What is the half-life of RU58841?

In rats given RU-58841 intravenously, Roussel-Uclaf measured a plasma elimination half-life of roughly one hour. There is no published human pharmacokinetic study, so no human half-life exists. The rat figure is the only number, and it describes the parent compound in blood, not how long it persists in scalp tissue after topical application.

RU 56279 is the N-desalkyl metabolite of RU-58841. It is itself antiandrogenic and is cleared from plasma much more slowly than the parent. In rats, only about 1% of RU-58841 was converted to RU 56279, compared with 77% for a sister compound, RU 56187, which did show systemic antiandrogen effects. The low conversion is the main reason RU-58841 behaved as a local agent in animals.

Can RU58841 lower testosterone?

An androgen receptor antagonist does not reduce testosterone production directly, and in animal studies RU-58841 left testosterone levels unchanged at topical doses. In theory, enough systemic antagonist could disrupt feedback and raise testosterone, as oral antiandrogens like flutamide do. Whether topical RU-58841 reaches that threshold in people has never been measured.

Does the vehicle affect systemic absorption?

Almost certainly. Solvent, concentration, surface area, skin condition and occlusion all change how much of any topical crosses the skin. None of these variables has been studied for RU-58841 in humans, which is one reason forum reports of 'systemic sides' are impossible to interpret: nobody knows what was applied, how, or what was in the bottle.

Why has nobody measured this in humans?

Because RU-58841 was shelved by Roussel-Uclaf in the 1990s before clinical development and nobody has funded human studies since. A pharmacokinetic study would be inexpensive by pharmaceutical standards, but there is no company with a commercial reason to run one for an unpatentable, unlicensed molecule.

RU58841 Half-Life & Systemic Absorption

Q: Does RU58841 go systemic?

Some of any topical compound reaches the bloodstream. The question is how much and whether it matters. In animals, topical RU-58841 produced strong local antiandrogen effects without measurable effects on the prostate or testosterone, which Roussel-Uclaf attributed to rapid clearance and very low conversion to its active metabolite. No human study has measured blood levels, so the human answer is unknown.

Key facts (as of October 2026)

The only RU-58841 pharmacokinetic data is a 1994 Roussel-Uclaf rat study by Cousty-Berlin and colleagues.
After 10 mg/kg intravenous dosing, RU-58841 cleared from rat plasma with a half-life of about 1 hour.
About 1% of RU-58841 was converted to the slow-clearing active metabolite RU 56279, versus 77% for the sister compound RU 56187.
Battmann et al. (1994, PMID 8136306) found topical doses as low as 1 microgram acted locally in hamsters, with no systemic antiandrogen effect up to 100 micrograms.
No human pharmacokinetic study of RU-58841 has been published as of October 2026.
No human half-life, blood level, or absorption fraction exists for RU-58841.

The short version

The only RU-58841 pharmacokinetic data is a 1994 rat study from Roussel-Uclaf: after intravenous dosing the parent compound cleared with a half-life of about one hour, and only about 1% was converted to its slow-clearing active metabolite, RU 56279.
That low metabolite formation is the mechanism Roussel-Uclaf proposed for why topical RU-58841 showed no systemic antiandrogen effect in animals while acting strongly on the skin.
There is no human pharmacokinetic study. No human half-life, blood level, or absorption fraction has ever been published. Claims of either "it never goes systemic" or "it definitely goes systemic" are not supported.

The question people are actually asking

"Does RU58841 go systemic?" is really three questions. How much of a topical dose gets through the skin? Once in the blood, how quickly is it cleared? And does whatever remains do anything at the androgen receptors in the rest of the body? For a licensed drug those would be answered by human absorption, distribution, metabolism and excretion studies. RU-58841 was developed by Roussel-Uclaf in the 1980s and shelved in the 1990s before any of that work was published in people. What exists is animal pharmacology, and it is better than nothing, so here it is in full.

The 1994 rat pharmacokinetic study

Cousty-Berlin and colleagues at the Roussel-Uclaf research centre in Romainville published the key paper in the Journal of Steroid Biochemistry and Molecular Biology in 1994 [1]. They gave rats 10 mg/kg of RU-58841 intravenously and followed plasma levels. Three findings matter.

The parent compound disappears quickly. RU-58841 was eliminated from plasma with a half-life "of the order of 1 h". That is fast for a lipophilic small molecule.
It forms a slow metabolite. Both RU-58841 and a sister compound, RU 56187, are converted to the same N-desalkyl metabolite, RU 56279, which is cleared much more slowly than either parent and is itself clearly antiandrogenic.
RU-58841 barely forms it. Estimated from area-under-curve comparisons, about 1% of RU-58841 was converted to RU 56279. For RU 56187 the figure was 77%.

The authors then measured systemic antiandrogen effects (prostate and seminal vesicle weights) for both parents and the metabolite and found a relationship: the more RU 56279 a compound formed, the more systemic activity it showed. Their conclusion was that RU-58841's profile, potent local antiandrogen activity without systemic effects, "can be related to its very low propensity to form the N-desalkyl metabolite". In plain terms: the parent is cleared too quickly to matter systemically, and it does not make enough of the slow metabolite to matter either. In rats.

What the earlier pharmacology paper adds

Battmann and colleagues' original 1994 characterisation [2] is the other half of the picture. In hamsters, topical RU-58841 shrank the androgen-dependent flank organ at doses as low as 1 microgram per animal while having no antiandrogen effect on the prostate and seminal vesicles and no effect on testosterone up to 100 micrograms. Given subcutaneously instead, 300 micrograms was needed to produce a local effect equal to 1 microgram topically, and systemic activity was weak even then. That is the "topical action" profile the molecule was designed for: a wide gap between the dose that acts on skin and the dose that acts on the rest of the body.

Pan and colleagues added a note of caution in 1998 [3]. In cell assays RU-58841 blocked DHT activation of the androgen receptor with potency comparable to hydroxyflutamide, the active form of a systemic prostate-cancer drug, and they observed that topical use "may induce systemic side effects" on that basis. In the same paper, however, topical application in stump-tailed macaques increased hair density and length with no systemic effects detected. The molecule is potent enough to matter if it gets through; the animal data says little gets through.

What none of this tells you

Every number above is from rodents or primates, after intravenous or controlled topical dosing of a known formulation. There is no human study measuring:

How much RU-58841 crosses human scalp skin from any given solvent.
Plasma concentration of the parent or of RU 56279 after topical application.
Human half-life of either compound.
Effects on testosterone, LH, oestradiol or any other hormone.
Whether repeated application leads to accumulation of RU 56279.

The last point deserves attention. The parent clears in about an hour in rats, but the metabolite clears "much more slowly". Even at 1% conversion, a metabolite that persists could in principle build up with repeated exposure. Whether it does in humans, and at what exposure, is unknown. That is the honest gap behind every forum thread about tiredness, libido or mood on RU-58841: those reports are uncontrolled, the material applied is usually unverified, and there is no measurement to anchor them to. We discuss the reports themselves in RU58841 side effects.

Why vehicle and formulation matter

Skin penetration depends on solvent, concentration, area treated, skin integrity and whether the site is occluded. A compound dissolved in a penetration-enhancing solvent and applied to an inflamed scalp behaves differently from the same compound in a simple alcohol base on intact skin. None of this has been characterised for RU-58841 in humans, and it is one reason the animal numbers cannot be transferred. It is also why the concentration and solvent actually in a bottle are the first things a researcher should verify, which is what our buying guide covers.

How this compares with pyrilutamide

Kintor designed pyrilutamide (KX-826) around the same idea: high receptor occupancy in skin, low transdermal absorption, and rapid metabolism to low-activity products. The difference is that Kintor has run human trials, and across several hundred patients and a 52-week open-label study it reported no drug-related sexual dysfunction and adverse-event rates similar to placebo [4]. That is still company-reported, and no human pharmacokinetic figures for pyrilutamide have been published either, but it is human data where RU-58841 has none. See Pyrilutamide clinical trials for the full record.

The honest summary

The best available evidence says RU-58841 was engineered to act locally and, in animals, it did: rapid clearance, minimal conversion to its persistent active metabolite, and no measurable systemic antiandrogen effect at topical doses. That is a well-designed molecule, not a proven safe one. The absence of human pharmacokinetic data means no supplier, forum or article can tell you what happens in a person, and anyone who claims certainty in either direction is guessing. Norwood Labs supplies RU-58841 for laboratory research only, publishes sample reports from a third-party analytical laboratory for the named samples, and makes no claim about safety in humans because none can be made.

References

Cousty-Berlin D, Bergaud B, Bruyant MC, Battmann T, Branche C, Philibert D. Preliminary pharmacokinetics and metabolism of novel non-steroidal antiandrogens in the rat: relation of their systemic activity to the formation of a common metabolite. J Steroid Biochem Mol Biol. 1994;51(1-2):47-55. PMID 7947350
Battmann T, Bonfils A, Branche C, et al. RU 58841, a new specific topical antiandrogen: a candidate of choice for the treatment of acne, androgenetic alopecia and hirsutism. J Steroid Biochem Mol Biol. 1994;48(1):55-60. PMID 8136306
Pan HJ, Wilding G, Uno H, et al. Evaluation of RU58841 as an anti-androgen in prostate PC3 cells and a topical anti-alopecia agent in the bald scalp of stumptailed macaques. Endocrine. 1998;9(1):39-43. PMID 9798729
Kintor Pharmaceutical. Long-term safety Phase III clinical trial of KX-826 for the treatment of AGA reached primary endpoint. Press release, 20 March 2025. kintor.com.cn

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RU-58841 5% Solution

50 mg/mL · published sample report.

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RU-58841 Powder

2 g / 5 g / 10 g · published sample reports.

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