... DHT literally causes calcification and scar tissue build up at the site of injured / damaged tissue in all areas of the body that ive studied; I dont see why it would be any different in the scalp...

The nutrients to the brain are supplied by cerebrospinal fluid circulation. It’s completely different than the vasculars that delivers blood and nutrients to hair follicles

 

[Selb]

I wrote some python to find a fuzzy match between genes regulated by androgenic alopecia and estrogen. Then pulled the ones that had opposite regulations (up vs down). I did a fuzzy match because I don't know the naming conventions for genes and I figured I'd pull anything that was somewhat close character-wise. So if you see widely different genes compared or duplicates, just ignore it. Also, there's only a few as I'm working based off data I find. If someone wants to contribute please provide data for upregulation/downregulation for estrogen and androgenic alopecia in the following format (U for up, D for down):

{ "CSPG4": "U", "MAP2K2": "U", "PTK7": "U", "GSTP1": "U", "CCND1": "U", "ERCC2": "U", "NFATC4": "U", "COL11A1": "U", "CTNNB1": "D", "MCM5": "D", "PDZK1IP1": "D" }

If you can't put in that format, it's fine, I can parse the data.

The results are here, process (AA or Estrogen), what gene it matches on, and what the regulation directions are, each 'match' indexed with the square brackets:

['[AA: Gene-CXCL10 U | Estro: Gene-BCL10 D]', '[AA: Gene-CXCL10 U | Estro: Gene-CXCL1 D]', '[AA: Gene-MMP12 U | Estro: Gene-MMP1 D]', '[AA: Gene-TSNFRS17 U | Estro: Gene-TNFRSF1A D]', '[AA: Gene-TSNFRS17 U | Estro: Gene-TNFRSF19 D]', '[AA: Gene-CCL13 U | Estro: Gene-CXCL1 D]', '[AA: Gene-CD38 U | Estro: Gene-CD36 D]', '[AA: Gene-CD38 U | Estro: Gene-CD34 D]', '[AA: Gene-COL1A U | Estro: Gene-COL6A3 D]', '[AA: Gene-COL1A U | Estro: Gene-COL12A1 D]', '[AA: Gene-CCL8 U | Estro: Gene-CCT8 D]', '[AA: Gene-PTGDS U | Estro: Gene-PTGDS D]']

I bolded the interesting ones.

 

[-G-]

I wrote some python to find a fuzzy match between genes regulated by androgenic alopecia and estrogen. Then pulled the ones that had opposite regulations (up vs down). I did a fuzzy match because I don't know the naming conventions for genes and I figured I'd pull anything that was somewhat close character-wise. So if you see widely different genes compared or duplicates, just ignore it. Also, there's only a few as I'm working based off data I find. If someone wants to contribute please provide data for upregulation/downregulation for estrogen and androgenic alopecia in the following format (U for up, D for down):

{ "CSPG4": "U", "MAP2K2": "U", "PTK7": "U", "GSTP1": "U", "CCND1": "U", "ERCC2": "U", "NFATC4": "U", "COL11A1": "U", "CTNNB1": "D", "MCM5": "D", "PDZK1IP1": "D" }

If you can't put in that format, it's fine, I can parse the data.

The results are here, process (AA or Estrogen), what gene it matches on, and what the regulation directions are, each 'match' indexed with the square brackets:

['[AA: Gene-CXCL10 U | Estro: Gene-BCL10 D]', '[AA: Gene-CXCL10 U | Estro: Gene-CXCL1 D]', '[AA: Gene-MMP12 U | Estro: Gene-MMP1 D]', '[AA: Gene-TSNFRS17 U | Estro: Gene-TNFRSF1A D]', '[AA: Gene-TSNFRS17 U | Estro: Gene-TNFRSF19 D]', '[AA: Gene-CCL13 U | Estro: Gene-CXCL1 D]', '[AA: Gene-CD38 U | Estro: Gene-CD36 D]', '[AA: Gene-CD38 U | Estro: Gene-CD34 D]', '[AA: Gene-COL1A U | Estro: Gene-COL6A3 D]', '[AA: Gene-COL1A U | Estro: Gene-COL12A1 D]', '[AA: Gene-CCL8 U | Estro: Gene-CCT8 D]', '[AA: Gene-PTGDS U | Estro: Gene-PTGDS D]']

I bolded the interesting ones.

What is your end goal and what does this show for people who don't understand this?

A part of me thinks there is enough snippets of knowledge on this forum (if we all combined it) to perhaps make some actual dents in this "problem".

 

[FCKW36]

So if we get phase 3 results in January 2021, how long will it need until it goes to market?

 

[NorwoodGuardian]

Can't wait to see.the power of minoxidil plus Samumed plus needling.

 

[Selb]

What is your end goal and what does this show for people who don't understand this?

A part of me thinks there is enough snippets of knowledge on this forum (if we all combined it) to perhaps make some actual dents in this "problem".

Basically, Estrogen is really the only thing that can regrow a significant amount of hair to the extent that you can go slick bald to Norwood 1.5. Anything else isn’t nearly as effective at the moment. Even if you block dht completely for example, the regrowth wouldn’t be the same as supplementing with estrogen. Why is that?

The assumption here is that there are processes in the body that are brought on by balding which may originally start with too much dht/AR sensitivity, but cascades into lack of regrowth for whatever reason. The follicles aren’t dead, so why wouldn’t they grow? Estrogen does something to reverse those cascading processes. And I think you can see what it’s doing by looking at gene expression

I’m taking the genes upregulated or downregulated by estrogen and comparing them to those upregulated or downregulated by androgenic alopecia. If there’s a gene match across both datasets plus they have opposite regulations (up vs down), that gene and diff fulfill the criteria.

The end goal is to take this list of differences in gene expression and see what process is estrogen really affecting to regrow hair and if we can possibly mimic it without estrogen

 

[NorwoodGuardian]

Basically, Estrogen is really the only thing that can regrow a significant amount of hair to the extent that you can go slick bald to Norwood 1.5. Anything else isn’t nearly as effective at the moment. Even if you block dht completely for example, the regrowth wouldn’t be the same as supplementing with estrogen. Why is that?

The assumption here is that there are processes in the body that are brought on by balding which may originally start with too much dht/AR sensitivity, but cascades into lack of regrowth for whatever reason. The follicles aren’t dead, so why wouldn’t they grow? Estrogen does something to reverse those cascading processes. And I think you can see what it’s doing by looking at gene expression

I’m taking the genes upregulated or downregulated by estrogen and comparing them to those upregulated or downregulated by androgenic alopecia. If there’s a gene match across both datasets plus they have opposite regulations (up vs down), that gene and diff fulfill the criteria.

The end goal is to take this list of differences in gene expression and see what process is estrogen really affecting to regrow hair and if we can possibly mimic it without estrogen

Can I drop it when I am back to Norwood 1.5?

 

[Selb]

Can I drop it when I am back to Norwood 1.5?

There have been people who have done that, yes. Problem is, feminization occurs. Like growing gyno.

But they also remain on dutasteride or finasteride. Sometimes the hair stays, sometimes it gets a bit worse. I think it depends on AR sensitivity.

 

[InBeforeTheCure]

If you also have on hand a good list of upregulated/downregulated genes for AA, that would be helpful. They don't need to have too many common genes in the estrogen dataset. I have a list already but it seems a bit short.

You can try these to start.

Go to the NCBI site and search under GEO datasets for more.

Differentially expressed genes don't replicate well at all between studies though. It's probably better to compare gene ontology and transcription factor target enrichment.

 

[-G-]

Basically, Estrogen is really the only thing that can regrow a significant amount of hair to the extent that you can go slick bald to Norwood 1.5. Anything else isn’t nearly as effective at the moment. Even if you block dht completely for example, the regrowth wouldn’t be the same as supplementing with estrogen. Why is that?

The assumption here is that there are processes in the body that are brought on by balding which may originally start with too much dht/AR sensitivity, but cascades into lack of regrowth for whatever reason. The follicles aren’t dead, so why wouldn’t they grow? Estrogen does something to reverse those cascading processes. And I think you can see what it’s doing by looking at gene expression

I’m taking the genes upregulated or downregulated by estrogen and comparing them to those upregulated or downregulated by androgenic alopecia. If there’s a gene match across both datasets plus they have opposite regulations (up vs down), that gene and diff fulfill the criteria.

The end goal is to take this list of differences in gene expression and see what process is estrogen really affecting to regrow hair and if we can possibly mimic it without estrogen

I do admire and appreciate your work and knowledge but is there more indication that estrogen is the answer? I feel like there is a million things that impact our hairloss and all in a lovely cascading effect.

 

[Selb]

I do admire and appreciate your work and knowledge but is there more indication that estrogen is the answer? I feel like there is a million things that impact our hairloss and all in a lovely cascading effect.

I wouldn’t say estrogen is the answer. I’d say estrogen leads to some reversal of some of those cascading effects enough to regrow hair. It’s basically working backwards from a known solution. As long as we can track down how it does that, then we can use it to our advantage.

 

[-G-]

I wouldn’t say estrogen is the answer. I’d say estrogen leads to some reversal of some of those cascading effects enough to regrow hair. It’s basically working backwards from a known solution. As long as we can track down how it does that, then we can use it to our advantage.

Fair enough. Well, good luck and keep us updated.

 

[kawnshawn]

So if we get phase 3 results in January 2021, how long will it need until it goes to market?

Can take the FDA from a few months to over a year to approve a new drug depending on a few factors.

Samumed is doing their phase 3 trial outside the US, so pray to god they do their due diligence with finalizing their study competently so that its up to snuff for the FDA's standards.

 

[nick123]

So if we get phase 3 results in January 2021, how long will it need until it goes to market?

This has already been said a few times, clinical trials should finish in January 2021. Compiling data should take a while, roughly 1-3 months. To fill in the actual FDA and EMA applications could take 3-6 months. FDA can take anywhere between 1-2 years to approve, the EMA usually take around 2 years to approve.

 

[MrJolly26]

It will be, for sure! Thing is if that will work better than what we already have or not...

Let´s see if 2021 will be a better year concerning hairloss.

Merry Xmas to you all, though I don´t like the new forum I keep reading you!

 

[Tom4362]

Gosh I just dont know what to expect from this product

 

[MrV88]

Let's hope the approval is faster in Turkey.

If they pay well enough I'm sure it will be faster approved then the Biontech vaccine.

 

[MrJolly26]

Sorry for asking, but I forgot again: is this going to be a lotion or a pill?

Thanks!

 

[FilthyFrancis]

Sorry for asking, but I forgot again: is this going to be a lotion or a pill?

Thanks!

It's going to be a suppository.

 

[Feelsbadman.jpg]

Activation of Wnt/β-catenin signaling is involved in hair growth-promoting effect of 655-nm red light and LED in in vitro culture model - PubMed

Activation of the Wnt/β-catenin signaling pathway plays an important role in hair follicle morphogenesis and hair growth. Recently, low-level laser therapy (LLLT) was evaluated for stimulating hair growth in numerous clinical studies, in which 655-nm red light was found to be most effective and...

pubmed.ncbi.nlm.nih.gov

Red Light Therapy also seems to activate this pathway.