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RU58841 Vs. Finasteride For Hair Loss Prevention

RU58841 Vs. Finasteride For Hair Loss Prevention – Which Is Better?


RU58841 vs. Finasteride.

As of now RU58841 is the most commonly used topical anti-androgen used for hair loss prevention, and Finasteride is the most commonly used 5α-Reductase inhibitor for hair loss prevention.

Which is better for hair loss prevention?

This is a common question I get asked and a dedicated post is long overdue.

Study Comparing RU58841 Vs. Finasteride Head To Head

While there are tons of anecdotal reviews comparing Finasteride to RU58841, there is very little scientific data for us to refer to.

There is some though that is worth delving into.

In this study, Finasteride was stacked up against RU58841 to see which would be more effective for hair loss prevention, and how much each would impact systemic hormone levels [R].

RU58841 was applied either in a 5% solution, a 0.5% solution, or just a vehicle with no RU58841 in it for 6 months to the bald scalp of 10 stump-tailed macaques.

The 5% solution was applied to 4 of the 10 bald stump-tailed macaques, the 0.5% solution was applied to 3 of the 10 bald stump-tailed macaques, and the vehicle with no RU58841 was applied to the last 3 of the 10 bald stump-tailed macaques.

The common dosing protocol for RU58841 is typically a 5% solution applied to androgenic alopecia affected areas, so this study was right in line with what we would want to see.

Oral Finasteride was given in a dose of 1 mg/kg/day for 6 months to 10 bald stump-tailed macaques.

An oral placebo was also given to 10 bald stump-tailed macaques.

Male stump-tailed macaques weigh on average between 9.7–10.2 kg, so that would equate to a Finasteride dosage of roughly 10 mg orally per day.

This dosage greatly exceeds the point of diminishing returns with Finasteride use, so this is also a great way for us to compare the efficacy of a standard dose of RU58841 to a maxed out dose of Finasteride.

The stump-tailed macaque has shown to be a suitable biological model for human androgenetic alopecia as it possesses hereditary balding characteristics similar in many respects to that of androgenetic alopecia in humans [R].

Results

Skin biopsies for micromorphometric analysis (folliculogram) were taken at 0 and 6 months for Finasteride treated macaques and at 0 and 4 months for RU58841 treated macaques.

The amount of anagen follicles (hairs in the active growth phase) and vellus follicles (short, thin, and barely noticeable hairs) enlarged to terminal size were compared to those in pre-treatment stages.

Anagen follicles increased an average of 88% with Finasteride.

Anagen follicles increased an average of 103% with 5% strength RU58841.

The growth of vellus follicles to terminal size (thick, strong, pigmented hairs that have fully matured) was 12% with Finasteride.

The growth of vellus follicles to terminal size was 26% with 5% strength RU58841.

The 0.5% strength RU58841 solution induced almost no effect.

Expectedly, the Finasteride placebo induced no effect.

The 5% strength RU58841 solution induced the most hair growth after only 2 months of treatment.

RU58841 was given less time to work and still significantly outperformed Finasteride in this study.

Although Finasteride significantly reduced DHT levels, DHT remaining and produced by Type I 5α-reductase isoenzyme still contributed to hair follicle miniaturization.

Because Testosterone and DHT both bind to the androgen receptor, a locally sufficient dose of an “AR blocker” (topical anti-androgen) appears to suppress Testosterone and DHT induced follicular regression more effectively than 5α-reductase inhibition.

Systemic Effects

Plasma RU58841 and metabolites (10-20 ng/ml) were detected in 2 of the stump-tailed macaques that were applied the 5% strength RU58841 solution at the 3 month mark of treatment.

Only 1 of the stump-tailed macaques had detectable plasma RU58841 and metabolites at at the 6 month mark of treatment.

RU58841 had no significant impact on serum DHT or Testosterone levels at any point.

Finasteride decreased serum DHT levels by about 70%, and Testosterone levels increased as a result of the 5α-reductase blockade.

If Estrogen levels were assessed in the Finasteride treated group, their Estrogen levels would have showed significant elevation as well as a result of increased aromatization.

My Concluding Thoughts On This Study

This study shows that RU58841 can go systemic when topically applied, although there is no effect on endogenous androgen levels.

First of all, I do believe that RU58841 can go systemic, in fact, I think it is an inevitable outcome.

However, the degree to which it goes systemic and if the amount that goes systemic will cause anti-androgenic side effects will be based on several factors.

These factors include but are not limited to endogenous androgen production, sex hormone metabolism, androgen receptor density and expression, scalp skin porosity, the dosage used, if there are open wounds on the scalp or not, the vehicle used, frequency of administration, and more.

Does this ensure side effects? No.

However, applying anything to your skin with a low enough molecular weight to be absorbed and not expecting it to go systemic at all is wishful thinking.

The molecular weight of RU58841 is 369.34 g/mol [R].

1 Da (dalton) = 1 g/mol.

The molecular weight of a compound must be under 500 Dalton to allow skin absorption (which RU58841 is) [R].

With that being said, RU58841 is well tolerated by the majority of users for a reason.

In the study, at the 3 month mark 2 of the stump-tailed macaques had detectable plasma RU58841 and metabolites.

By the 6 month mark, only 1 of the stump-tailed macaques had detectable plasma RU58841 and metabolites.

If there was a cumulative drug effect we would have seen more animals with detectable metabolites after an additional 3 months of dosing, not less.

What most fail to consider is that RU58841 is non-steroidal and acts as a competitive silent antagonist of the androgen receptor.

This means that even if RU58841 goes systemic, by creating a blockade of the androgen receptor, RU58841 prevents the negative feedback androgens would normally create via the hypothalamic–pituitary–gonadal axis (HPG axis) in men.

By binding to androgen receptors, RU58841 will induce anti-androgen effects without reducing serum androgen levels in the body.

Finasteride on the other hand works by directly crushing DHT levels rather than by occupying androgen receptors.

The ideal treatment would be a topical non-steroidal anti-androgen or SARM with a high binding affinity, and harmless metabolites void of anti-androgenic activity upon systemic absorption.

Achieving Complete Hair Loss Protection By Addressing The Androgen Receptor, Not Just 5α-Reductase

When you inhibit 5α-Reductase with Finasteride or Dutasteride, serum Testosterone and Estrogen levels increase will increase.

A common mistake is to ignore the fact that scalp Testosterone levels rise dramatically after inhibiting 5α-Reductase.

This occurs to an even greater degree with Dutasteride use, and I believe is the reason why some men experience accelerated hair loss after switching from Finasteride to Dutasteride.

Typically, most men will see better results with Dutasteride as scalp DHT is almost always going to be more of a problem than scalp Testosterone.

However, the consequent spike in scalp Testosterone levels with Dutasteride use is significant, and Testosterone will bind to androgen receptors and induce miniaturization just the same.

5 mg of Finasteride resulted in a 23% increase in scalp Testosterone levels with a concurrent 41% suppression of scalp DHT levels.

0.5 mg Dutasteride resulted in a 99% increase in scalp Testosterone levels with a concurrent 51% suppression of scalp DHT levels.

This is why the androgen receptor needs to be addressed, not just nuking 5α-reductase with Dutasteride.

Scalp Testosterone will still slowly chip away at your hair, regardless if DHT is there or not.

In addition, Finasteride is insufficient to completely eliminate scalp DHT, which also needs to be taken into account and addressed.

When you inhibit 5α-reductase, that Testosterone that would have otherwise converted to DHT doesn't just disappear, it remains as the parent hormone, thus raising total Testosterone levels in the body.

Dutasteride doesn't just randomly stop working one day, Testosterone and other endogenous androgens are still eating away at your hair, just at a much slower pace than DHT would.

Steroidogenesis Chart

The only way to prevent other androgens from binding to androgen receptors and miniaturizing hair follicles is by competing with them for androgen receptor binding.

That's where the therapeutic promise of topical anti-androgens, anti-androgens in general, selective androgen receptor modulators, and other similar compounds that bind to androgen receptors can come into play and provide a compounding level of protection when needed, or as a form of monotherapy on their own if sufficient.

If you only inhibit 5α-reductase with Finasteride, not only will you have residual amounts of DHT, but you will also have a spike in scalp Testosterone that is totally unaccounted for.

Unfortunately, you can't just partially inhibit 5α-reductase and expect complete protection for life unless you have very mild hair loss to begin with.

Permanent prevention can only be achieved by addressing the androgen receptor itself.

For some individuals, Finasteride monotherapy will be sufficient to stave off hair loss for a couple decades, but that residual DHT and spike in Testosterone will continue to chip away and eventually win in the end.

For some with aggressive hair loss, Finasteride monotherapy isn't even sufficient in the short-term.

At the end of the day, regardless of how aggressive your hair loss is, prevention is mediated via the androgen receptor.

Other treatment options may be implemented that interact with different downstream mechanisms in the cascade of events that lead to hair loss, but they will unlikely prove sufficient to completely mitigate androgenic alopecia on their own, and will be best utilized as an adjunct treatment to achieve a compounding level of protection with other compounds.

Which Is Better For Hair Loss Prevention?

RU58841 and Finasteride work via different mechanisms of action.

They shouldn't be pitted against one another as neither are likely to prove sufficient to completely prevent hair loss on their own.

DHT has a much higher binding affinity than RU58841, but Testosterone doesn't.

Those with very aggressive hair loss would likely need to use a massive dose of RU58841 to compete with all of their scalp DHT and Testosterone.

On the other hand, Finasteride can significantly decrease DHT levels, but causes a subsequent spike in scalp Testosterone that goes completely unaccounted for that will still work in tandem with the residual DHT to miniaturize hair follicles.

A more complete level of protection would be achieved by using both Finasteride and RU58841, not one or the other.

Finasteride will significantly reduce the amount of scalp DHT, and leave a hormonal environment that RU58841 is more capable of dealing with.

RU58841's binding affinity is at least as high as Testosterone, so if most of the DHT is cleared out of the way, RU58841 only has to compete with Testosterone and a much lower amount of DHT.

Expecting RU58841 to out-compete all endogenous DHT and Testosterone without any assistance when its binding affinity is several times lower than DHT is a strategy that would likely only work long-term for someone with mild hair loss.

The dose and frequency of administration relative to the half-life needs to be kept in mind as well.

There's a dose-dependent response with all drugs, including anti-androgens.

Just because a 5% RU58841 solution applied once per day proves sufficient for one guy, that doesn't mean that dosage will be sufficient for you too.

Hair loss is basically just a giant chess match where the most efficacious treatments will either knock out the opponent (decrease endogenous androgen levels), or occupy a more advantageous position on the chess board (binding to androgen receptors).

The more chess pieces you have, the better your chance of winning against the finite number of opponent chess pieces.

This is why certain anti-androgens with very poor binding affinity can still be effective in a clinical setting.

An anti-androgen dosed very aggressively will eventually overpower Testosterone and DHT just by sheer volume (e.g. Bicalutamide).

The same applies for RU58841, assuming it gets absorbed, which will boil down to scalp skin porosity, vehicle, and so on.

If you opted for CB-03-01 instead of RU58841, the same concept would apply, it would just need to be dosed even more aggressively until sufficient AR binding is achieved.

For those prone to side effects, that strategy may be the better alternative with CB-03-01 rather than RU58841 as it seems that the metabolites of CB-03-01 may be better tolerated at higher dosages than those of RU58841.

The binding affinity of CB-03-01 is much lower than RU58841 though and it is very cost prohibitive, so for the time being, that strategy is likely not viable for most.

Where To Buy RU58841

Most RU58841 sources 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 RU58841 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 the only companies I currently use for my own personal research:

(Greater Than 99% Purity: FTIR, HPLC, GC-MS, LC-MS & NMR Tested)

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

Chemyo – 10% off coupon code “DC10”

Anageninc – 5% off coupon code “DC5”

14 thoughts on “RU58841 Vs. Finasteride For Hair Loss Prevention – Which Is Better?”

  1. Would you recommend using mk-667 for temporary use just to speed up the shedding phase of finasteride or RU? If so, at what dose would you use until satisfied results?

    1. I don’t know what a 5% solution test means. I’ve made a solution with a higher concentration than 5% before if that’s what you’re asking.

  2. In a cycle of 200 primo EW 200 test EW and anavar 30 ED. It is worth using oral dutasteride / finasteride. Or will it not do any anti hair loss effect and I will also be reducing the potency of the therapy compounds? Thank you

  3. Hi Derek,

    If using minoxidil in addition to RU, should they be applied at the exact same time (RU, wait til dry, then minox)? Or, is it a okay to apply minox in the morning and RU at night?

    I see you noted the drying time of PG/ethanol RU to be less than a minute. However, I have noticed that I get a persistent (visible and feelable) “greasiness” left on my scalp after applying (after shower too). It lasts a long time and I’m wondering why this is and worried that it’s interfering with the effectiveness of my subsequent minoxidil application. Thoughts?

    Thanks!

    1. Maybe. Who knows for sure. I don’t have before and after ultrasounds on a giant sample of guys before and after RU. Anecdotally it seems to be well-tolerated for most, but there are a minority of individuals who report chest pains on it. More people report chest pains on Minoxidil than RU from what I’ve seen, and that is the most readily available over the counter compound for hair loss.

  4. Derek,

    Does RU protect against other metabolites of other steroids besides Testosterone?, for example other members of DHT family even though as outlined in your article RU has a weaker binding affinity to AR than DHT or 19nor Families or other Test Based Family of steroids ?

  5. Hi Derek,

    Can you clarify, you put RU and then minox on at night for convenience. You shower in the morning (so 8-10 hours later). So you have an ”RU free” scalp 16-14 hours of the day.

    Do you put minox foam on in the morning after the shower?

    Thank you

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