Man applying topical SARMs for hair loss prevention

The Therapeutic Promise Of Topical SARMs For Hair Loss Prevention

After reviewing the molecular weight of some of the most promising SARMs developed, I theorized that they could potentially be prepared in a topical solution for hair loss prevention.

As you probably already know, Selective Androgen Receptor Modulators (SARMs) are a class of androgen receptor ligands that bind to androgen receptors and exert tissue selective anabolic effects with a relative lack of androgenicity when compared to traditional anabolic steroids.

The end goal of their continued development is more or less to create the ultimate anabolic agent that can completely offset tissue loss as a result of musculoskeletal degenerative diseases, with a complete absence of androgenic activity in the body.

While certain SARMs are closer to reaching this goal than others, the perfect SARM has yet to be developed.

However, that doesn't mean that the SARMs currently developed cannot be leveraged in some capacity for a variety of potential applications.

As alternatives to oral SARMs, topical SARMs may be a promising area of research in the fight against hair loss.

This article highlights the reasons why I believe there is such therapeutic promise in topical SARMs for hair loss prevention.

Role Of Androgens In Causing Hair Loss

Despite there being a cascade of events that lead to hair loss, the presence of too many androgens is ultimately what causes follicular miniaturization.

However, the effects of exogenous androgens on the human body will inevitably vary between individuals due to several dependant factors in this cascade.

As a rule of thumb, raising androgen levels via exogenous androgens will generally initiate or accelerate hair loss for someone who is hair loss prone.

Unfortunately, anabolic steroids will unavoidably bring along some degree of concurrent androgenic activity.

Our natural endogenously produced steroids are not an exception to this, and the androgen load in the body needs to be addressed in some capacity to attenuate, or even reverse hair loss.

Standard Treatments For Hair Loss: Finasteride And Dutasteride

Finasteride and Dutasteride are medications designed to treat hair loss by inhibiting the enzymatic process responsible for DHT production.

This means that they are not anti-androgens that bind to androgen receptors, but rather they prevent the body from converting testosterone into the much more androgenic metabolite dihydrotestosterone (DHT) by inhibiting the enzyme 5-alpha reductase.

A 5 mg dose of Finasteride per day will inhibit approximately 70 percent of the body's systemic DHT, in comparison to 0.5 mg Dutasteride; which inhibits 90 to 99 percent of the body's systemic DHT.

For most individuals, androgenic activity caused by DHT will be minimized after Dutasteride serum concentrations have peaked in the body, as there will simply be barely any DHT left.

However, even with a high dose of Dutasteride, scalp DHT levels may not be diminished enough to completely deprive the tissues of DHT, and there is a substantial concurrent spike in scalp testosterone levels as a result of the blockade created at 5-alpha reductase.

Not only is there potential for residual scalp DHT, but you if you rely on a 5-alpha reductase inhibitor as a form of hair loss prevention monotherapy you will still have a significant amount of testosterone unaccounted for in your body that still has its own inherent androgenic activity.

I've posted a video on this before, where I review my over one year long experiment with Dutasteride where I lowered my DHT to undetectable levels and increased my testosterone levels into borderline supraphysiological territory.

The inherent androgenicity of testosterone was still substantial enough to progress my androgenic alopecia.

In fact, I still had all the characteristics of androgenic activity:

  • facial hair growth
  • body hair growth (albeit notably reduced, which is to be expected)
  • high libido
  • morning wood and good erectile quality
  • hair loss

In contrast to 5-alpha reductase inhibitors, a compound that reduces androgenic activity in the scalp by effectively targeting the androgen receptors would be more efficacious in staving off further hair loss progression.

This is what prompted the development of anti-androgens.

Transgender Hormone Therapy (Male-To-Female) For Hair Loss Prevention

During the process of male-to-female gender transitioning, one of the first things doctors would do is prescribe estrogen or an estrogen analog to crush endogenous testosterone levels while increasing feminine hormones.

They may also introduce anti-androgens to the protocol to further reduce the amount of androgenic activity in the body.

One of the side effects of gender transitioning via anti-androgen and estrogen therapy is significant scalp hair regrowth, and complete reversal in even some of the most extreme cases.

In some instances, men with nearly slick bald heads have grown back pre-puberty heads of hair via this kind of protocol.

While this is clearly the most extreme method of reversing androgenic alopecia, you can't argue with the results it produces in individuals who feel the risk/reward is worth it, or simply desire to become more feminine.

Certain non-steroidal anti-androgens that interact with androgen receptors are designed to compete with testosterone and DHT for androgen receptor binding, while other steroidal anti-androgens work through slightly different mechanisms, albeit still working around the biological target of endogenous androgens (the androgen receptor).

For the sake of not overcomplicating this section with too much scientific jargon, I'm going briefly summarize the pharmacodynamics of the two most commonly used anti-androgens in the hair loss prevention community, and elaborate on how SARMs may stack up to them.


Bicalutamide is a non-steroidal anti-androgen that is recognized for its affinity to androgen receptors, thus preventing testosterone and DHT from binding and transcribing their effects in tissues.

Bicalutamide is a highly selective competitive silent antagonist of the androgen receptor, and is often utilized in androgen deprivation protocols, both clinically and experimentally.

A common feature of pure anti-androgens, such as Hydroxyflutamide and Casodex (Bicalutamide), is their relatively weak binding affinity for the androgen receptor, 50–100 times less than that of Testosterone [R].

On paper, it doesn't seem like Bicalutamide would be very effective at preventing hair loss because of its weak binding affinity.

However, the typical prescribed dosages of Bicalutamide are high enough that so much of the drug gets into the system that it essentially overpowers testosterone and DHT for androgen receptor binding.

The logic behind this protocol is basically that the drug is poor at what it is designed to do, and for it to work it needs to be dosed extremely high until there is just so much of it circulating in the body that it overpowers testosterone and DHT by sheer volume.

The half-life of Bicalutamide is 5-10 days as well (depending on single vs. continuous dosing), consequently allowing serum concentrations of the drug to accumulate far more over time.

By creating a blockade of the androgen receptor, bicalutamide prevents the negative feedback androgens would normally create via the hypothalamic–pituitary–gonadal axis (HPG axis) in men.

As a result of this, luteinizing hormone (LH) spikes in the body as the body recognizes a need to produce more androgens.

After LH spikes, the gonads produce more testosterone, and more of that testosterone 5-alpha reduces into DHT, as well as aromatizes into estrogen.

150 mg Bicalutamide per day in men has shown to increase testosterone levels by 59-97%, increase estrogen levels by 65-146%, as well as increase DHT, SHBG and prolactin to a less significant degree.

This significant spike in estrogen will often lead to estrogenic side effects during Bicalutamide monotherapy.

Gynecomastia is a very common occurrence during Bicalutamide monotherapy.

Cyproterone Acetate

In contrast to the non-steroidal anti-androgen Bicalutamide, the steroidal anti-androgen Cyproterone acetate works by suppressing testosterone production directly, as well as competing for androgen receptors.

Cyproterone acetate is one of the first anti-androgens developed, but it is still one of the most effective to date for hair loss prevention.

With that being said, it has also shown to be one of the most side effect ridden compounds used for this purpose.

Cyproterone acetate was originally clinically deployed to “treat” hypersexuality and sexual deviation.

It was also used to delay precocious puberty.

When puberty begins before age 8 in girls and before age 9 in boys, it is considered “precocious puberty”.

As cyproterone acetate was used both in full grown men as well as pre-pubescent children, the conflicting findings in its pharmacodynamics have led to differing conclusions on how it works in the body, but for the sake of this article being about full grown men preventing hair loss, we will obviously be evaluating the clinical data on full grown men.

Cyproterone acetate causes a prompt drop in LH and FSH levels, and consequently a massive drop in testosterone levels.

In a study conducted on healthy male sexual offenders, dosing 50 mg cyproterone acetate twice daily caused testosterone levels to fall to subnormal levels within 1 week [R].

Eflect of cyproterone acetate on sexual oflenders - testosterone levels before and after taking cyproterone acetate

Cyproterone acetate has the highest anti-androgenic activity of any other clinically used progestin.

Despite it having a fairly weak binding affinity when compared to DHT and testosterone, Cyproterone acetate works similarly to Bicalutamide in that it accumulates during daily dosing because of its 1.6–4.3 day half-life, and also is dosed high enough clinically to increase serum concentrations high enough to a point whereby it can effectively compete for AR via sheer volume.

In addition, because Cyproterone acetate significantly reduces testosterone production (and by extension DHT production) via its progestogenic activity, there are less endogenous androgens for Cyproterone acetate to compete with for AR as it accumulates, consequently making it very effective at displacing androgens at AR and inducing systemic anti-androgen activity.

Cyproterone Acetate Vs. Bicalutamide

Steroidal anti-androgens have largely been replaced now by non-steroidal anti-androgens clinically, but cyproterone acetate and spironolactone are still commonly used in the management of feminizing hormone therapy.

Cyproterone acetate is more effective at reversing hair loss than Bicalutamide anecdotally, but also comes with a significantly elevated risk profile associated with its use.

Maintaining Masculinity Vs. Your Hair

While oral anti-androgens certainly work to reduce androgenic activity in the scalp, they also will often cause a variety of undesired side effects.

Aside from the actual health concerns in regards to hepatotoxicity, musculoskeletal degeneration, and more, the main thing we are going to focus on is the effect anti-androgens have on your literal manhood.

Expectedly, anti-androgens can cause feminization, loss of libido, erectile dysfunction, as well as muscle and bone loss.

Now, like I mentioned, non-steroidal anti-androgens like Bicalutamide are substantially better in this regard, whereby they will not cause musculoskeletal degeneration, will maintain relatively normal sex hormone levels, and do not have many of the drawbacks of steroidal anti-androgens [R].

However, that doesn't mean that they are ideal, as they can still throw off the balance of androgens to estrogens in the body and prevent you from improving your body composition.

Anything inhibiting testosterone from binding to androgen receptors in muscle and bone and transcribing anabolic effects will get in the way of your body composition goals at the end of the day.

Inhibiting DHT and testosterone from binding to androgen receptors systemically will also impede countless physiologic processes that are facilitated via endogenous androgens in the body.

This isn't a flaw of the drug necessarily, as it is doing exactly what it was designed to do.

However, androgen deprivation does not complement most of our goals as men, nor does it complement our health and quality of life.

We want androgen deprivation in the scalp only, with no alteration of our systemic hormones or health markers.

Obviously this is easier said than done, or else we would already have a topical anti-androgen available that stays localized, has a higher binding affinity than DHT, and has no systemic absorption.

This compound does not exist, so we have to make do with our current pharmacology and understanding of pharmacodynamics.

Oral Anti-Androgens Vs. Topical Anti-Androgens

Many would question why we don't just use Cyproterone acetate or Bicalutamide topically to achieve this.

The reason why these fall short as topical treatments essentially boils down to the fact that their binding affinity is poor, and their success as anti-androgens is largely achieved via their accumulation in the body systemically.

When it comes to topical treatments, we don't want something with a week long half-life, as it will start to accumulate in the body and cause systemic anti-androgen effects.

The ideal compound would be something that has a short half-life, a high binding affinity for androgen receptors, and acts as a highly selective competitive silent antagonist in the scalp exclusively.

The closest we have come to this so far is RU58841, with CB-03-01 showing therapeutic promise as well despite having a much lower binding affinity.

A compound that does not convert to deleterious metabolites systemically is also advantageous, as there will unavoidably be some level of systemic absorption with any molecule that is small enough to penetrate the stratum corneum after topical application.

While current topical anti-androgens commercially available do work for some individuals, there are limitations to each which I have delved into before.

There is no perfect treatment at the moment, but in this article I elaborate on something I feel is worth further exploration when it comes to creating a strong localized androgen receptor blockade with as minimal of a systemic impact as possible.

How Anti-Androgens Are Related To SARMs For Hair Loss

At the end of the day, how does this all intertwine with SARMs?

The bodybuilding community, the hair loss prevention community, and the research between them actually intersects in many ways that are commonly overlooked.

I first realized the therapeutic promise of SARMs in a hair loss prevention capacity when I saw someone stop their hair loss cold turkey with the SARM S4 and exogenous Estradiol.

What many don't realize is that non-steroidal SARMs like S4 were synthesized using the chemical structure of traditional anti-androgens like Bicalutamide as their backbone.

The most promising SARMs exhibit binding affinities several times higher than these anti-androgens, and I feel are an extremely promising area of untapped research for hair loss prevention.

Chemical structures of hydroxyflutamide, bicalutamide, aryl proprionamide ligands.

Some SARMs at certain dosages have shown to be as anti-androgenic as compounds like Bicalutamide and Hydroxyflutamide, more anti-androgenic than Finasteride, but with the benefit of actual tissue selective anabolic activity in muscle and bone.

Basically, some SARMs can prevent hair loss better than Finasteride, as well as traditional anti-androgens, all while allowing supraphysiological muscle growth.

The reason this is possible is that most SARMs have much higher binding affinities than traditional anti-androgens and can be far more effective at competing with endogenous androgens for AR binding and activation.

In addition, because they are tissue selective, once they bind to androgen receptors, they induce anabolic activity in muscle and bone with a relative lack of androgenicity in other tissues like the prostate and scalp.

I detail how this works further in one of my older articles called “Do SARMs Cause Hair Loss? | Can SARMs Prevent Hair Loss“.

Oral SARMs also lower SHBG and can have a suppressive effect on endogenous androgen production at high enough dosages (and even low dosages with some SARMs).

Through this suppression, SARMs can lower the androgen load in the body even further.

With long-term use, certain SARMs may suppress endogenous testosterone production enough that the use of estrogen alongside the SARM becomes a necessity if aromatization is no longer satisfactory to maintain healthy estradiol levels.

This presents an interesting scenario whereby androgen levels can be crushed to nearly undetectable levels via a non-steroidal SARM, and the additional negative feedback provided by the exogenous estradiol being added to the protocol to maintain therapeutic estrogen levels.

The end result of this is essentially a heavy duty anti-androgen protocol that can maintain significantly more muscle mass than what is possible via traditional androgen deprivation therapy.

However, oral SARMs obviously have their limitations as suppression of endogenous androgens is going to result in decreased libido, drive, and overall masculinity.

While many who use traditional anti-androgens don't care about this as they simply want the most efficacious way to nuke their hair loss, there are going to be many individuals who want to minimize the systemic impact of any treatment they deploy to keep their hair.

This is where I believe there is therapeutic promise in topical SARMs.

Difference Between Topical SARMs For Hair Loss And Topical Anti-Androgens

SARMs and anti-androgens are both effective at inhibiting gene transcription via androgen receptor competition.

By competing against endogenous androgens for androgen receptor binding, topical anti-androgens like RU58841 and CB-03-01 are effective at preventing hair loss completely for some individuals with mild hair loss, and moderately effective at providing at least a decent foundation of protection for some individuals with more aggressive hair loss.

One limitation of topical anti-androgens is that they work in a dose-dependent manner, but can wreak havoc if they get systemic.

As I showed earlier with Bicalutamide, the higher volume of drug present, the more difficult it is for testosterone and DHT to bind to vacant androgen receptors.

With anti-androgens its not as simple as increasing the dose until it works though, as topical solutions will go systemic to some extent, and the more drug you introduce to your system, the more anti-androgen activity you will get systemically.

For someone with aggressive hair loss, chasing the volume approach with topical anti-androgens to overwhelm the endogenous androgens present in the scalp may lead to significant systemic side effects before adequate androgen receptor competition to prevent hair loss is even achieved.

SARMs on the other hand will have a negligible impact on endogenous androgen production when trickling into the system in trace amounts, and will not induce anti-androgen activity in muscle and bone even if a substantial amount of it does get into the bloodstream.

SARMs Anti-Androgens
Comparable Binding Affinity To Testosterone For Androgen Receptors SOME SOME
Transcription Of Anabolic Affects YES NO
Transcription Of Androgenic Affects MINIMIZED NO
Side Effects To Systemic Introduction MINOR MAJOR

How SARMs May Complement Finasteride Or Dutasteride

As DHT has a binding affinity higher than all SARMs, and significantly higher than all anti-androgens, if sufficient AR competition could not be achieved locally via a SARM or anti-androgen to stave off androgenic alopecia, then a 5-alpha reductase inhibitor could then be looked at as a potential adjunct treatment to use concurrently.

By dropping systemic DHT levels via 5-alpha reductase inhibition, competing for AR becomes significantly easier for us as we have compounds at our disposal that are actually comparable to testosterone in binding affinity.

The 500 Dalton Rule For The Skin Penetration Of Chemical Compounds And Drugs

The molecular weight of a compound must be under 500 Dalton to allow skin absorption [R].

Larger molecules cannot pass the corneal layer.

The Dalton is used as a unit of molar mass, especially in biochemistry.

1 Da (dalton) = 1 g/mol.

The Most Promising SARMs For Hair Loss Prevention

Taking S4 (Andarine) as an example, you can see that the molecular weight is 441.4 g/mol [R].

Because S4 has a molecular weight of 441.4 daltons, it can pass the corneal layer and work to some extent topically.

I'm using S4 as an example simply because it seems to be the most hair safe SARM of all to date via oral administration, and is also the only SARM I have seen used topically so far.

It is also the only SARM I've seen used orally in conjunction with exogenous estradiol for over a year straight so far with great success and no notable deleterious effects to liver enzymes or other health markers that are commonly impaired with high dosages of oral SARMs.

With that being said, S4 isn't without its potential issues itself.

SARMs are still uncharted waters, but there are several that have been well tolerated in a clinical setting at dosages several times higher than what we would be using for hair loss prevention, or even for muscle growth in a bodybuilding context in a few token scenarios.

While S4 has shown to be the most promising SARM in a hair loss prevention context to date, I am confident that other alternatives with improved binding affinities, high tissue selectivity, and high tolerability clinically in actual human subjects would likely result in similar positive outcomes if the dosing was nailed down.

For example, LGD-4033 has a molecular weight of 338.25 daltons and has shown to be well tolerated in humans at dosages as high as 22 mg per day orally [R].

It has also binds to the androgen receptor with an extremely high affinity (Ki of ~1 nM), which is superior to every other SARM tested on humans with comparable tissue selectivity.

In addition, a preclinical rodent model showed that it has greater than 500-fold selectivity of muscle tissue to prostate when compared to testosterone.

LGD-4033 Selectivity For Muscle To Prostate Compared To Testosterone
LGD-4033 Selectivity For Muscle To Prostate Compared To Testosterone

A greater than 500:1 anabolic to androgenic selectivity would make LGD-4033 the most tissue selective SARM to date.

However, in practical application, LGD-4033 seems several times more androgenic than S4, although it is also several times more anabolic milligram for milligram.

Some individuals even report hair loss with LGD-4033 use.

Context is key here though, as the individuals reporting hair loss are using dosages 10x higher than the dosage being evaluated in humans clinically, and it is not clear whether this is telogen effluvium or actual androgenic alopecia progression even in these mega-dosing cases.

This is what I mean by the dosing needs to be nailed down with these compounds, as haphazard overdosing could easily lead to unexpected androgenic activity, or induce telogen effluvium via a significant shift in endogenous hormones.

There is no SARM that is completely devoid of androgenic activity, so dose response needs to be carefully assessed when experimentation is done with these compounds.

Anabolism as a Systemic Effect of Topical SARMs for Hair Loss

One of the limitations of anti-androgens is that when they go systemic they can induce anti-androgenic activity in other tissues.

SARMs on the other hand bind to androgen receptors and induce tissue selective anabolic activity.

So, the theory here is that we can potentially use a lower dose of a SARM topically than we would need with an anti-androgen, and achieve a substantial anti-androgenic effect via a much lower dosage, and even if it were to go systemic to some extent, then the worst that happens is we get some anabolic activity in muscle and bone.

In theory, it sounds great, but SARMs will still suppress endogenous androgen production to some extent, lower SHBG, and potentially induce some hepatic stress when systemic.

However, the degree to which this occurs should be much lower than what occurs with traditional anti-androgens.

This is all theoretical at the end of the day, as SARMs may not even compete for AR activation in the scalp.

However, anecdotally via oral administration it seems fairly obvious that they do in all tissues in the body, despite having “selective” action.

If a topical anti-androgen works, then a topical SARM should work in a similar way.

SARMs are essentially just chemically modified anti-androgens with better binding affinity and anabolic activity after all.

Efficacy Profile Of Topical SARMs For Men Wanting To Retain Masculinity

For many men, hair is a huge part of their identity and plays a massive role in looking good.

Unfortunately, we've been put in a position biologically where the more androgens in our body, the more expedited our hair loss progression will be, and all effective anabolic agents have some level of androgenicity.

So, in a perfect world, we would be able to utilize SARMs (or something like SARMs) to selectively occupy androgen receptors in the scalp, and leave the rest of the body alone.

Topical SARMs For Hair Loss Prevention: A Viable Long-term Strategy?

While SARMs are still very new, there are already SARMs with comparable binding affinities to testosterone that have shown to have no virilizing effects in women at fairly high dosages orally.

Topically, we may be able to achieve more localized action on androgen receptors and minimize the systemic impact in the body.

I believe there are better ways to manage hair loss than blindly crushing androgen levels with primitive medications.

SARMs may or may not be the answer, but they are certainly a step forward and could very likely be used effectively as a form of monotherapy in some users, or as an adjunct treatment alongside tried and true compounds that do a significant amount of the heavy lifting, and then let a SARM clean up the mess leftover.

Are SARMs perfect?

No, they aren't.

However, some of the SARMs currently developed may already have more therapeutic promise for some individuals than traditional anti-androgens used for hair loss prevention.

At the very least, they are worth exploring more in this context, and I believe are potentially a more progressive way to go about handling excessive androgenic activity via AR activation in the scalp.

In addition, injectable SARMs are a new area I'm researching that may also have therapeutic promise as well.

How To Create A Topical SARM

The ideal scenario would be that we mix a SARM into a topical solution that has shown to not only be very tissue selective with a high binding affinity, but has also shown to be well-tolerated in humans in a clinical setting with no deleterious outcomes, and then apply that solution topically to bind locally to androgen receptors and compete with testosterone and DHT for AR activation.

Standard vehicles (the carrier solution you mix the compound in for topical application) should work similarly to anti-androgens.

My guess is that a 70% ethanol/30% propylene glycol vehicle would suffice.

A PEG 400 mixture may be a useful alternative vehicle for those with intolerance to propylene glycol, or those with vehicle-dependent contact allergy to SARMs in either propylene or hexylene glycol [R].

Adding a bit of DMSO or daily microneedling with a short length pretreatment may need to be incorporated for absorption for those with less permeable skin.

What concentration the solution should be remains up in the air and will need to be determined via experimentation.

Following the dosage outlines used in a therapeutic setting, we can get a well-tolerated starting point.

For example, with LGD-4033, orally it has a tissue selective anabolic effect at dosages as low as 0.1 mg per day, and has shown to be well-tolerated as high as 22 mg per day.

The most notable clinical trial on LGD-4033 utilized 0.5 mg, 1 mg and 2 mg orally for 12 weeks.

LGD-4033 exhibited encouraging safety and tolerability, and there were no drug-related serious adverse events in the study [R].

A good starting point would be 0.5 mg LGD-4033 per day topically, with the dosage titrated up accordingly based on dose-response.

The only SARM I've seen used topically to date is S4.

As S4 does not have any human data, we had to design the protocol based around anecdotal findings and extrapolated clinical data on rodent models.

Anecdotally, orally administered S4 does not induce night vision side effects until around 30-50 mg per day.

A topically administered dosage of 25 mg per day produced a very quick reduction in sebum in the scalp, which is a very obvious marker of reduced androgenic activity.

Scalp itch was also severely decreased, with no notable side effects.

Notably, the individual who I oversaw who did this experiment gets horrible side effects from every single hair loss prevention compound he has tried.

He's one of the unfortunate ones who gets brutal 5-alpha reductase inhibitor side effects, systemic anti-androgen side effects with topical anti-androgen use, and even severely impaired sleep with PGD2 inhibitors.

The fact that he had no issues with topical S4 was very promising, and piqued my interest in the area even more (which is partially what has led me to my current injectable SARMs experiment I am conducting on myself).

Does that mean this is a viable long-term strategy?

That remains to be seen with further experimentation.

To be clear, this is still a theoretical approach to topical hair loss prevention, and is geared mostly towards individuals who have experienced negative side effects with 5-alpha reductase inhibitors, RU58841 and CB-03-01.

Where To Buy SARMs

Most companies do not third party test their products, nor do they have any satisfactory level of quality control whatsoever.

I strongly advise that before you buy SARMs from a company online you thoroughly evaluate their track record, their third party test results, and how they are marketing their products in general.

These Are My Current Trusted/Go To Companies For Third Party Tested 99%+ Pure SARMs:

Science.bio – 10% off coupon code “DC10”

Chemyo – 10% off coupon code “DC10”

Amino Asylum – 20% off coupon code “DC20”

Swiss Chems – 25% off coupon code “DC25”

Disclaimer: The information included in this article is intended for entertainment and informational purposes only. It is not intended nor implied to be a substitute for professional medical advice. Prior to buying anything, check that it is compliant where you live with your current government laws.

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45 thoughts on “The Therapeutic Promise Of Topical SARMs For Hair Loss Prevention”

  1. Is the guy you mentioned, who was using topical S4, still running that? If so, please keep us up to date on the efficacy of this, and any side effects.

    I look forward to your further research in hair loss prevention.


        1. camille leprevost

          hey bro. did you tried topical sarm finally for hair loss ? if yes can you contact me by email. thanks for your help

      1. Derek, you are light years ahead of anyone on hair loss and hormones. Great job! Keep up the good work . I have severe issues with DHT inhibition. DHT has and Test has protective effect on nerves. Without it my sleep degrades and my sense of well being and immunes system goes down. Gonna try the s4 approach and see if it can be selective for the scalp

  2. Really interesting stuff thanks Derek, I notice Ostarine is also under that 500 g/mol at 389.33. I have a bunch of that laying around I may experiment with.

  3. Derek my man!, awesome video like usual, ok so If on my research subject I wanted to experiment with lgd because the molar mass is less than 500, would I be good to apply on the scalp as is if its oral lgd or would I still use a mix of 50ml of let’s say k and b solution? As far as adding in oral estrogen down the line one would just know if they started not feeling too good huh? And last question is when it comes to hair transplants the one thing I dont understand is that even if the back hairs are applied to the front, wont androgens reak havoc on those hairs too? Or those back hairs arent sensitive to androgens ?

    1. You shouldn’t need estrogen with topical SARMs. The goal is localized site specific anti-androgen activity with a topical SARM. Estrogen would be part of a makeshift HRT regimen for those who need to get very aggressive with their regimen on oral or injectable SARMs.

      1. So when applying to myresearch subject there is no need to mix it with a different solution to penetrate? The lgd-4033 in oral sarm form is set for application? Just looking for an effective plan b incase my first solution for my subjects hair doesnt work out.

    1. I’ve used topical Estrogens before (17β-estradiol as well as Estriol) and it made no difference at all. 17β-estradiol is much stronger than 17α-Estradiol.

  4. So when applying to myresearch subject there is no need to mix it with a different solution to penetrate? The lgd-4033 in oral sarm form is set for application? Just looking for an effective plan b incase my first solution for my subjects hair doesnt work out.

    1. I don’t know what vehicle you are using as is, but ideally you would want to get raw powder so then you can choose the vehicle you want. If one doesn’t work well, then microneedling can be done to increase absorption, or things like DMSO can be looked at to increase penetration.

      1. So solutions from chemyo arent ideal to just apply to the scalp since they are already in liquid form? Raw powder solutions are more ideal to topical administration for whichever sarms one decides to try out on their research experiment?

        1. Well first of all, they don’t use the same vehicle for every product (they detail their vehicles on the product pages). Second, the advantage to raw is that you can make your own vehicle based on your individual needs. That isn’t to say the vehicles they are using won’t work, but obviously the greatest flexibility comes from starting from scratch is all I’m saying.

  5. Hey Derek, you hypothesized that lgd 4033 at .5 mg would be a good place for a test rat to begin experiments at, do you not think that LGD is too tissue selective? In your opinion would lgd show the most promise in this application or is there another sarm with a lower side profile that you think holds more promise to run first. My rat is eager to test and run blood work and log/report findings and labs if you want to coordinate with me.

    1. As I’ve personally overseen someone with aggressive loss do well with S4, I would try that myself before LGD, but with that being said, LGD has actually been tested on humans in multiple trials orally at much higher dosages, so at the end of the day its up to you. Another guy testing out my theory just reported better results using topical S23 than RU58841, so we will likely get more insight as more reports come out. S23 is one of the most androgenic SARMs, but it has one of the highest binding affinities, so a lot of this will likely come down to individual response and dosage.

      1. Could you tell me what dosage of S23 did he use and was he on gear or not? How bad was his balding? Had he tried anything prior? Thanks Derek for all the info I’m willing to try this myself.

  6. Hey man,

    I just sent you an email but I now see that you also have a comment section so then more people might profit from your response.

    First of all, thanks for all your awesome work. I have been following you for quite a while now and the quality of your platform keeps on growing!

    Summary of my question if you do not feel like reading the rest: Can topical dutasteride still be effective despite the molecule being 528 daltons? There seems to be some evidence that it still should work and that its molecular weight is actually the reason why people do not seem to be getting side effects from it (despite having gotten them from finasteride).

    Lately, I am seeing some anecdotal signs from people having success with topical dutasteride. I was always convinced that topical dutasteride was never studied because it had a molecular weight of 528 daltons and therefore not able to pass through the outer layer of the skin.

    I did some research on the topic and apparently, the situation seems to be a bit more nuanced. I found this: “This rule doesn’t necessarily mean that all skincare ingredients are ineffective above 500 Daltons. However, for products that need to get to the lower layers of skin, which includes most actives in cosmetics, molecular weight should be below 500 Daltons.” (source: https://www.aaextracts.com/the-500-dalton-rule/).

    “There is a hair transplant clinic in Belgium that kind of uses that as a reason why they believe in the success of dutasteride. They claim:
    “The idea behind topical dutasteride has to do with the chemical properties compared to finasteride. At the molecular level, dutasteride is more difficult to deliver as a topical agent to be absorbed through the skin due to the size of dutasteride molecules. They are larger than those of finasteride. This difficulty however becomes an advantage as the difficulty to get past the subcutaneous layer may prevent systemic absorption. The molecular size prevents deep penetration. In addition, dutasteride has a high lipophilicity of 4.94, compared to 3.03 of finasteride, which means it is less water-soluble than finasteride or more “greasy”. This higher lipophilicity can in theory help dutasteride to remain in the skin longer as these properties tend to preclude the paracellular and follicular routes of ingress into the skin.”

    Thank you in advance brother. Keep up the good work!


    1. Yes it can, and it has shown to be. Just because something is 28 daltons over the “limit” that doesn’t mean that 0% of it makes it through. I’ve seen blood work of guys on topical Dutasteride showing systemic suppression of DHT, so it is definitely getting into the blood in some capacity.

      1. Thanks man! I have not seen any scientific evidence on this but do you know if Dut has a flat response curve like finasteride? Are you still on Dut btw? I remember that you were not happy with its efficacy due to the lack of protection from your high test levels.

  7. My friend Swim has been using 25mg/0.8ml of s4 in the 70/30 Ethanol to PG ratio for the last week as suggested. He has seen a reduction in hairs in the hair catcher from an uncountable number to now less than 10. He said he might try 25mg per 2 or 3ml with the next batch as its hard to cover all the spots with 0.8ml.

    Is there some reason he should be aware as to why you wouldn’t use a more diluted concentration?

    1. That’s great news man. Not a lot of people testing this theory out so I’m happy to hear that. Well ultimately if you dilute it more you’re delivering less active compound, so it is a dose response assessment. If 25 mg per 2-3 mL works, or even less than that, then why go above it? Just common sense. If it doesn’t work, then you either need a higher dose, a different vehicle, or a different compound entirely.

  8. Hey Derek,

    Great post, thanks for sharing.

    I am new to hair loss prevention and am deciding if I should start with RU or a topical SARM like S4. The topical SARM sounds like the better option overall however dosing and efficacy seem somewhat unclear. Would RU be your first go to ? I’m currently doing micro needling, nizoral, red light therapy and Mk677.

    Thanks for your time.

  9. Hi Derek, about topical Sarm for hair loss now after some time can you tell me if they were useful for blocking loss/regrowth and if so which is the best between lgd or s4? Thanks

    1. hey derek,
      I am interested by the same info as luke up there. Can you give any feedback on the efficacy of topical sarms for hair loss since some dude tried your theory by now.
      Moroever i have read anecdotally that some upreglating sensibility to T and DHT can occur after stopping sarm, increasing hair loss even more. I think the dude was using sarm via pill or injection though.

      Thanks for your feedback

  10. Ive been running topical s4 and I think 25 mg is severely overkill. I almost wonder if 10 mg is plenty or less. I think its dose dependent. So if I took osterine maybe I would need more. But if your not taking anything I think 25 mg is too much I’m slowly lowering dose and seeing if shedding remains the same. I dropped it to 12 mg and shedding remained the same.

    I think the S4 works in that once the receptors are filled anything more is just a waste. Finasteride is 1mg. I wonder if 1 mg of topical s4 is enough. I will continue to lower it and see where the shedding starts again.

    1. You’re comparing an anti-androgen to a 5-ar inhibitor. If you want more useful metrics at least compare the milligram amount to another topical anti-androgen with similar binding affinity.

    2. hey jacob, also heavily interested with your experiment, so you are basically saying that 12 and 25 mg of topical s4 made your hairloss worse ? can you say for how long did you try that experiment and what is the vehicule that you used.

      Moroever can you tell us more about if you find a dosage of topical S4 that stopped your hairloss and your current regimen.

      Your feedback is very much appreciated as myself i would like to try topical sarm as i can’t use ru58841 and finasteride wich gave me side effect.

      Thanks for your help bro

      1. Im debating if it made it worse or if im just in a shedding phase. I’ve been having huge sheds not sure if that’s what topical sarms are meant to do. So the side effects I got were I would go to sleep and then wake up at like 4 in the morning then stay awake for 2 hours then go back to bed

        At 6mg I have noticed no sides but I got a massive shed after 2-3 days. Im taking 12.5 mg of mk-677 and doing minoxidil. Since the half life of S4 is 4 hours I took the idea of its still in my hair for a day and a half so I was using it for 3 days a week at 25 mg. I think I’m gonna do 6.25 mg for a week then check my sheds then do roughly 8.33mg something there then 12.5 mg and see if it affects sheds at all.

        I looked up and noticed some people got sides like waking up in the middle of the night from other farms. I wonder if RU or topical sarms like finasteride have a shed phase then regrowth phase cause if they don’t I might wanna switch over to another sarm other than S4 but of course the more androgenic it is the more likely whatever sides I get on S4 they would be worse I would assume.

        I see what you mean Derrick. Ok what do you think milligram for milligram would be a similar anti androgen?

    3. Ok im convinced S4 set me back possibly time to try lgd and s23 see if there’s any effect there. But s23 being so tissue selective will be interesting

  11. What would you recommend for someone that does not take exogenous androgens and has had systemic effects from topical ketoconazole?

    Need a strategy other than minoxidil, AR5-Is, or antiandrogens. Right now left with microneedling and peptides of questionable efficacy.

    Topical sarms are interesting. Maybe one with more selectivity towards the scalp will be known from these sorts of tests. <500 daltons I expect significant systemic absorption, and thus suppression of an HPTA that is without exogenous hormones.

    SARMS with excess of 1000 Dalton’s (if they exist) would be safer and still possibly efficacious IMO.

  12. Derek,
    Any update on this? I know several people are running experiments; I am wondering if you have heard back.

    I’m going to get the pre-finastride blood work done after I cut & stabilize around 12% bf to reduce E, & I’m thinking of running the following protocol on my lab subject:

    .25g fin 3X week
    Topical solution of RU & S4 EOD, low dose.
    2ml Castor Oil oral, everyday
    Derminator 2, 1.5mm once a week, with more shallow version conducted intermittently to increase porosity as needed.

    29 yo male.
    6’ 2”, 200 lbs
    15% bf
    No gear.
    NW 2.25 receder not a profuse thinner.
    Thick, dark hair with good density.

    Risk Aversion: moderate, willing to take calculated risk.

    Rationale for protocol:
    Reduce the risk of adverse symptoms, & capitalizing on minimal effective doses and synergistic effects of a multi-pronged approach.

    Reducing Serum DHT by 4o-60%, & using a topical mix applied at the scalp of S4 & RU to compete with Test & DH for AR sites.

    Let me know your thoughts.

    1. Do you get bad sides from fin. I’ve considered trying 0.25 mgs but I get bad sides from fin like headaches, lack of sleep and lower libido. Were you getting low sides on 0.25mgs as opposed to 1mg?

  13. I applied 25mg of S4 onto my scalp for 3 days. I waited 1-2 weeks to see if it went systemic and, in fact, it did. I experienced high estrogen symptoms such as bloat, libido issues, and my small gyno become hard, which isn’t usual. The S4 didn’t reduce my hair loss, in fact it made it worse, but it probably was due to the high T that built up in my body from introducing an exogenous substance. I will try a much lower dose next time, maybe 5mg, and see if I can reduce the amount that goes systemic.

  14. It’s important to note that molecular size is just one of many factors, and not even the most important, affecting a molecule’s ability to pass through the stratum corneum. Everything else being equal, yes, a smaller molecule will be able to permeate through the stratum corneum better. Two more important factors are whether the molecule can “hitch a ride” on a membrane transporter, and the polarity of the molecule. A highly polar molecule, or ion, such as sodium, will not diffuse through a cellular membrane. Similarly, for instance, glucose (a polar/hydrophilic molecule) requires a membrane transporter to get inside cells.
    A lipophilic molecule will have a much easier time diffusing through the nonpolar cellular membrane.

    Another thing that can allow a molecule to pass through is the concomitant use of a permeability enhancer, such as dimethyl sulfoxide. This can allow, to varying degrees, larger lipophilic substances as well as polar substances to pass through the phospholipid bilayer that makes up our cellular membranes. It can work too well, in some cases, where it actually makes a medication less effective by driving a medication too far, creating a deep transdermal delivery rather than shallow, or even topical. A notorious example of this is some compounding pharmacies that don’t do proper research on pharmacodynamic properties of certain drugs and drug combos, and put anesthetics such as lidocaine with DMSO for the assumed “deeper delivery”. Often used for dermal procedures, such a compound would actually benefit by the exclusion of DMSO.

    Anyway, just some food for thought regarding the molecular weight of compounds. It’s just one piece of the puzzle, but it’s important to consider other aspects of both the molecule, and any excipients it may be paired with.

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