EmergingResearch compound

RU58841 (PSK‑3841 / HMR‑3841)

Peripheral non-steroidal AR antagonist (NOT a 5α-reductase inhibitor) – Roussel-Uclaf 1992 designer. Topical AGA research chemical. Phase II terminated 1996 due to systemic feminization. Modern UGL formulations' local-only claim has sparse supporting data.

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RU58841 (PSK-3841 / HMR-3841) vial

WHAT IS RU58841 (PSK-3841 / HMR-3841)?

Detailed overview

**IMPORTANT mechanism-clarification**: RU58841 (PSK-3841 / HMR-3841) is **NOT** a 5α-reductase inhibitor (like finasteride/dutasteride), but a **peripheral androgen receptor (AR) antagonist**. Designed by Roussel-Uclaf laboratory in 1992 (Sawaya 1997 PMID 9224249) for topical treatment of androgenetic alopecia (AGA): the compound competitively binds AR at scalp follicular tissue, blocking the downstream effect of DHT (and testosterone) androgenic signaling – **it does NOT inhibit DHT conversion, but rather neutralizes the DHT effect at the hair-follicle level**. Phase II clinical trials were terminated in 1996 by the industrial producer (Hoechst Marion Roussel, later Sanofi-Aventis), after feminizing effects (gynecomastia formation, sexual dysfunction) appeared in test populations on systemic absorption. Modern UGL formulations (5% solution in ethanol/propylene glycol) base their local-only claim – via rapid serum esterase inactivation – on sparse in vivo data with contradictory case reports of systemic effects. Tier 2 (research-level, Phase II terminated, UGL-only). Designer-purple accent `#a78bfa` per spec § 3.3. **NOT** a 5AR substrate mechanism – classified under the 5AR sub-section due to use-case grouping convention (AAS hair-loss-prevention shared goal with finasteride/dutasteride).

Mechanism

Peripheral non-steroidal AR antagonist (NOT a 5AR inhibitor!) – scalp follicular AR binding blockade

Dosing (research-only)

5% solution in ethanol/propylene glycol, 0.5-1 mL once daily scalp application

Half-life

Topical minimal systemic absorption (claim), effect ~24 h

Onset

Scalp AR blockade immediate, hair stabilization 3-6 months (in vivo data sparse)

Legal status

NO FDA/EMA approval, NO HU/PL Rx, research-chemical vendor only, WADA banned (S1 anabolic agent related)

Data console

Lab data

/lab/molecular-data.jsonLIVE
> Androgenic:AnabolicN/A (AR antagonist, NOT AR agonist) – NOT AAS
> AR bindingAR Ki ~0.5 nM (competitive antagonist, vs DHT ~5 nM, testos…
> Active half-lifeEffect ~24 h per application (claim, in vivo confirmation incomplete)
> Detection windowWADA-accredited LC-MS/MS sparse data – research-chemical context urine detection 1-2 weeks post-topical application (in vivo data minimal)
> AromatizationNo direct aromatization. Peripheral AR blockade → steroid axis NOT affected. (If absorbed systemically, AAS activity could be blocked – gyno-emphasizing risk feminization throughout the body.)
> HepatotoxicityTopical low hepatic; in case of in vivo absorption, hepatic stress data are incomplete – caution in research-chemical context.

Safety

Side effects, stop signs, contraindications

Side effects · 6

  • Systemic feminizing effects with meaningful absorption: gynecomastia, reduced libido, erectile dysfunction, deteriorating sperm quality (the documented reason for the 1996 Phase II trial termination).
  • Local scalp irritation, itching, redness and contact dermatitis, mainly from the ethanol/propylene glycol vehicle (the most common, well-documented local effect).
  • NO long-term (6+ months) safety data: the endocrine and reproductive risks of chronic absorption are unknown because clinical development stopped at Phase II.
  • UGL/research-chemical sourcing risks: purity often <90%, unstable solution (potency <50% after 6 months at room temperature), vehicle-contamination allergy – the actual active content is not guaranteed.
  • Systemic AR blockade may suppress the anabolic effect of a concurrent AAS or SARM cycle if the compound is absorbed (receptor-level antagonism, not a mechanism conflict).
  • Mood symptoms: the Phase II monitoring protocol explicitly tracked IIEF-5 (sexual function) and PHQ-9 (depression), pointing to possible psychological complaints alongside sexual dysfunction.

Contraindications · 7

  • Contact with a pregnant partner: with systemic absorption the AR antagonist could theoretically disrupt fetal male sexual development – avoid when a partner is pregnant or planning pregnancy.
  • Fertility planning / active conception intent: not recommended for users planning children due to documented sperm-quality deterioration and sexual dysfunction.
  • Not indicated for prophylactic use in those not predisposed to AGA: with research-chemical status and absent safety evidence the risk-benefit balance is unjustifiable.
  • Topical only: NEVER take orally – the compound is intended for the scalp alone; ingestion drastically raises the risk of systemic AR blockade and feminizing effects.
  • Long-term chronic use (>12 months): in vivo safety data are missing and Phase II was halted precisely over systemic side effects – chronic use is not supported.
  • Prohibited for competitive athletes: banned by WADA under S1 (Other Anabolic Agents) as an AR modulator, both in and out of competition.
  • Damaged/inflamed scalp or ethanol/propylene glycol sensitivity: the vehicle can trigger contact dermatitis and increases systemic absorption when the skin barrier is compromised.

Related Performance Compounds

Same therapeutic category

Studies

Related research and clinical findings

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MolekulaX Editorial Team·Source-verified · PubMed · FDA · EMA
Updated: June 19, 2026

The information here is for educational and scientific purposes only. Performance-enhancing compounds (AAS, prohormones, stimulants, doping agents) are illegal without prescription in Hungary and most of the EU, and carry serious health and legal risks. WADA bans them in competitive sport. This is NOT a usage guide, and we do not encourage any illegal use. If you do use them, medical supervision and regular bloodwork are ESSENTIAL. Severe endocrine, cardiovascular, hepatic and psychiatric side effects are possible.