I’m currently at somewhere between NW1-NW1.5.
I’m 33yo and my father is bald. My hair loss is not very noticeable to others but I know it’s gotten thinner/recessed a bit over the past few years, especially since starting “TRT” (200mg/week) and blasting occasionally (375mg/week).

Just wanted to share my protocol, will report back in a few months;

1mg oral finasteride daily. Avoiding minoxidil for my first year because when I tried topical fin/min a few years ago it caused an aggressive shed that scared me and led me to discontinue treatment.

6iu HGH daily
I notice this makes my hair and nails grow really fast. I also think it could also help negate some of the potential side effects from the finasteride as my body adjusts to it.

4mg GHK-CU daily
I’m gonna cycle this, but on this protocol for the next 8weeks). I’m aware this doesn’t stop MPB but it does extend the anagen phase of hair follicles and I think it could be helpful paired with finasteride.

1mg BPC-157 daily (500mcg AM/PM)
I know this isn’t great for hair loss, but it has a synergistic effect with HGH upregulating growth hormone receptors at mRNA and protein levels, which I think could be helpful for hair growth.

500mcg KPV daily
From what I’ve read this could help with scalp inflammation, helping me to avoid extreme sheds.

2 capsules Biotin/Collagen/Keratin vitamin (nutraharmony vitamin, also has nettles, grape seed extract, etc….)
I know hair vitamins do nothing to stop balding, but I think they could help speed up potential regrowth from the finasteride.

2% ketoconazole shampoo 2-3x/week

4.5mg Low-Dose Naltrexone daily
I take this to manage a chronic illness but I’ve heard it can be helpful with hair loss so thought I’d add it.

To further reduce scalp DHT and soothe inflammation

I’ve been so freaked out by the horror stories about DHT blockers that I’ve put off treatment for years. I’ve decided to approach it with a positive attitude, an aggressive holistic protocol, and enjoy the journey :) I have high hopes that, as my hair is still pretty decent, within a couple years I could have better hair than I did in my early 20s.

Ranking of the most promising future approaches, based on a deep dive AI analysis:

1. PP405 — most promising “regenerative” candidate

If I had to pick the most exciting possible breakthrough, it would be PP405. Its appeal is that it is not just another anti-androgen. It is designed to reactivate dormant hair-follicle stem cells and restart growth from follicles that are still present but inactive. In Pelage’s phase 2a trial, 78 men and women used PP405 or placebo for four weeks; it was well tolerated, no systemic absorption was detected, and at week eight, 31% of treated men with more advanced hair loss had a greater than 20% increase in hair density, versus 0% on placebo. Phase 3 studies were expected to begin in 2026. 

The caution: this is still early. The study was small, short, and exploratory for efficacy. So PP405 is the most “cure-like” conceptually, but not yet the most proven.

2. Clascoterone 5% — most promising near-market drug

Clascoterone 5% topical solution may be the most realistic near-term advance. It blocks DHT at the follicle’s androgen receptor without the same kind of systemic DHT suppression as oral finasteride or dutasteride. Cosmo reported phase 3 results in 1,465 men across two studies, with both hitting target-area hair-count endpoints; one showed a 5.39x relative improvement versus vehicle and the other 1.68x, with adverse events similar to vehicle. Regulatory submissions in the US and Europe were being prepared after 12-month safety follow-up. 

The caution: the headline “539% improvement” is a relative-to-placebo figure, not “five times more hair.” It is likely to be a useful anti-androgenic maintenance/regrowth drug, not a baldness cure.

3. AMP-303 — promising injectable, but less mature

AMP-303 is interesting because it is an intradermal injectable aimed at stimulating regrowth after a treatment cycle rather than requiring daily application. Amplifica reported a randomized, double-blind, placebo-controlled first-in-human trial in men aged 18–45 with AGA. It found AMP-303 was safe and well tolerated, and a statistically significant proportion of subjects had more than 15% increase in non-vellus hair count versus placebo at 60 days, and more than 10% at 150 days. 

The caution: this is still early and company-reported. It needs larger trials, peer-reviewed data, durability data, and clear comparison with minoxidil/finasteride.

4. Stem cells, exosomes, microRNA — scientifically exciting, clinically messy

Stem-cell and exosome approaches are biologically plausible because AGA involves follicular miniaturisation, dermal papilla dysfunction, and stem-cell dormancy. There are small human studies suggesting adipose-derived stem-cell extracts or conditioned media can improve density, and newer exosome/microRNA work is intriguing. But the field is not yet standardised: different clinics use different preparations, doses, sources, and protocols.

The fat-derived stem cells + ATP approach you mention is promising but still preclinical. A 2025 mouse-model study found that adipose-derived stem cells supplemented with ATP improved hair regrowth in a DHT-induced AGA model, especially in male mice. 

The caution: mouse hair regrowth is notoriously easier than human scalp regrowth. I would not yet put this above PP405, clascoterone, or AMP-303.

5. Near-infrared / low-level laser therapy — useful adjunct, not a cure

Low-level laser/light therapy has better evidence than many people assume. A 2024 systematic review/meta-analysis found significant increases in hair density in androgenetic alopecia patients after LLLT compared with placebo. 

The caution: benefits are usually modest and require ongoing use. I would view laser caps/combs as an adjunct to medical treatment, not a standalone cure.

6. Deoxyribose sugar — fascinating but very early

2-deoxy-D-ribose generated buzz because it stimulated hair regrowth in an animal model of androgenic alopecia. The hypothesis is that it may promote angiogenesis and follicular activity, somewhat overlapping with the vascular-growth logic of minoxidil.

The caution: it is animal-model evidence, not a validated human treatment. Cheap, clever, and worth watching, but nowhere near clinical readiness.

7. JAK inhibitors — powerful, but mostly for alopecia areata, not male pattern baldness

JAK inhibitors are a breakthrough for alopecia areata, an autoimmune hair-loss disease, not classic androgenetic baldness. The National Alopecia Areata Foundation lists FDA-approved JAK inhibitors including baricitinib, ritlecitinib, and deuruxolitinib for severe alopecia areata. 

The caution: unless a man has an autoimmune alopecia component, JAK inhibitors are not the logical treatment for male pattern baldness.

8. Immune-regulating microneedle patch — wrong disease target for most balding men

The microneedle patch that teaches T cells not to attack follicles is also aimed at alopecia areata, not androgenetic alopecia. MIT described it as a potential treatment for the autoimmune disease alopecia areata, using immune-regulating molecules to halt the autoimmune attack on follicles. 

Very promising for autoimmune hair loss; probably not central for male pattern baldness.

Bottom line

The most promising “cure-like” candidate is PP405, because it aims to wake dormant follicle stem cells rather than merely slow DHT damage.

The most promising near-term approved-drug candidate is clascoterone 5%, because it already has large phase 3 male AGA data and a clean topical anti-androgen rationale.

The most practical current strategy remains: stabilise DHT damage with finasteride/dutasteride or future clascoterone, stimulate growth with minoxidil or future PP405/AMP-303, and use transplantation where follicles are already gone. A real cure will probably be a combination protocol, not one magic molecule.

The key thing is that the “cure” probably won’t be one thing. It will likely be a stack: something to stop androgen-driven miniaturisation, something to wake dormant follicles, and eventually something regenerative or transplant-like for areas where follicles are truly gone. PP405 is the one I’d watch most closely.

Has anyone tried ketoconazole solution or cream on the scalp? I know a lot of people try the shampoo, but that only stays on your scalp for 5 minutes. I’m looking for alternatives to 5ar inhibitors.

Just curious, is anyone in any of the veradermics phase 1, 2, or 3 trials on here, that is seeing results? It will be a game changer for me if it can work on nw5-7 people.

Thanks

Other than the patent readings that claim 46% of men had a visible effect and consistent regrowth in woman up to a “striking” degree is there any anecdotes or newer information? The only guy i can find that consistently used it was Derek from more plates but his hair is near pristine anyways so any percent change is minimal and he didn’t say how long he was on topical estrogens. One other even less informed anecdote from 2017.

What has me curious is how many biological males that take estrogens for hormone replacement claim estrogens have been anabolic for their hair, and also the plethora of examples of hair-loss recovery faster and more unexpected than with dut-min. It’s much easier to find nw6 men regrow the vast majority of their hair while on estrogen than with conventional androgenetic options.

I want to explain something that has been driving me insane.

We have been stuck with the same two treatments for decades. Finasteride, discovered by accident, lowers DHT and minoxidil, discovered by accident, grows hair through a mechanism we still don't fully understand. Both require lifelong use. Neither addresses the root cause. One messes with your systemic hormones while the other stops working the moment you quit.

Why is this still the standard of care in 2026? The answer is not that the science is too hard. The answer it seems is nobody has funded the one experiment that would unlock a permanent solution.

I think this might make what I think clear.

The single most important fact about hair loss that nobody talks about.

Every bald man has hair follicles on the back of his head that are completely immune to DHT. These follicles never miniaturize. They never fall out. They keep growing thick terminal hair until the day you die. We know this for a fact because hair transplant surgeons move these follicles to the top of the scalp and they just keep growing. They do not need finasteride to survive. They are naturally resistant. This means the cure for hair loss already exists on your own head. The resistant follicles have the same DNA as your bald follicles. Same genes, same person and same blood supply. The difference is entirely epigenetic. The resistant follicle reads the genome one way. The susceptible follicle reads it differently. Same book, different chapter.

If that is true, and it is, then the cure is not a drug you take forever. The cure must be a treatment that changes how your susceptible follicles read their own DNA. You flip them from the susceptible program to the resistant program. You do it once. The change is stable because epigenetic states are heritable across cell divisions. The follicle now reads DHT the way your donor area reads DHT. It ignores it.

Every technology to do this already exists.

This is not science fiction because every component required has been demonstrated.

Single-cell ATAC-seq can map exactly which genes are open and closed in individual cells. We can take a resistant follicle and a susceptible follicle from the same person and see every molecular difference between them. The technology has existed for years but it costs a few thousand dollars per sample.

Once you have that map, someone (maybe an AI model trained to do this) can identify the smallest number of changes needed to flip a susceptible cell into a resistant one. Which transcription factors need to be turned on. Which need to be silenced. This is causal inference on a regulatory network. The same computational tools already do this for cancer drug discovery. Nanoparticles in the 300 to 600 nanometer range naturally accumulate in hair follicles when applied topically. This has been demonstrated in multiple studies. You do not need to inject anything because you rub it on. The particles fall into the follicle opening and reach the dermal papilla at the base. We can load those particles with mRNA to turn on specific genes and siRNA to turn off specific genes. mRNA and siRNA therapies are already in clinical use. Lipid nanoparticles have established safety profiles from the COVID vaccines and cancer therapies.

So what is missing?

I believe a comprehensive single-cell comparison of resistant occipital follicles versus susceptible vertex follicles from the same individuals across a meaningful cohort. Roughly fifty men. Two small punch biopsies each. Single-cell ATAC-seq and RNA-seq on the dermal papilla cells. This experiment would cost somewhere in the low six figures. A few hundred thousand dollars which is pocket change compared to what gets spent on clinical trials for drugs that will never cure anything. Academic hair loss research has been trapped in the DHT suppression paradigm for thirty years.

What a permanent solution would actually look like.

You apply a topical formulation once. Maybe once a week for a month. The nanoparticles deliver a defined set of transcription factors and silencing RNAs to your dermal papilla cells. Over the course of a few weeks, the susceptible follicles shift their epigenetic state to match the resistant follicles on the back of your head. The change may be stable. Your follicles now read DHT the way your donor follicles read it. They stop miniaturizing, they recover over subsequent hair cycles and you do not need to keep applying anything. The cure is permanent because the epigenetic change is permanent.

For areas where follicles are completely gone, you would need a second component. Stem cell activation to wake up dormant miniaturized follicles, or cell therapy to repopulate empty sites. But for the majority of men who still have hair, however thin, the reprogramming alone would halt loss and recover significant density.

Why am I posting this here?

I want someone to explain why this hasn't been done, not why it might not work. We can argue about the specific transcription factors and delivery efficiency. That is what experiments are for. I want to know why the one experiment that would answer those questions has never been funded. Is there a technical barrier I am missing? Is someone already doing this and I haven't found it? Or is this genuinely a case where a solvable problem remains unsolved because the incentives of the research ecosystem do not align with solving it?

If you work in biotech, if you are a researcher, if you know someone who knows someone, tell me why this is not already underway. Because from where I stand, the science is done. The tools exist. The bottleneck is a single publicly available dataset that would cost less than a McMansion in the Bay Area. That cannot be the reason we are all still rubbing minoxidil on our heads and hoping for the best.

So I wanted to make a more detailed post about Finasteride and Dutasteride induced insomnia since I feel like this is a common topic which however does not get sufficient recognition in the hairloss community and it has become somewhat of a taboo to talk about side effects.

However this poses a real problem for many people trying to take Finasteride or Dutasteride in order to save their precious hair or for those who maybe have to take it because of an enlarged prostate.

I am in no way claiming that Finasteride or Dutasteride "ruined my life", are unsafe drugs or cause permanent side effects.

Since Finastaride and Dutasteride are the only current serious long-term treatment options for male-pattern baldness, there are many people on treatment that are still trying to make it work for them. So this post is supposed to eventually help people that are struggling with this specific side-effect but still want to stay on treatment to maintain their hair until the next generation of hairloss treatments arrives.

Is this even a real side effect?

When posting about this people often argue that it's nocebo, the issue might be caused by another health issue and would in no way be related to hairloss drugs, or that since it has not been mentioned in most of existing scientific literature about those drugs it's likely not a real issue. I beg to differ.

I was not able to find any study on Finasteride or Dutasteride that mentions insomnia or disrupted sleep as a side effect. However it has been commonly reported on online-forums like hairloss talk or here on reddit. Some posts even date back to the year 2005.

Also according to the data of the FEARS-database Finasteride ranks in the top 5 drugs by ROR for Insomnia. ROR meaning reporting odds ratio, a metric that is being used for drug safety monitoring.

Another possible reason that might made it harder for Finasteride to be associated with Insomnia as side-effect is that this side-effect does not necessarily occur immediately after starting the drug. It might just appear after several months, maybe after Finasteride reached a steady state level. As an example I really like the post made by u/Swimming-College6384 who uploaded his sleep data of his Garmin Fenix, although I would not like to agree on his hypothesis of the cause.

Sleep related side-effects that are being reported

• Trouble falling asleep
• Trouble staying asleep
• Sleep fragmentation
• Worse subjective sleep quality
• Lacking tiredness in the evening, no yawning for example (personal experience)

What might be the cause? (Disclaimer: AI-slopped hypothesis)

Often when looking up the topic people or ai-slop point towards neurosteroids. However I would rather argue that cortisol plays a significant role in the insomnia caused by Finasteride and Dutasteride. Often users report awakening after just 2-6 hours of sleep, while not being able to fall back asleep. My hypothesis is that the cause of this could be that their cortisol levels might elevate too early during the night due to 5ar inhibition.

Slop graphic for normal Cicardian-Rythm

As illustrated for a normal circadian rhythm cortisol rises during the night and gives the body a wake-up signal in the morning.

Apparently there is a process called A-ring reduction taking place in the liver that involves 5alpha-reductase. This metabolic process is partially also responsible for reducing active cortisol to an inactive metabolite. A possible explanation could be that there are a subset of people that take 5alpha-reductase inhibitor drugs, who can't properly compensate for this inhibition and thus have reduced cortisol clearance. As a consequence cortisol becomes elevated in their system as 5ar-inhibition rises over time and eventually reaches a steady state.

This could lead to cortisol rising earlier than normal during sleep and staying elevated during the day. Therefore explaining why people experience waking up earlier without being able to fall back asleep and the other mentioned sleep related effects.

My personal experience

I personally have been taking Finasteride for about 3 years on dosages ranging from 1mg daily to 0.25mg daily and last October I swapped to 0.5mg Dutasteride every other day. I am a young healthy male without prior history of sleep or mental health issues, a healthy and active lifestyle and I take my sleep hygiene very seriously. Obviously I tried to determine that Finasteride actually is the cause of my sleep issues by stopping the drug for a short amount of time with a noticeable improvement of my sleep quality. Also lowering the dosage from 1 mg a day to 0.25mg a day helped me. I was able to get 8 hours of often fragmented sleep on 0.25mg while just being able to sleep for 3-5 hours on 1mg of Finasteride. As already mentioned prior in my case I also noticed a gradual worsening of my sleep issues over time.

Another thing I noticed was that on Finasteride things that usually would not affect my sleep started to wreck it. Like working out late, eating meals later in the evening or having any sort of conflict before bed. Without proper sleep hygiene I wouldn't enjoy going to bed at all anymore.

Initially whenever starting higher doses of Finasteride or Dutasteride I felt a little more sluggish or groggy, which I would attribute to an altered testosterone to estrogen ratio which eventually normalizes over time. To avoid that I sometimes took the pill before bed to avoid that side effect. Over time however I had to start taking Finasteride in the morning in order to achieve better sleep. This may be explained by Finasteride before bed increasing inhibition of any replenished and yet uninhibited 5ar enzymes and a consequentially lower cortisol clearance than if one takes Finasteride in the morning.

Another observation I made which I could not really explain to myself at first was that whenever I was on vacation, although having to sleep in a bit noisier environment my sleep seemed of better quality than when I was sleeping at home.

Since swapping to Dutasteride I actually sleep better than I would on 1mg of Finasteride, although 6 Months might not be enough time to be able to to tell yet, since my sleep still could worsen in the future. Unfortunately I also feel like this observation may would contradict my hypothesis since Dutasteride is supposed to be a stronger 5ar type 2 inhibitor than Finasteride is.

Recently I started tracking my sleep data using sleep² with a polar h10 sensor in order to gain more insights about my sleep quality and how my behaviours and experiments affect my sleep quality. I have been experimenting with glycine and magnesium bisglycinate with mixed results.

Solution attempts

Ideas I explored or plan to explore further:

- Taking Pill in the morning
- Trying Dutasteride instead of Finasteride
- Taking a smaller dose (might not achieve desired hair outcome for everyone)
- Glycine / Magnesium bisglycinate
- l-theanin
- apigenin
- ashwaganda
- zinc

I'm looking forward to receiving your ideas and thoughts on the matter and would like to gather ideas to experiment with, in order to achieve better sleep quality while enjoying the benefits of Finasteride or Dutasteride. If my hypothesis was to be somewhat correct I would assume anything that could lower cortisol or increase cortisol clearance would be of benefit.

Thank you for reading!