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    RU-58841 molecular structure

    RU-58841

    OtherPreclinical

    Also known as: RU58841, 5-RU, ManemMaxing

    RU-58841 (also known as PSK-3841 or HMR-3841, and commonly written simply as RU in hair-loss forums) is a non-steroidal androgen receptor antagonist originally developed by Roussel Uclaf (later absorbed into Sanofi) in the late 1980s and early 1990s. The compound was designed as a potential topical treatment for androgen-dependent skin conditions — including androgenic alopecia (male pattern hair loss), acne, and hirsutism — by blocking dihydrotestosterone (DHT) at the androgen receptor at the site of application, without requiring systemic enzyme inhibition like 5-alpha reductase inhibitors (finasteride, dutasteride). The intended use case is elegant in principle.

    CAS: 154992-24-211 PubMed Studies
    Last reviewed:
    11
    PubMed Studies
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    Preclinical
    Research Stage

    Overview

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    At A Glance

    Mechanism

    RU-58841 is a non-steroidal androgen receptor (AR) antagonist with a chemical structure unrelated to testosterone, DHT, or the steroidal antiandrogens (cyproterone acetate, spironolactone). Its pharmacology was characterized in the early 1990s by teams at Roussel Uclaf, most nota

    Dose Range
    25 mg - 50 mg topical daily (dissolved in vehicle)mcg
    Potential Benefits
    Prevention of hair follicle miniaturizationHair loss reduction (androgenic alopecia)Topical application minimizes systemic effectsAlternative to finasteride without systemic 5-AR inhibition

    Mechanism of Action

    RU-58841 is a non-steroidal androgen receptor (AR) antagonist with a chemical structure unrelated to testosterone, DHT, or the steroidal antiandrogens (cyproterone acetate, spironolactone). Its pharmacology was characterized in the early 1990s by teams at Roussel Uclaf, most notably Battmann et al. (1994) and Battmann et al. (1998).

    The core mechanism:

    • Androgen receptors (ARs) in the cytoplasm and nucleus of target cells — including dermal papilla cells in hair follicles — bind DHT (the primary androgen driver of male pattern hair loss) with high affinity.
    • Bound AR-DHT complex translocates to the nucleus, dimerizes, binds androgen response elements on DNA, and drives gene expression that in genetically susceptible hair follicles promotes miniaturization and shortened anagen phases.
    • RU-58841 competes with DHT for AR binding. When RU-58841 occupies the receptor, DHT cannot bind, downstream transcriptional activation does not occur, and the follicle is spared from the androgen-driven miniaturization signal.
    • Unlike steroidal antiandrogens, RU-58841 is a "pure" antagonist — it does not produce partial agonist activity at the AR. This pure-antagonist behavior is shared with drugs like bicalutamide (approved for prostate cancer) and flutamide (approved historically for prostate cancer).

    Why topical delivery was the goal:

    • Systemic AR blockade causes predictable consequences — gynecomastia, reduced libido, testicular atrophy, changes in LH/FSH/testosterone, and potential liver toxicity (the reason flutamide was withdrawn in most markets).
    • Topical application to a defined skin surface should in principle allow AR blockade at the target tissue while minimizing systemic exposure.
    • RU-58841 was specifically engineered with properties intended to promote rapid metabolism upon absorption, so that any fraction reaching systemic circulation would be cleared before accumulating.

    Why topical delivery did not fully succeed:

    • Preclinical pharmacokinetic studies, including rat and primate work, demonstrated that measurable systemic RU-58841 appears after topical application, with plasma concentrations rising into the range where systemic AR effects become detectable.
    • Human phase I data (limited, mostly in unpublished Roussel Uclaf reports referenced in secondary literature) showed hormonal changes suggesting partial systemic absorption.
    • The degree of systemic effect is dose- and vehicle-dependent — higher concentrations, larger application areas, occlusion, and solvents like DMSO that improve skin penetration all increase systemic exposure.

    Potency relative to other antiandrogens:

    • RU-58841 is markedly more potent than spironolactone as an AR antagonist.
    • It is comparable to or more potent than bicalutamide in AR-binding affinity assays.
    • Against DHT at the hair follicle level, animal studies suggest single-digit to low-double-digit micromolar concentrations in topical vehicle produce strong follicle protection.

    Downstream effects on the hair follicle:

    • Reduced DHT-driven miniaturization signaling
    • Preservation of anagen phase duration
    • Protection against terminal-to-vellus hair transformation
    • In preclinical macaque studies by Pan et al. and related groups, topical RU-58841 produced measurable hair regrowth in animals with androgen-induced alopecia, at doses lower than those required for topical minoxidil to produce similar effects.

    The mechanism summary is that RU-58841 is a potent, pure AR antagonist with a theoretical ideal topical use case for androgenic alopecia, undermined in practice by enough systemic absorption to produce partial systemic antiandrogen effects in humans — the exact problem its designers were trying to solve.

    Overview

    RU-58841 (also known as PSK-3841 or HMR-3841, and commonly written simply as RU in hair-loss forums) is a non-steroidal androgen receptor antagonist originally developed by Roussel Uclaf (later absorbed into Sanofi) in the late 1980s and early 1990s. The compound was designed as a potential topical treatment for androgen-dependent skin conditions — including androgenic alopecia (male pattern hair loss), acne, and hirsutism — by blocking dihydrotestosterone (DHT) at the androgen receptor at the site of application, without requiring systemic enzyme inhibition like 5-alpha reductase inhibitors (finasteride, dutasteride).

    The intended use case is elegant in principle. 5-alpha reductase inhibitors such as finasteride and dutasteride work systemically by reducing DHT conversion from testosterone everywhere in the body — including in tissues where you want DHT to stay intact. That's why oral finasteride carries the side-effect profile that made it famous: sexual dysfunction, post-finasteride syndrome, mood changes in a subset of users. RU-58841, by contrast, was designed to be applied only where DHT is unwanted — on the scalp, for hair loss — and to then be metabolized before reaching systemic circulation. On the scalp, it would compete with DHT at the androgen receptor in dermal papilla cells, protecting follicles from miniaturization. Off the scalp, it would theoretically not exist at meaningful concentration.

    In practice, Roussel Uclaf's own preclinical and phase I work suggested that RU-58841 absorbed through the skin in amounts sufficient to cause measurable systemic antiandrogen effects — suppression of testosterone-driven organ weights in animal studies, and in human volunteers, hormonal signals suggestive of partial systemic androgen blockade. This was not what the developers wanted, and the compound was quietly shelved in the mid-1990s. It never made it to a registered clinical trial for hair loss, never received regulatory approval anywhere, and essentially disappeared from the pharmaceutical pipeline.

    Despite that abandonment, RU-58841 has had an extraordinary underground second life in the hair-loss community. From the early 2000s onward, research-chemical suppliers began selling RU-58841 powder to individual buyers who self-compounded topical solutions in ethanol, propylene glycol, and related vehicles. An active Reddit, TressLess, and independent blog ecosystem emerged around RU-58841 use as a "topical-only finasteride alternative" — frequently marketed with a claim of equivalent hair regrowth potency and dramatically reduced systemic side-effect risk. That claim is partially supported by animal data and partially refuted by the absorption problems that caused its original abandonment, and the honest user experience on forums reflects both outcomes.

    This entry takes the position that RU-58841 is a research-grade compound with plausible topical efficacy for androgenic alopecia and genuine systemic-absorption risks that have not been adequately characterized in humans. It is not a supplement. It is not approved for any human use in any jurisdiction. Users engaging with it are accepting the full research-chemical risk profile. For comparisons, see finasteride (if available), topical minoxidil, and the FDA-approved topical antiandrogen clascoterone for acne. For related research-chemical landscape discussion, see aminotadalafil.

    Chemical Information

    IUPAC Name

    Not yet available

    CAS Number

    154992-24-2

    Molecular Formula

    C17H18F3N3O3S

    Molecular Mass

    489.41 g/mol

    Dosing & Protocols

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    Interactions

    Interaction Matrix

    Contraindications

    Absolute contraindications:

    • Women of childbearing potential — antiandrogen exposure during pregnancy can cause ambiguous genitalia in male fetuses; topical use during pregnancy is contraindicated, and theoretical transfer to a partner is a consideration
    • Men actively trying to conceive — theoretical fertility effects, even with topical application
    • Pregnancy and lactation — absolute avoidance
    • Adolescents under 18 — effects on androgen-dependent developmental processes are not characterized
    • Individuals with known prostate cancer or strong family history without oncologic evaluation (antiandrogens interact with prostate biology)
    • Active hepatic disease or hepatitis — non-steroidal antiandrogens as a class can cause hepatotoxicity
    • Known hypersensitivity to RU-58841 or vehicle components
    • Active scalp dermatitis, open wounds, or infection in the treatment area
    • Recent hair transplant surgery (wait for healing per surgeon's guidance)
    • Inability to commit to basic monitoring

    Relative contraindications requiring careful consideration:

    • Concurrent oral antiandrogen use (bicalutamide, flutamide, high-dose spironolactone) — additive systemic effects
    • Concurrent high-dose 5-ARI therapy (oral dutasteride at full daily dose) — compound systemic antiandrogen load
    • Baseline low testosterone or hypogonadism — already compromised androgen status
    • Gynecomastia or strong family history of gynecomastia
    • Mood disorders (depression, bipolar) — antiandrogens may worsen mood symptoms in some individuals
    • Concurrent major medication with CYP3A4 interactions (effect on RU-58841 metabolism uncharacterized)
    • Use of DMSO or other high-penetration vehicles
    • Chronic corticosteroid use
    • Prior adverse response to finasteride or other antiandrogens

    Drug interactions:

    • Oral and topical antiandrogens — additive
    • Systemic CYP3A4 inhibitors — effect on RU-58841 metabolism unclear
    • Anticoagulants — unclear interaction, monitor if concurrent use
    • Topical corticosteroids — may alter skin penetration; use separated in time if both needed
    • Other topical hair loss products (minoxidil, topical finasteride, clascoterone) — generally compatible but apply separately with time between

    Populations requiring specialist oversight:

    • Men with cardiovascular disease (antiandrogens can affect lipid profile)
    • Men with diabetes (antiandrogens can affect insulin sensitivity)
    • Men with metabolic syndrome or obesity (baseline hormonal imbalance may be accentuated)
    • Transgender users of gender-affirming hormone therapy (RU-58841 would compound feminizing antiandrogen therapy; this is a legitimate but specialized use case requiring endocrinology management)
    • Men with any history of liver disease, hepatitis, or hepatotoxic drug exposure

    Baseline evaluation before initiating RU-58841:

    • CBC with differential
    • Comprehensive metabolic panel (emphasis on liver enzymes: ALT, AST, ALP, bilirubin)
    • Testosterone (total and free), SHBG, LH, FSH, estradiol, prolactin, DHT
    • Lipid panel, fasting glucose, A1c
    • Thyroid panel (TSH, free T4)
    • Vitamin D, ferritin, zinc if considering nutritional cofactors
    • PSA for men over 40 (baseline, annual)
    • Scalp examination and standardized photography for response tracking
    • Review of medications, supplements, and medical history
    • Review of family history of hormone-sensitive conditions

    Monitoring during RU-58841 use:

    • Monthly self-assessment: nipple sensitivity/gynecomastia signs, libido, erectile function, mood, energy, testicular sensation
    • Every 3–6 months: full hormonal panel, liver function
    • Every 12 months: lipid panel, A1c, PSA (men over 40), standardized scalp photography
    • Immediate discontinuation for: new-onset breast tissue growth, jaundice or dark urine, severe mood changes, any prostate or urinary symptom changes, severe skin reaction

    When to reduce dose or discontinue:

    • Any new systemic antiandrogen side effect that does not resolve with concentration reduction
    • Any liver enzyme elevation beyond 3x upper limit of normal
    • Persistent libido loss or sexual dysfunction
    • New gynecomastia or breast tissue changes
    • Severe scalp irritation unresponsive to vehicle adjustment
    • Lack of response after 9–12 months of adherent use

    Drug testing considerations:

    • RU-58841 is not on the WADA prohibited list as of 2026
    • It is not tested for on routine drug panels
    • Forensic or specialized anti-doping testing could identify it in users competing in specialized testing programs
    • No known cross-reactivity with standard workplace drug panels

    Post-discontinuation considerations:

    • Expect a shedding phase 2–3 months after stopping, lasting 3–6 months
    • Hair density typically returns to pre-treatment baseline over 6–12 months
    • If concurrent oral finasteride and minoxidil are maintained, the shedding from RU discontinuation alone may be modest
    • Some users report persistent post-discontinuation symptoms; if this occurs, medical evaluation is warranted

    The overall contraindication framing: RU-58841 carries a meaningful risk profile related to partial systemic antiandrogen absorption. For any reader who cannot execute the monitoring infrastructure described above, approved alternatives (oral finasteride, oral dutasteride, topical finasteride, topical clascoterone, minoxidil) are the correct path. These alternatives have more data, more regulatory oversight, and more predictable safety.

    Research Disclaimer

    This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.

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    Protocols, calculator & safety for RU-58841

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    2 vendors · 2 listings

    Research Score

    31

    11 PubMed studies

    Quality Indicators

    Data Completeness

    100%
    Description
    Mechanism of Action
    Chemical Data
    Dosing Protocols
    Safety Profile
    PubMed Studies
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    Vendor Listings

    Research Credibility

    11PubMed studies

    Quick Facts

    Molecular Weight

    489.41 g/mol

    CAS Number

    154992-24-2

    Trial Phase

    Preclinical

    Research Disclaimer

    This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.

    Frequently Asked Questions

    Is RU-58841 safe to use for hair loss?

    RU-58841 is a research chemical with no regulatory approval in any jurisdiction. Preclinical data support topical efficacy against androgenic alopecia, but human efficacy has never been validated in published randomized controlled trials, and the original developer (Roussel Uclaf) abandoned the compound in the 1990s after phase I data showed measurable systemic absorption leading to partial systemic antiandrogen effects. 'Safe' in this context means: for some users, at conservative concentrations, with appropriate monitoring, the risk may be acceptable relative to severe hair loss. It does not mean safe in the way FDA-approved minoxidil or finasteride are safe. Users should treat RU-58841 as an experimental compound, start with approved alternatives first, and commit to laboratory monitoring if using chronically.

    How does RU-58841 compare to finasteride?

    RU-58841 and finasteride attack the same problem (DHT-driven follicle miniaturization) from different angles. Finasteride is an oral 5-alpha reductase inhibitor that reduces systemic DHT production by blocking its synthesis from testosterone. It is FDA-approved, extensively studied in RCTs, and works for most men with androgenic alopecia. Its major drawback is systemic side effects in a subset of users — sexual dysfunction, mood effects, occasional persistent post-finasteride syndrome. RU-58841 is a topical AR antagonist that blocks DHT from binding its receptor at the follicle, with the theoretical advantage of topical-only action. In practice, RU-58841 produces measurable systemic absorption, so its side-effect profile overlaps with finasteride's to some degree. Most hair-loss clinicians recommend finasteride first due to evidence and regulatory status. RU-58841 is typically added to, or substituted for, oral finasteride in users with inadequate response or intolerable systemic side effects from oral therapy.

    Is RU-58841 legal?

    RU-58841 is not approved for human use by the FDA, EMA, or any other major regulatory authority. It is not scheduled as a controlled substance in most jurisdictions, which means personal possession for research purposes occupies a gray area that varies by country. Selling RU-58841 as a supplement or cosmetic is illegal in the United States and most developed markets. Some vendors market 'research-only' labeled product that is not explicitly illegal to purchase in many jurisdictions but is not authorized for human use. Users should understand that customs seizures and enforcement actions do occur. For a legal topical AR antagonist, topical clascoterone (Winlevi) is FDA-approved for acne and available off-label for alopecia by prescription.

    What concentration and dose should I use?

    Research-community convention is 2.5–5% solution in 60/40 or 70/30 ethanol/propylene glycol vehicle, applied once daily at 0.5–2 mL per application to dry scalp. Start conservative (2.5% if sensitive, 5% if more aggressive) and increase only if needed. Volume depends on treatment area — 0.5–1 mL for focal treatment (vertex or hairline only) versus 1–2 mL for full scalp. Duration before assessing response should be at least 3 months, ideally 6 months. Avoid DMSO-containing vehicles as a beginner; they dramatically increase systemic absorption. Do not exceed 7.5% concentration without substantial monitoring infrastructure.

    Will RU-58841 cause gynecomastia or sexual side effects?

    Partial systemic absorption of RU-58841 is well-documented in the preclinical and limited human phase I literature, and user-reported gynecomastia, libido changes, and erectile dysfunction occur in a meaningful minority of long-term users at 5%+ concentrations. Estimates from forum-reported outcomes suggest 5–20% of users experience gynecomastia-like symptoms (nipple sensitivity, early breast tissue development) within 3–12 months. Higher concentrations, larger application areas, DMSO vehicles, and concurrent oral antiandrogens increase risk. Users with baseline gynecomastia risk, mood disorders, or hypogonadism should approach RU-58841 with particular caution. Monthly self-monitoring for these symptoms is essential. Immediate discontinuation is warranted if gynecomastia-like symptoms appear.

    Can I stack RU-58841 with minoxidil and finasteride?

    Yes, and in fact the standard 'top-tier' hair-loss stack referenced in the community combines topical minoxidil 5% twice daily, oral finasteride 1 mg daily (or oral dutasteride), and topical RU-58841 5% once daily, often with ketoconazole shampoo, microneedling, and low-level laser therapy as adjuncts. The rationale is that each component addresses a different mechanism — minoxidil affects follicle vascular supply and cycle duration, oral 5-ARI reduces systemic DHT, and RU-58841 blocks DHT at the follicle receptor. The stacking is well-tolerated for most users, but systemic antiandrogen effects from RU-58841 plus oral finasteride are additive, so users should monitor carefully and be willing to reduce or discontinue components if side effects emerge. Start one intervention at a time to allow attribution of effects.

    How long before I see results?

    Realistic expectations: visible improvement typically starts at 3–6 months, with peak response at 9–12 months and maintenance thereafter. The first 4–8 weeks may involve a transient shedding phase as follicles transition from telogen to anagen. Users who see no visible improvement by 9 months on an adherent RU-58841-containing stack should reconsider the protocol, verify product purity, confirm that underlying drivers of hair loss are being addressed (iron, thyroid, stress, scalp health), and potentially discontinue. Standardized photography (same angle, lighting, hair length every 3 months) is much more reliable than subjective mirror assessment for tracking response.

    What is the typical side effect profile at the scalp?

    Local side effects include scalp dryness, itching, redness, and flaking — mostly attributable to the ethanol and propylene glycol vehicle rather than RU-58841 itself. Contact dermatitis from PG occurs in a subset of users. Initial shedding in the first 4–8 weeks is common and typically resolves as new anagen hair replaces shed follicles. Severe local irritation warrants vehicle change (lower ethanol percentage, addition of glycerin, or switch to alternative vehicles). Systemic side effects (covered in other FAQs) are separate from local scalp effects and are the more important safety concern.

    How do I find a trustworthy RU-58841 supplier?

    This is among the most difficult questions in the RU-58841 conversation. Research-chemical supply chains are unregulated, vendor quality varies enormously, and the market rotates as regulators shut down sources. Best practices: request and review a certificate of analysis (HPLC, ideally ≥98% purity, from a recognized third-party lab); favor vendors with a long track record in research-chemical forums and consistent user feedback; start with a small quantity to verify quality before committing to a bulk purchase; compound your own solution from verified powder rather than buying pre-mixed solutions where concentration is unverifiable; understand that even reputable vendors occasionally ship degraded or underdosed product, and that customs seizures are a real risk in stricter jurisdictions. If you cannot access a trustworthy supplier, do not substitute with a questionable one — use approved alternatives (topical finasteride, topical clascoterone) through legitimate pharmacy channels instead.

    What should I do if I have hair loss but don't want to use research chemicals?

    The honest answer is that most hair-loss users achieve excellent outcomes with approved therapies and never need RU-58841. First step is a proper dermatologic or telehealth hair-loss evaluation to confirm androgenic alopecia versus alternatives. Optimize approved pharmacotherapy — topical minoxidil 5% twice daily, oral finasteride 1 mg daily for men (women use different protocols), and consider oral dutasteride if finasteride response is inadequate. Add adjuncts — ketoconazole shampoo 2% 2–3x weekly, microneedling 1.0–1.5 mm weekly, low-level laser therapy, PRP injections every 4–6 weeks for several sessions. Optimize lifestyle — sleep, stress, training, protein and micronutrient intake. Emerging approved topical options — topical finasteride (FDA-reviewed, increasingly available through compounding pharmacies and some telehealth services) and topical clascoterone (FDA-approved for acne, off-label for alopecia) — now occupy much of the therapeutic space that RU-58841 was historically used to fill. For most users, a well-executed approved-therapy stack is as effective as anything involving RU-58841 and carries substantially less risk. See the full compound library and stack protocols for broader body-hacking approaches that support hair health indirectly.

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