EJ Jones

Thanks, Melvin. I saw some older posts about Vert where it was mentioned that you asked Dr. Bisanga about it and he kind of blew it off, but my understanding is that this interview took place prior to the pig trial. If you do decide to ask, I would make sure to emphasize the pig trial as it's recognized as the "gold standard" for animal skin experiments. Best, EJ

Here's a quote straight from the presentation booklet written by the researchers at Stanford-- "Results: Grossly and histologically, verteporfin treatment significantly reduced scarring and promoted skin regeneration, including recovery of hair follicles/glands (Figure 1A-B). Verteporfin-treated wounds were both significantly less stiff (Figure 1C) and stronger (Figure 1D) than PBS-treated wounds, with mechanical properties similar to those of unwounded skin. scRNA-seq identified two novel fibroblast subpopulations, one enriched in regenerating (verteporfin) wounds and unwounded skin, the other enriched in scarring (PBS) wounds (Figure 1E-F; clusters 1 and 4, respectively). Pseudotime trajectory constructs demonstrated putative state transitions between these two populations, which were supported by prospective FACS isolation and force manipulation in a 3D culture system. Conclusion: One-time local administration of verteporfin following injury significantly reduces scarring and induces regenerative healing in a large animal model."

Hey all, Long time lurker first time poster. I'm not one to get hyped about "new research" or "potential cures" when it comes to hair loss. Usually, I assume the worst and just expect such news to wither away without any actual progress. However, i must admit that Verteporfin and the Stanford scar research seems promising, so much so that I truly believe this drug could make noticeable improvements on scarring if it were used on a patient today. The story starts back in 1987, when Michael Longaker was working as a surgeon performing lifesaving surgeries for fetuses at UCSF. Longaker was asked by one of the surgeons to find out why the fetuses they were saving through surgery never formed any scars, and the question sent him down a rabbit hole for the next several decades. Scars are formed because they can cover wounds faster than normal skin can. This avoids death from extensive blood loss and potential infections, but also leaves us with thick scars that are unable to produce hair follicles or sweat glands. Longaker discovered that mechanical stress plays a large role in the formation of scars-- fetuses have more "gelatinous" skin without tension, meaning that they tend to heal without scars. Cells, mainly proteins called fibroblasts, detect mechanical stress when a wound is made, setting off the engrailed gene and forming a scar. Through experiments with mice fibroblast cells, Longaker found that you can stop the engrailed genes expression by using a soft gel that prevented mechanical strain. This is interesting, but doesn't really help us since we don't have soft gel for skin and we're not mice. However, through the same experiment and with the use of stress-inducing plastic, Longaker was able to successfully block the engrailed gene from expressing itself using a chemical that blocked mechanical strain signaling. This leads us to Verteporfin, a drug that has been approved by the FDA for macular degeneration for decades. Longaker identified this drug as a potential blocker for mechanical strain, and performed an experiment on mice with great success. So much so, that an AI algorithm which looked for differences between the Verteporfin-healed skin and normal skin saw NO DIFFERENCES. Not only was the skin fully healed, it, most importantly, GREW BACK THE HAIR on the affected area. Now again, who cares about mice? We don't have the same skin as them, and how many times have we heard about a "cure" tested on mice that translated poorly to humans? Well, this is where the pigs come in. It is well known that pig or "porcine" skin is one of the best available large-animal models that translates to humans. An article by Artur Summerfield notes that "The porcine skin has striking similarities to the human skin in terms of general structure, thickness, hair follicle content, pigmentation, collagen and lipid composition. This has been the basis for numerous studies using the pig as a model for wound healing, transdermal delivery, dermal toxicology, radiation and UVB effects." So, the next logical step would be to test it on pigs, right? Well, it appears that such an experiment has been performed by the same team. It worked. What is the next step, then? How does this apply to hair? At the end of the day, I'm just a novice when it comes to all of this stuff and I'm not a doctor, but I would very curious to see how this plays out if a hair transplant surgeon decides to try it. Even if the scar is not completely healed by Verteporfin, even if it doesn't grow back all the hair taken from the donor zone, I expect that there will be at least some improvements if this drug is added to the mix based on the pig model. If we get even a 50% success rate in terms of regrowing hair taken from the donor zone, this could increase the lifetime donor supply substantially. Think about it-- there are already doctors out there bringing Norwood 7's back to a full head of hair WITHOUT the use of this drug, so imagine what they could do with 50% MORE hair. At the end of the day, I'm holding my breath. This is incredibly promising and could make it so that a lot of guys don't have to wait for hair cloning (which I honestly don't think will ever happen in our lifetimes), but the history of the hair loss industry tells me that I shouldn't get my hopes up. Any doctors care to chime in on this? What are your thoughts? Do you find this promising at the very least?