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There are currently two very promising non conventional treatments in clinical trials at the moment, these might compliment each other very well if the first one doesn't restore full coverage.
Finasteride, dustasteride, minoxidil and hair systems might be a thing of the past, relatively soon.
These are:
1) HMI-115.
2) Verteporfin during transplants.
HMI -115
Lets talk about HMI-115 first. The redditor tired45453 laid it out perfectly and made it very easy to understand, so I will essentially copy his bulletin points:
Now, a user with the username of moeman32 has been a part of this clinical trial, he was posting updates on /r/tressless semi regularly, which he was not allowed to do, and he almost got kicked out of the trial because of it, as some sad moron essentially ratted on him to the researchers who were conducting this trial.
17 days ago, however. He posted this subtle post, you can read two of the comments he replied to and make your own conclusion.
Verteporfin
There is a megathread about Verteporfin on hairrestorationnetwork that you can view here.
So what is Verteporfin? TLDR it's a drug that prevents the pathways to scarring.
So the idea is to massively increase the amount of donor hairs that can be used for a transplant.
Say that your a Norwood 6-7, likely you won't be a candidate for a hair transplant unless you have a huge density in the donor area as well as thick hair.
The idea here, is to harvest hair follicles, then inject verteporfin into the donor area.
The tissue recovers in a much more physiological fashion, and even the harvested hair follicle might return.
This is being experimented on by a handful of hair transplant surgeons currently, as the first trial by Dr. Barghouthi showed great promise.
Finasteride, dustasteride, minoxidil and hair systems might be a thing of the past, relatively soon.
These are:
1) HMI-115.
2) Verteporfin during transplants.
HMI -115
Lets talk about HMI-115 first. The redditor tired45453 laid it out perfectly and made it very easy to understand, so I will essentially copy his bulletin points:
- Effect of HMI-115 was discovered by accident in a similar manner as Finasteride. Was being used to treat endometriosis, when Bayer noticed mice regrew hair.
- Bayer was not interested in researching HMI-115's potential effects on AGA, as they had pivoted towards women's issues. However, Rui-Ping Xiao, who was working with them, asked to test the drug on bald, stumptailed macaques. This is where we get the pictures showing hair growth through four years. Bayer agreed, and when the results came in she formed HopeMed Inc., and purchased the global rights to the drug from Bayer in 2019.
- The bald, stumptailed macaques are unique in hair-loss research in that they experience AGA in the same way humans do. DHT causes their follicles to miniaturize, and they go bald in a similar pattern as us. Previous hair-loss treatments such as Finasteride and minoxidil show similar efficacies in macaques as they do in us. Hair transplants work for them, just like for us.
- To clear up some confusion regarding results on the macaques: The observation period is still ongoing. The macaques did not lose all their hair after four years. Furthermore, slight regression was experienced after cessation of the 6-month treatment in some of the macaques. However, that slight regression stabilized soon after cessation, and the macaques experienced regrowth far after cessation of treatment. Again, the observation period is still ongoing. The macaques have kept their hair for four years and counting.
- There was no plateau reached during the 6-month study, meaning there could have been potentially greater gains had the treatment continued.
- Completely bald areas responded the best.
- HMI-115 would be effective for diffuse thinners and for those struggling with telogen effluvium.
- Inhibiting serum prolactin levels will not work, as the hair follicle produces its own prolactin.
- HMI-115 works because it is a prolactin receptor antagonist that targets the PRL receptors on the follicle.
- HMI-115 has already undergone a Phase I trial in women. The FDA greenlit Phase II for AGA already back in early 2022, but Australia did not. The reason for this is that the FDA allowed them to extrapolate safety data from Phase I for endometriosis, but Australia denied them.
- The current Phase I trial is essentially a formality. They term it Phase Ib.
- No serious adverse effects reported in the Phase I trial in women. Relevant quote regarding side effects:
- 14 genes were found upregulated in frontal vs vertex scalp. At least 10 of them are upregulated by prolactin receptor signaling, and 2 others induce prolactin secretion. Many of these genes are also upregulated by Wnt inhibition.
- Prolactin receptor in follicles may play a role in alopecia areata.
- DHT induces increased prolactin production. DHT doesn't directly cause miniaturization; DHT binding to follicles increases prolactin, which in turn causes miniaturiaztion. DHTs role in hair loss is finally adequately explained.
- The role of prolactin in hair loss has been known for two decades now. No research has been done because no one bothered to develop a prolactin receptor antagonist.
- At least in certain blood cells PRLR expression increases in adulthood as GHR expression decreases. This coincides with the time when men start losing their hair. Additionally, newborns have extremely high levels of serum prolactin, 100-300ng/ml, well beyond hyperprolactinema levels of 20ng/ml. This could be why newborns lose hair in the male pattern baldness pattern, and lends some credibility to the theory that PRLR expression is responsible for the hair loss pattern found in Androgenetic Alopecia. Prolactin levels return to normal in the weeks to months before babies regrow their hair.
Now, a user with the username of moeman32 has been a part of this clinical trial, he was posting updates on /r/tressless semi regularly, which he was not allowed to do, and he almost got kicked out of the trial because of it, as some sad moron essentially ratted on him to the researchers who were conducting this trial.
17 days ago, however. He posted this subtle post, you can read two of the comments he replied to and make your own conclusion.
Verteporfin
There is a megathread about Verteporfin on hairrestorationnetwork that you can view here.
So what is Verteporfin? TLDR it's a drug that prevents the pathways to scarring.
So the idea is to massively increase the amount of donor hairs that can be used for a transplant.
Say that your a Norwood 6-7, likely you won't be a candidate for a hair transplant unless you have a huge density in the donor area as well as thick hair.
The idea here, is to harvest hair follicles, then inject verteporfin into the donor area.
The tissue recovers in a much more physiological fashion, and even the harvested hair follicle might return.
This is being experimented on by a handful of hair transplant surgeons currently, as the first trial by Dr. Barghouthi showed great promise.
