r/HairlossResearch

Hair loss has been making my life harder. I’m currently using vitamin D, minoxidil and some other anti hair loss shampoos but progress has been pretty slow. My dermatologist had me check my thyroid and other vitamins too but everything else came back normal.

I’ve seen people mention Precision Pep Co like GHK-Cu for hair loss so I started looking into them.
Does anyone know of good human research on GHK-Cu or other peptides for androgenetic alopecia?

I’m a 20 year old healthy male that went through depression 2 years ago which rapidly accelerated my hair loss and I am mostly recovered from it now but I train MMA from anyone’s experience or from someone’s research will either of these 2 effect me from doing MMA or no?

so i've been going down a rabbit hole looking at hair loss research lately. spent way too much time reading studies about what actually works and what's just marketing. honestly it's kind of depressing how many ingredients are just thrown into products without any real evidence.

there's actually been some decent research on specific ingredients though. caffeine has some evidence for reducing shedding and stimulating growth . adenosine is another one that's been tested . but apparently most ingredients in anti-hair loss shampoos haven't actually been tested at all . like 20 out of 36 commonly used active ingredients have zero clinical trials behind them . that's insane.

a friend recommended this hair loss shampoo and conditioner set to me a while ago and i've been using it for a few months. actually been seeing some results which is surprising. less shedding, hair feels thicker.

now i'm trying to figure out what's in it that's actually working. like is it one of the ingredients with clinical data or something new. there's a study on a shampoo with DMG-Na and caffeine that showed significant improvement in hair density and anagen/telogen ratio after 24 weeks . also some interesting stuff on Wnt/β-catenin pathway activation in hair follicle cells .

anyway. just curious if anyone else has looked into the science behind these products. what ingredients do you actually trust based on research? i feel like there's so much hype and marketing around hair loss stuff that it's hard to know what's legit.

Hey i have been 1 mg 3x a week finasteride for more than 3 months now in still shedding pretty much sa. e as before the hairs falling Is Very thick hairs and when i check the end of the hair i dont think its miniaturised should i switch To Everday or switch to dutasteride

In 2024, Amplifica announced “promising” phase I data for AMP-303, with some subjects experiencing an increase in terminal hair counts of more than 15% after one session [1]. The compound is described as a novel polysaccharide, so it appears to be based on hyaluronic acid [2]. Treatment was given on one side of the scalp and placebo on the other. The 15% increase was observed only in a subset of participants, and this was compared with baseline not placebo. This type of post hoc analysis can be misleading. They did not state that no one in the placebo group showed a more than 15% increase in hair count. What they found is that the number of subjects experiencing a greater than 15% increase in non-vellus hair count on the treatment side was significantly greater than the number subjects experiencing this level of response on the placebo side. They did not report how much hair growth increased compared with placebo. With even a small response to the drug, or random noise, it is easy to find a threshold that magnifies the significance of it. The difference between treatment and placebo could be only one percent and you could still potentially identify a threshold at which the number of subjects experiencing that extent of hair growth is significantly greater in the treatment group. Comparing responders on the treatment side to responders on the placebo side would be a more reliable comparison. We don’t know how many people responded on both sides, or from what baseline their hair counts increased. The lower the baseline reading, the less significant a 15% change becomes. Isolating responders for their comparison suggests that the treatment group as a whole did not demonstrate a significant change relative to placebo, and that even in responders there was a significant amount of hair growth on the placebo side. The press release teases a small signal that some subjects may have responded, while saying nothing of the magnitude or consistency of the response.

According to a new paper from Jiangnan University, the optimal HA molecular weight for hair growth is 268.1 kDa, demonstrating the most potent modulation for each growth factor and hair growth [3]. Medium-MW HA promotes hair growth via CD44-mediated ROS induction and phosphorylation of AKT, followed by stabilization of β-catenin. AKT stabilizes β-catenin by inactivating GSK-3, and facilitates nuclear entry via direct phosphorylation of β-catenin at ser552 [4]. However, priming of β-catenin by phosphorylation at ser45 by the destruction complex is required before GSK-3 can phosphorylate it. GSK-3-mediated regulation of β-catenin is largely AKT-independent, so the effect on Wnt signaling is more limited than canonical Wnt activation and insufficient to activate LEF1 in the absence of Wnt ligands [5]. All forms of HA stimulated VEGF in vitro and in vivo, while also inhibiting TGF-β1. Medium- and high-MW HA also markedly increased ALP and DPC migration in vitro. This suggests it has potential to extend anagen with repeated treatments, but the dermal papilla is already under oxidative stress. HA-mediated ROS generation was transient in vitro; however, the authors still caution that application of HA in such conditions may be inappropriate. Upregulation of ROS and β-catenin was more modest for High-MW HA. Pretreatment with NAC prevents ROS and β-catenin upregulation, indicating that β-catenin upregulation is dependent on ROS induction. AKT inhibition abrogated ROS generation. Taken together, the results suggest that CD44 activates AKT, while AKT-mediated ROS stabilizes its activity, thereby potentiating Wnt activation via inhibition of GSK-3 and/or direct targeting of β-catenin. Functional experiments were only performed in DP cells in vitro, while transcriptomic analysis was performed on whole mouse skin [3]. The functional location for the anagen-inducing effect of osteopontin-CD44 in vivo is in epithelial cells, but it may mirror the same regulatory network as HA, since transient ROS induction activates HFSCs [6][7].

Effects of hyaluronic acid on AKT and CD44 in human DP cells. I+II = low-MW, III= medium-MW, IV = High-MW

Effects of HA on growth factors in human DPCs in vitro

Downregulation of AKT doesn’t appear to be a contributing factor to Wnt suppression in AGA. Phosphorylated AKT and SGK1 are upregulated in bald dermal papilla cells, possibly to compensate for Wnt downregulation [8][9]. It fails to fully compensate, and it may exacerbate DPC stress.

Protein levels of TGF-β1 in bald and non-bald follicles. Activated Smad2 and Akt in bald and non-bald DPCs

In mice, medium-MW HA stimulated hair growth more robustly than other molecular weights, with earlier anagen induction, longer length, and the largest hair diameter. The amount of hair growth observed correlated with β-catenin expression in mouse skin. Measurements were taken at day 14 when treated follicles were in full anagen VI, but control follicles had only just begun entering anagen. Thus, the HF diameter increase may not meaningful. All treatments also markedly increased IGF1, and modestly inhibited BMP4 in mouse skin. Regulation of VEGF and TGF-β1 were also validated in vivo [3].

Stimulation of hair growth in mice with hyaluronic acid

Amplifica has a second CD44-based treatment in the preclinical stage [10]. AMP-203 is confirmed to be osteopontin, so AMP-203/AMP-506 might be osteopontin combined with HA and a third CD44 ligand, which could be serglycin or IGFBP4 based on their patents [11][12].

Amplifica identified this pathway by investigating transcriptional alterations in hairy moles to isolate proteins that might drive ectopic hair growth [6]. While the approach is intriguing, caution is needed when interpreting results. Body hair follicles are fundamentally different from scalp hair follicles. That which promotes body hair growth won’t necessarily promote hair growth on the scalp or in AGA. This is most obvious when observing the opposing effects of DHT and estrogen between the two regions. DHT is trichogenic in body hair, promoting vellus-to-terminal conversion, while on the scalp it promotes terminal-to-vellus conversion. DHT might even promote body hair growth via some of the same mechanisms that Amplifica has discovered. It’s possible that some trichogenic transcriptional targets of DHT in body hair have the inverse effect on scalp hair due to differential accessibility/availability of downstream effectors, or a weaker stress response [13].

The response to 17β-Estradiol is the inverse of that to DHT. It’s the most potent known stimulator of vellus-to-terminal conversion in frontal hair follicles, yet it retards body hair growth. Interestingly, osteopontin is the second most downregulated gene in male frontotemporal human follicles treated with 17β-Estradiol ex vivo. It’s possible that the observed downregulation is the result of negative feedback from upregulation of its CD44 receptor, but that would also suggest that supplementation of the ligand is insufficient.

Downregulation of osteopontin in frontotemporal human hair follicles by estrogen

Osteopontin is upregulated near the bulge in hairy moles, and knockout abrogates the precocious anagen phenotype in mice. Knockout also reduces wound-induced hair neogenesis, suggesting osteopontin might be useful for WIHN. The same phenotypes are observed in CD44 knockout, and in conditional mice treated with osteopontin, indicating that the effects of osteopontin on hair growth are mediated by epithelial CD44 [6].

Anagen progression depends on bidirectional signaling between the DP and epithelial cells. Osteopontin may enhance epithelial cell activation, which in turn enhances DP signaling, but if that DP signaling is resistant to activation in AGA, the effect would be limited. CD34+ cells were not compromised by CD44 knockout in mice [6]. This is an important epithelial cell population that’s depleted in AGA and dependent on DP signaling [14]. Osteopontin also promoted anagen entry in human occipital hair follicles grafted onto mice. It likely does the same in frontal hair follicles, but the more important question is how long it can prolong anagen in these follicles, and it’s doubtful that it can meaningfully increase hair diameter.

Follicum previously trialed an osteopontin fragment that is mutated to prevent binding of integrins while retaining its hair growth promoting ability. In preclinical testing it demonstrated a stronger effect in vivo than natural osteopontin [15]. The company published modest results from their clinical trial in 2020. After 3 months, the total hair count increased by 1.08/cm² vs placebo, while total anagen hairs increased by 8.16/cm² vs placebo [16].

AMP-601 is the last drug in Amplifica’s pipeline; it’s SCUBE3. Its function depends on whether it is secreted or membrane bound. UCI shows that it’s secreted from the DP to activate TGF-β receptors in epithelial cells, and that TGF-β inhibition abolishes SCUBE3-induced hair growth effects [17]. Presumably, it relieves the SMAD1-mediated quiescence program in HFSCs, which would trigger anagen but not reverse miniaturization [18]. Genetic studies suggest a causal role for TGF-β in AGA [19], but it appears to be overactivation in the DP driving it [8]. SCUBE3-null mice experience only a modest delay in anagen entry, with no other reported hair growth defects. Since TGF-β is a potent catagen-promoting factor upregulated by DHT, this seems less promising than HA, which inhibits TGF-β1 [3]. While not demonstrated by UCI, SCUBE proteins also facilitate Hedgehog activation by acting as chaperones for Shh, transporting it from the producing cell to the target cell [20]. SCUBE3 is likely a safer method of potentiating Hedgehog activity than activating Hedgehog with a smoothened agonist because its capacity to activate the pathway is rate-limited by Shh transcription. It’s also unlikely to significantly alter pathway activation in AGA.

23M with androgenetic hair loss. I'm researching RU58841 and would like to hear from people who have actually used it.

For those currently using RU58841:

• How long have you been using it?

• Are you using it alone or with finasteride/minoxidil?

• Did you notice reduced shedding or regrowth?

• Have you experienced any side effects?

• Has anyone used it for 1+ year?

I'm particularly interested in long-term experiences and side effects, rather than asking whether I should use it.

I'll add my scalp photos/current routine below for context.

Very disappointing, but expected. Gave it 12 months but all signs point to scam. Avoid the gray market fellas. Real minoxidil liquid is dirt cheap, safe, and works. https://www.hairrestorationnetwork.com/topic/78323-my-honest-review-of-folligenz-10-liposomal-minoxidil-sulfate/

Hey I am on finasteride never visited dermatologist!

How to find out if I have any side effects?

Hey! I’m going through menopause, and have been losing tons of hair for a few years. I had an ablation several months ago and the 14 day Holter monitor test + my Apple watch haven’t noted a single episode of Afib since the ablation.

Is anyone here on Rogaine for hair loss? Is it helping you?

Seen a lot of people who seem to vouch for RU, I recently started a couple weeks ago so to soon to tell if it is having any impact.

I am wondering though, is it actually effective, can it really stop MPB and lead to some regrowth. I've seen a lot of people saying it can and some impressive pictures but would love some more insight.

Has anyone found Liposomal/Encapsulated AHK CU... I've looked everywhere but I can't seem to find anywhere that sells this... Any clues ?

I started taking finasteride on January 2025. I remember taking 1mg once every 3 days considering all the sides I heard about. By March-April, I was having stomach issues, where after 7-8 hours of taking the pill i had extreme stomach pain and had diarrhea.

By July, I pinpointed it to being the drug causing it, figured it was a secondary ingredient causing this, and asked my pharmacy for a brand switch (to Sandoz). I started taking Sandoz and had 0 side effects! Everything was great taking it once a day for 8-9 months until April 2026. That’s when I started regetting the same sides as I was back with the first brand. One thing I noticed was that the April batch had changed the packaging and colour, which might have meant that they changed the inactive ingredient in the pill. After trying to take it for another few days, I had to stop taking it.

Flash forward to June, I switched brands again to PMS, but instead of getting 30 pills, tried with a sample of 7 to see if I react to it. I was able to take it once a day for 7 days, and ordered the full 30 pack. When I started taking the 30, by the 7th or 8th pill, I started to get the same side effects again, this time a bit later. I had to stop, and switched brands again. I wasn’t able to take more than 1 pill in that other brand, as I had the same sides.

Flash forward to now, I stopped taking fin for a bit and my stomach still feels weird and not completely healed. I find I am a lot more sensitive to lactose and caffeine now. Not sure how this happened, and why I was able to sustain finasteride for 9 months straight. Wondering if anyone had similar experience and what you might suggest

Basically I have been taking dut since the last 3 months to no avail. I think I'm seeing even worse hairloss now . Should I add 1mg fin ?

Hello lovely people- finasteride is a complete no go for me.

What are some alternatives I try that has some success PP405 from every chem? Clasterone?

Let me know I’ll try anything at this point…help a brother out