He’d have to establish that the proprietary component, GPI 1485, is what’s doing the magic. My understanding of the trial is that he didn’t do this.
It’s kinda like all the expensive hair growth formulations that have special proprietary blend of this and that but also, unsurprisingly, include minoxidil and maybe even consulting with their experts who prescribe finasteride too!
Name escapes me, but there’s a VERY expensive hair treatment that’s heavily advertised now. It’s “all natural” and has great “clinical” data to back it up. Thing is… that data was on WOMEN whose type of hair loss responds really well to biotin. Unsurprisingly, biotin is a primary ingredient. Of course, it’s mostly men buying it. Marketing is often evil and without conscience.
Thanks for this explanation. It makes a lot of sense.
My post wasn’t only directed to this particular product but the lack of research and effort to bring any product to market that deals with the issue of greying especially in the premature form. As compared to the availability and R&D towards countless other products for countless other dermatological conditions.
Also, for anyone interested, there’s another company that has a product in their pipeline for hair graying. Although they’ve been quite lately. It’s called Eirion Therapeutics out of Massachusetts. Apparently the main component being a PAI-1 inhibitor.
Interesting… I was going to say earlier in this conversation that the closest class of products that might be somewhat comparable to the Rivertown gray hair repigmentation formulation might be something like botox…
But for the Gray Hair product, they are very early in the development cycle:
ET-02 (Topical) and ET-03 (Oral) Small Molecule for Androgenetic Alopecia, Hair Greying, and Other Dermatologic Conditions
ET-02 and ET-03 contain the same small molecule that is being developed for the topical and oral treatment of androgenetic alopecia (male or female pattern baldness), and hair greying. Eirion utilizes a different therapeutic approach than other products for androgenic alopecia that are commercially available or in development. ET-02 and ET-03 targets a novel and compelling mechanism of action that we believe corrects a dysfunction in the hair follicle stem cell that is the cause of alopecia.
To Eirion’s knowledge, ET-02 and ET-03 are the only pharmaceutical products in development for hair greying. Eirion believes hair greying is also due to a defect in the stem cells in the hair follicle.
ET-02 and ET-03 have the potential to be effective in treating other medical dermatologic indications (not yet disclosed).
Also came across this while searching on Eirion, on hair regrowth:
JAK INHIBITORS AND BEYOND
A game changer for managing alopecia areata is the use of oral Janus kinase (JAK) inhibitors, according to Shapiro. “They can also be used to treat certain forms of scarring hair loss,” he said. “Overall, JAK inhibitors have the highest chance of success for alopecia totalis or universalis.”
Shapiro favors the JAK inhibitor tofacitinib at a dose of 5 mg, twice a day. Newer JAK inhibitors, such as baricitinib (Olumiant, Eli Lilly and Company), have also proven to be effective.
“Patients, though, need to be monitored for [adverse] effects; namely the immune system through a complete metabolic panel, a complete blood count, and testing of triglyceride and cholesterol levels,” Shapiro said.
Related research:
Results:
A systematic review and meta-analysis was performed according to PRISMA guidelines. From 30 studies and 289 cases, there were 72.4% responders, good responders 45.7% and partial responders 21.4%. Mean time to initial hair growth was 2.2 ± 6.7 months, and time to complete hair regrowth was 6.7 ± 2.2 months. All 37 recurrences occurred when treatment was ceased after 2.7 months. Oral route was significantly associated with response to treatment compared to topical therapy.
“Alopecia” just means hair loss in general. Alopecia areata/totalis/universalis is a specific autoimmune form of hair loss which can be helped by jak inhibitors (although oral Jak inhibitors are pretty scary in their potential side effects, so have to weigh the pros/cons). I’ve prescribed a topical Jak inhibitor for alopecia areata on the face with good results. I haven’t seen any research with androgenetic alopecia (i.e. male/female pattern baldness) and Jak inhibitors, but these drugs are far too dangerous to use orally as a cosmetic treatment IMO. Topically maybe, but they’re probably way too expensive to be feasible at this point, even if they do work.
I’ve not done the research on this topic, but do you think there are dosing alternatives that may reduces the risk of the side effects? (e.g. pulsed dosing, lower level dosing, etc.?)
Thank you. I was under the impression the selective JAK1-inhibitors come with less invasive side effects (Filgotinib, Upadacitinib), is that not the case? Edit: I mean to remember reading some studies that indicated selective JAK1-inhibitors could also suppress the SASP in senescent cells.
I’m actually pretty new to JAK inhibitors myself and am only familiar with the very few which have recently become available for use in dermatology. I’d expect lower or less frequent doses to be less toxic but also less efficacious, although I suppose it depends on the degree of immunosuppression that’s needed. I’m not convinced they’ll have any effect on androgenetic alopecia, but time will tell.
There are lots of patentable rapamycin mtorc1 inhibitors, from simple fluorine hydrogen swaps, to new testable versions of mtorc1 inhibiting peptides. Also, the two rodent studies where rapamycin causes 60% greater lifespan are math statements of group behavior where some of the rodents may have actually gained more than 70% longevity, and finding out what makes the strong responder mice so responsive can be a second drug, or a new area on the rapamycin molecule.
I agree/am hopeful about your point about finding a superior derivative.
My point is that they need to find that patentable derivative first, have it work on its own in mice first AND also be vastly superior to rapamycin. In that scenario the VCs will circle, not now.
I just ordered your list of compounds, plus ethoxidglycol (which I believe is the same as trancutol). I was thinking of adding eriodictyon angustifolium (yerba santa) to it. I’ll let everyone know how it all goes.
Mixing threads, but it got me thinking…I have Ell-Cranell Alfatradiol because it’s the only way I could find source 17-alpha estradiol. Would adding some transcutol make the 17-alpha E more likely to work systemically?
I know nothing about transcutol. How much do you need to add as a percentage to improve absorption?
I am not a fan of Janus Kinase inhibition, but my understanding is that the JK responds to IL-10 and reduces or increases NF kappa B. NF kappa B transcribes for SLC25A1 which provides substrate to create Acetyl-CoA in the Cytosol which is then available to acetylate the histone in the nucleus.
Insufficient Acetyl-CoA means no acetylation and stem cells don’t differentiate and turn sensecent or partially senescent.
The interesting aspect of this is that IL-10 is part of SASP so SASP can cut SLC25A1 and result in stem cells turning senescent.
My experience with increasing acetylation is that this initially gets defunct hair follicles to produce very weak very fine white hairs, then you get stronger white hairs and then you get pigmented hairs.
My view on Rapamycin is in that in improving the quality of mitochondria it feeds into the same process also increasing Acetyl-CoA in the nucleus.
I think Minoxidil operates in a different way increasing the blood flow and hence diluting the effect of IL-10.
I thought about prescribing myself some minoxidil and was reading through the side effects and lo and behold one of the common side effects is actually hair colour change…
I tried to get some today, the pharmacy didn’t have it in stock but I think if you keep the dose low (like 1mg/day) which works for hair growth the side effects should be minimal, the most important would be hypotension, tachycardia and pericarditis (<- that last one is one to monitor…)
