Topilutamide
Not medical advice. PepTutor summarizes fallible research and community signal for trained practitioners; some compounds are research-only, unapproved, controlled, jurisdiction-dependent, or labeled not for human consumption.
Maintenance-focused hair-loss protection: blocks androgen receptors in scalp follicles so DHT, testosterone, SARMs, and DHT-derived AAS have less ability to drive miniaturization.
Topical does not mean irrelevant: watch libido, mood, testicular ache, scalp tolerance, and the expected early shed before judging failure.
Maintenance-focused hair-loss protection: blocks androgen receptors in scalp follicles so DHT, testosterone, SARMs, and DHT-derived AAS have less ability to drive miniaturization. It is a follicle AR blocker, not a regrowth drug by itself.
Low systemic-risk design, but not a zero-risk cosmetic. Rapid serum hydrolysis and inactive metabolites support the safety thesis; a minority of users still report testicular ache, mood changes, or libido reduction. Early shedding in the first 6–12 weeks is expected and should be separated from true treatment failure.
A topical AR blocker for people who need downstream androgen coverage without systemic DHT suppression. It is most rational for finasteride-intolerant users and enhanced users whose hair-loss pressure comes from direct AR activation where finasteride cannot help.
Moderate and profile-dependent. The strongest clinical anchor is one small Czech trial in men with AGA (n=43) showing an anagen/telogen ratio shift from about 76% to 87%; community reports mostly support shedding reduction and maintenance. The 95.9% in vitro AR-suppression figure is pharmacology, not proof of superior scalp outcomes.
Intro
Topilutamide (sold as Eucapil, also called fluridil) is a topical nonsteroidal antiandrogen (NSAA) developed specifically for androgenetic alopecia (AGA).
It belongs to the perfluoroacylamido-arylpropanamide chemical class — distinct from prostate-cancer NSAAs such as flutamide and bicalutamide, and distinct from the steroidal antiandrogen clascoterone. It is not a peptide or hormone; it is a small-molecule AR antagonist engineered for dermal delivery with a built-in systemic safety mechanism: rapid hydrolysis in blood. Topilutamide competitively blocks the androgen receptor (AR) in follicular cells, preventing DHT and testosterone from binding and initiating the miniaturization cascade. Crucially, it acts downstream of DHT synthesis — it does not reduce systemic DHT or testosterone levels. This means it blocks androgenic stimulation regardless of whether that stimulus comes from endogenous DHT, testosterone, DHT-derivative AAS (masteron, proviron, winstrol), or direct AR-activating compounds like SARMs. Eucapil has EU cosmetic product approval in the Czech Republic and Slovakia, where it is manufactured by Interpharma Praha (an Otsuka Pharmaceutical subsidiary). It is not approved as a pharmaceutical drug for AGA anywhere. Its patent expired in 2020. Topilutamide has been in community use since approximately 2003, predating clascoterone's clinical development, making it the original modern topical NSAA for AGA — though a substantially lower internet footprint (~15,900 Google results for 'fluridil' versus hundreds of thousands for competitors) limits available community documentation.
Observed Effects
The only published clinical trial of topilutamide for AGA is a 2002 Czech double-blind placebo-controlled study (n=43 men).
The anagen-to-telogen ratio improved from approximately 76% to 87% in the treatment arm — an 11-percentage-point shift representing a meaningful reduction in the proportion of follicles in the resting/shedding phase. Higher anagen percentage means fewer follicles cycling into telogen at any given time, consistent with slowing AGA progression. No sexual side effects or libido changes were reported in the trial. No Phase II or III trials have been published since.
Community efficacy: Reports consistently describe topilutamide as effective for shedding reduction. Multiple users document bringing active shedding down to replacement-level (~20 hairs per day) within 2–6 weeks of starting Eucapil. Some users achieve near-complete cessation by adding oral minoxidil (2.5–5 mg/day). Stop-and-start experiments confirm treatment dependency: shedding resumes within days of stopping Eucapil, returning to pre-treatment rates, which confirms ongoing treatment is required for continued benefit. Hair quality improvement (increased caliber and appearance of retained hairs) has been reported as a secondary observation in multi-month users.
Limitations: Topilutamide is not a cure for AGA — it is a maintenance treatment. The evidence gap between in vitro potency data and clinical outcomes is real. No head-to-head trial against finasteride, minoxidil, or clascoterone has been published. Community and clinical consensus strongly supports early intervention: anti-androgens can rescue and maintain miniaturized follicles but cannot regenerate follicles absent for extended periods.
Field Reports
Positive reports are consistently documented for shedding reduction. A representative first-person account: Eucapil alone reduced shedding from heavy loss to approximately 20 hairs per day within weeks; adding oral minoxidil achieved zero morning shedding by month 4, with existing hair noticeably improving in quality. This user's stop-and-start experiment — stopping Eucapil after successful treatment, then restarting — confirmed shedding resumed within days and reversed when treatment resumed. Another documented profile: SARM-associated shedding that was unresponsive to topical minoxidil resolved after adding Eucapil, consistent with SARMs activating follicular AR directly and bypassing the finasteride-addressable pathway entirely.
Adverse experience reports: A minority of community users report testicular ache, genital discomfort, mood changes, and libido reduction — effects that should not occur based on the marketed systemic-inertness profile. These remain unexplained mechanistically; nocebo and individual absorption variability are the most plausible explanations. A distinct subpopulation appears to be sensitive to all antiandrogens regardless of class — this group reports consistent side effects across finasteride, dutasteride, RU-58841, clascoterone, and topilutamide. This is separate from typical finasteride-intolerant users who are the primary topilutamide target population.
Onboarding expectations: Initial shedding increase in the first 6–12 weeks is common and expected — resting (telogen) hairs are shed as follicles are reactivated into anagen. This is not treatment failure. Full assessment of shedding reduction should not occur before month 3. Treatment is indefinite; stopping resumes loss at the pre-treatment rate.
Community Consensus
Topilutamide occupies a specific niche in the AGA treatment community: the finasteride-intolerant user's safer topical AR blocker.
The community positions it between clascoterone, which has stronger modern clinical/regulatory support, and RU-58841, which has a larger user base and stronger potency reputation but more metabolite anxiety.
Three use cases dominate. First, finasteride intolerance: users who cannot tolerate 5-AR inhibition but still want an antiandrogenic scalp mechanism. Second, enhanced-user hair protection: SARM and AAS users treat topical AR blockade as the mechanism that can cover direct receptor activation, DHT derivatives, and residual scalp androgen exposure that finasteride misses. Third, add-on use: people already using minoxidil, ketoconazole, and/or 5-AR inhibitors who still shed and want receptor-level coverage.
The consensus is specific rather than broadly bullish: topilutamide is a reasonable maintenance tool when safety architecture matters more than maximum potency, but it is not the first pick for users who want the strongest possible topical AR antagonist. The usual comparisons are: RU-58841 for potency and user footprint; clascoterone for formal drug-development evidence; pyrilutamide for higher-affinity investigational AR blockade; topilutamide for hydrolysis-limited systemic exposure and long EU cosmetic use. Stacking multiple topical AR blockers is treated as redundant. Sourcing friction, cost, and fluridil/flutamide naming confusion remain practical problems.
Risks & Monitoring
In the 2002 Czech clinical trial and per the Eucapil manufacturer (Interpharma Praha), topilutamide produced no adverse effects on libido, sexual performance, or systemic hormonal parameters.
The manufacturer states the compound is not systemically absorbed at topical doses, consistent with its t½ ~6h serum hydrolysis profile.
Community-reported effects are the main caveat. A minority of users describe testicular ache, genital discomfort, depressed mood, or reduced sex drive despite the marketed systemic-inertness profile. The mechanism is not established; plausible explanations include nocebo effect, individual variation in skin absorption or hydrolysis rate, formulation overuse, or undocumented low-level systemic activity at high-frequency application. A small intolerance phenotype appears to react poorly across many antiandrogen classes, including finasteride, dutasteride, RU-58841, clascoterone, and topilutamide; that group should treat symptoms as a stop signal rather than assuming topical delivery guarantees tolerance.
Initial shedding increase is common. As follicles shift out of telogen and back toward anagen, resting hairs shed. This telogen-effluvium-style phase usually lasts 6–12 weeks and does not by itself indicate treatment failure. Full assessment should wait until roughly month 3 unless systemic-type symptoms appear.
Class context matters. Oral NSAAs carry substantially higher adverse effect burdens at therapeutic doses. Flutamide in a 20-year study of 120 hyperandrogenic women showed 54.2% adverse effect incidence, 11 cases of mild hypertransaminasemia, and 1 case of acute fatty liver. Bicalutamide at 50 mg/day can produce severe cardiac and autonomic effects within weeks. Topilutamide's hydrolysis mechanism is meant to avoid that systemic exposure; class-level oral NSAA risks should not be copied onto topical topilutamide, but the antiandrogen symptom reports keep it from being a purely frictionless add-on.
For Women
Monitoring Panels
REQUIRED is a real safety gate. RECOMMENDED is the prudent default. OPTIONAL covers symptoms, risk factors, or tighter tracking.
Given community reports of unexpected antiandrogenic-type symptoms despite marketed systemic inertness, documenting baseline libido and mood before starting Eucapil provides a clear reference for evaluating any changes during treatment.
Topilutamide should not affect serum testosterone (acts at receptor, does not inhibit synthesis), but baseline data is useful if unexplained symptoms develop. Relevant for users combining topilutamide with SARMs or AAS where hormonal status monitoring is already appropriate.
HPTA monitoring for users combining topilutamide with compounds that suppress the HPG axis (SARMs, AAS, GnRH analogs). Topilutamide itself is not expected to suppress HPTA; monitoring is relevant to the stack context, not to topilutamide specifically.
Evaluate for emerging antiandrogenic-type symptoms. If testicular discomfort, mood changes, or libido reduction are present, consider whether they are resolving (nocebo), persistent (trial discontinuation warranted), or dose-timing correlated.
Avoid With
Do not combine Topilutamide with the following. Sorted highest-severity first.
Why:Receptor-level redundancy — both topilutamide and RU-58841 occupy androgen receptors in scalp follicles. Combining them provides no additive benefit at the receptor level while doubling cumulative compound load and any potential absorption burden.
What to do:Community consensus: 'pick one.' If switching from RU to topilutamide for safety reasons, RU's parent half-life is 1h but its cyanonilutamide metabolite persists 20–25h; allow a few days washout before starting topilutamide.
Why:Same mechanism class: topical AR antagonist. Stacking two topical AR blockers at the same receptor site provides no additive receptor-occupancy benefit and increases total compound application to the scalp. Clascoterone is steroidal; topilutamide is nonsteroidal — both compete for the same AR binding site.
What to do:No clinical or community data supports combining these. Choose one based on evidence preference (clascoterone has Phase 3 data) or regulatory status.
Why:Topical AR antagonist class redundancy. Community explicitly advises against stacking: 'No, pick one. They work similarly except pyrilutamide has higher binding affinity.'
What to do:If potency is the priority, pyrilutamide's higher binding affinity makes it the stronger single choice. If safety profile is the priority, topilutamide's inert metabolites and EU cosmetic approval are the advantages.
Why:Aromatase inhibitors suppress estrogen, and estrogen deficiency independently causes hair loss through a mechanism entirely separate from DHT-driven AGA. AI-induced hair shed is documented as one of the most severe AGA-adjacent presentations — particularly with letrozole and anastrozole. Topilutamide does not address the estrogen-deficiency mechanism.
What to do:Enhanced athletes using topilutamide + aggressive AI management may experience AI-induced shedding that is unresponsive to topilutamide. Estrogen management strategy should be evaluated separately from AGA protection when planning on-cycle protocols.
Protocols By Goal
Finasteride-intolerant users: Replace finasteride with Eucapil 1 mL/day as the anti-androgenic mechanism, and maintain minoxidil 5% BID (or oral 2.5–5 mg/day) as the growth stimulant.
Optionally add ketoconazole shampoo 2×/week. The mechanism substitution is pharmacologically sound: topilutamide provides receptor-level androgen blockade; the biological outcome (reduced follicular androgen exposure) is similar. Efficacy data is thinner than finasteride's clinical record, but the mechanism is valid.
Enhanced athletes (AAS/SARM users): Eucapil 1 mL/day as the primary scalp AR blocker. SARMs directly activate AR without 5-AR conversion — finasteride provides zero protection. DHT-derivative AAS (masteron, proviron, winstrol) bypass 5-AR entirely. Topilutamide works because it blocks at the receptor regardless of the androgen source. Optional add: microdose finasteride (0.25–0.5 mg/day) if using non-DHT-derivative androgens (testosterone, nandrolone). Add minoxidil 5% BID or oral 2.5–5 mg/day. RU-58841 is more widely used in this population; topilutamide is preferred by users concerned about RU's cyanonilutamide metabolite (t½ 20–25h).
Standard stack add-on (continued shedding on finasteride + minoxidil): Add Eucapil 1 mL/day to the existing protocol. Provides downstream AR blockade for the ~40% of scalp DHT that 5-AR inhibitors leave intact. Addresses residual DHT at the receptor level — complementary, not redundant.
Minimalist evidence-based protocol (no systemic agents): Eucapil 1 mL/day + Oral minoxidil 2.5–5 mg/day. This two-agent protocol covers AR blockade + growth stimulation without any systemic DHT reduction or HPTA involvement. Community's most-documented combination with the clearest efficacy signal.
Dosing Details
Standard dose: 1 mL of 2% Eucapil solution (20 mg topilutamide) applied to dry scalp once daily. Application method: part the hair in the thinning area (crown, temples, frontal hairline) and apply the dropper directly to exposed scalp skin. Brief massage improves distribution. The ethanol/propylene glycol vehicle evaporates within 10–15 minutes; hair can be restyled afterward.
Timing: Most users apply in the evening. If stacking with topical minoxidil, AM (minoxidil) / PM (topilutamide) is the standard split to avoid the hydrophobicity incompatibility — do not apply both simultaneously.
Wash protocol: Manufacturer recommends washing hair no more than once weekly to preserve scalp residency time. Community practice varies — some users report adequate results while washing 2–3 times per week. Conservative approach: wash 1–2 times per week and apply after washing.
Duration: Indefinite maintenance. Like all current AGA treatments, topilutamide does not cure the underlying androgen sensitivity — it suppresses the mechanism while present. Stopping resumes the pre-treatment rate of loss.
Stacks & Alternatives
The most-documented community combination. AR blockade (topilutamide) + growth stimulation (minoxidil) cover two mechanistically distinct AGA pathways with no overlap. One user documented zero morning shedding at 4 months after Eucapil alone achieved only replacement-level loss. Oral minoxidil (2.5–5 mg/day) has superior bioavailability vs topical. These two compounds are compatible in AM/PM split dosing.
Three-mechanism protocol without systemic hormonal agents. AR block (topilutamide) + growth stimulation (minoxidil) + local anti-androgenic/anti-inflammatory activity (ketoconazole). Apply topilutamide and topical minoxidil at different times (AM/PM); ketoconazole shampoo 2×/week during washing. This is the standard AGA triple-mechanism approach for finasteride-intolerant users.
Finasteride at 0.25–0.5 mg/day achieves significant scalp DHT reduction at lower systemic exposure than the standard 1 mg dose. Topilutamide provides downstream AR blockade for residual scalp DHT. Minoxidil stimulates growth. This combination addresses all three addressable steps in the AGA cascade: reduced DHT production + receptor blockade + follicle growth stimulation.
Dutasteride inhibits both Type I and Type II 5-AR isoforms, achieving ~60% scalp DHT inhibition despite near-zero serum DHT. Topilutamide addresses the remaining ~40% of scalp DHT via receptor blockade. Oral minoxidil provides systemic growth stimulation. The most mechanistically complete non-injectable AGA protocol available without synthetic androgens.
Alternatives
Stack Cost
Topilutamide creates low-to-moderate stack tax: the compound itself is topical and hydrolysis-limited, but the burden rises when it is used as part of multi-drug hair-loss or enhanced-user protocols where symptom attribution, topical scheduling, and redundant AR blockers become the real constraints.
The article reports unexpected antiandrogenic-type symptoms in a minority of users despite the systemic-inertness claim. Libido, mood, and genital/testicular discomfort need baseline tracking so true intolerance is not confused with normal early shedding anxiety.
Daily scalp application is simple, but topilutamide's vehicle should not be layered simultaneously with topical minoxidil or other water-based products. AM/PM splitting becomes the practical rule in most stacks.
RU-58841, clascoterone, pyrilutamide, and topilutamide all compete at the topical AR-blocker layer. Combining them adds scalp compound load and sourcing complexity without a supported additive receptor-occupancy benefit.
The article's clinical anchor is one small 2002 trial in 43 men, with the rest of the practical signal coming from community use and pharmacology. That makes it harder to treat response timelines, side-effect rates, or comparative efficacy as settled.
Documented topical formulations reduce uncertainty, while non-standard compounded or raw-active approaches create quality and formulation questions.
- ·Pick one topical AR antagonist; do not stack topilutamide with RU-58841, clascoterone, or pyrilutamide unless a clinician has a specific reason.
- ·Separate topilutamide from topical minoxidil by time of day; apply to dry scalp and let the vehicle evaporate before layering other products.
- ·Do not judge failure during the first 6-12 weeks if the only issue is increased shedding; reassess around month 3 unless systemic-type symptoms emerge.
- ·For SARM or AAS users, treat topilutamide as scalp AR coverage only; it does not make the underlying androgen cycle safer or less suppressive.
- ·Stop or de-escalate if libido, mood, genital discomfort, or testicular ache is persistent and dose-timing correlated.
- ·Baseline libido, mood, and genital/testicular comfort notes before starting.
- ·Week 4 and week 8 symptom check focused on antiandrogenic-type symptoms.
- ·AM/PM topical schedule when using minoxidil or other scalp treatments.
- ·Optional testosterone, LH, and FSH only when stack context or symptoms make attribution unclear.
- ·Sourcing preference for the documented Eucapil formulation over unvalidated raw-powder compounding.
The application is easy, but correct use requires understanding the difference between AR blockade, 5-AR inhibition, and growth stimulation. It is a poor blind first choice for someone who has not tried standard AGA basics or cannot track early shedding versus systemic-type intolerance.
- ·Trying to combine multiple topical AR blockers.
- ·Currently reacting poorly to several antiandrogen classes.
- ·Expecting regrowth in long-bald areas rather than maintenance of miniaturizing follicles.
- ·Using AAS/SARMs and assuming a scalp topical manages systemic cycle risk.
- ·Unable to tolerate or track libido, mood, or genital/testicular symptom changes.
There is no expected endocrine recovery problem and no taper requirement. The main off-ramp issue is loss of benefit: shedding can resume within days to weeks after stopping because the follicle AR blockade is no longer present.
- ·Return of pre-treatment shedding rate.
- ·Confusing rebound shedding with a new systemic problem.
- ·Loss of maintenance gains if no alternate AGA mechanism replaces it.
Choose one topical AR blocker and evaluate it long enough to judge response before switching.
Set a 12-week assessment window unless adverse systemic-type symptoms appear.
Use topilutamide only as scalp AR coverage; monitor and manage the underlying cycle separately.
Prefer the documented Eucapil formulation or verify compounding quality before judging the molecule.
The article has no pregnancy safety data and antiandrogen exposure is theoretically concerning for fetal androgen signaling.
These symptoms are unexpected but repeatedly reported in a minority of users; persistent or dose-correlated symptoms undermine the systemic-inertness assumption for that individual.
Mechanism redundancy adds compound load without supported additive benefit.
AI-induced hair loss can occur through estrogen-deficiency mechanisms that topilutamide does not address.
Practical Setup
Quality and formulation: Topilutamide is best discussed through documented topical formulations rather than import routes or raw-powder sourcing.
Vehicle composition matters significantly for scalp residence time and topical bioavailability, and non-standard compounded versions add quality-control uncertainty.
Application compatibility: Topilutamide's hydrophobic ethanol/propylene glycol vehicle is incompatible with simultaneous application of water-based products. Do not mix with minoxidil topical solution. Apply topilutamide to completely dry scalp; allow the vehicle to evaporate before applying water-based treatments. AM/PM split is the most practical multi-compound approach.
Naming hazard: Fluridil (topilutamide) and flutamide are entirely different compounds. Fluridil = topilutamide (topical NSAA, hydrolysis-limited, marketed as systemically inert). Flutamide = first-generation oral NSAA used in prostate cancer, with hepatotoxicity risk and documented systemic antiandrogenic effects. Community members researching 'fluridil' risk encountering flutamide safety data and applying wrong conclusions in either direction.
Early intervention: Community and clinical data alike strongly support starting treatment early — at first signs of temporal recession or crown thinning, while miniaturized follicles still have viable roots. Completely bald areas of extended duration are unlikely to respond to AR blockade. The best time to start is before hair loss is visually obvious to others.
Formulation caveat: post-patent compounding is theoretically possible, but standardized vehicles and bioavailability validation matter more than raw active availability.
Mechanism Deep Dive
Topilutamide functions as a competitive antagonist at the androgen receptor (AR). At the follicular level, DHT binds AR and initiates the transcription cascade that drives follicle miniaturization in genetically susceptible individuals. Topilutamide occupies the AR ligand-binding domain, preventing DHT and other androgens from activating the receptor. Unlike finasteride and dutasteride — which inhibit 5-alpha reductase and reduce DHT production — topilutamide acts at the receptor itself, downstream of synthesis. This downstream mechanism is critical: it is effective regardless of the source of the androgenic stimulus, including direct AR-activating compounds such as SARMs that entirely bypass the 5-AR conversion pathway.
A key mechanistic insight from corpus data: scalp DHT is partially independent of serum DHT. Scalp tissue has paracrine 5-AR activity, and miniaturizing follicles locally upregulate 5-AR in response to hypoxia, generating DHT in situ. Serum DHT suppression via finasteride achieves only ~40–60% scalp DHT reduction even at maximum dosing; dutasteride suppresses serum DHT to near-zero but still only inhibits scalp DHT by approximately 60%. Topilutamide's receptor-blocking mechanism addresses the residual scalp androgen exposure that synthesis inhibitors leave uncovered — making it additive rather than redundant to the 5-AR inhibitor class.
Pharmacokinetics: Applied topically, topilutamide penetrates the stratum corneum and acts locally on follicular cells. Any compound that enters systemic circulation undergoes rapid hydrolysis at physiological temperature (t½ ~6 hours at 37°C), becoming undetectable below 5 ng/mL at 48 hours. The two hydrolysis products — BP-34 (confirmed devoid of antiandrogenic activity) and trifluoroacetic acid (negligible body burden at topical doses) — are both inactive. This pharmacokinetic profile is the basis for topilutamide's marketed systemic safety claim.
In vitro potency data: In LNCaP prostate cancer cells (a standard AR-expression assay model), topilutamide's active form (BP-766) suppressed DHT-stimulated PSA expression by 95.9% ± 6% at 10 μM versus bicalutamide at 11% ± 3% and hydroxyflutamide at 6% ± 7% at equivalent concentrations — suggesting 9–15× higher AR binding affinity than first-generation NSAAs in this model. The Wikipedia entry for topilutamide explicitly notes that 'more research is required to validate' this finding in clinical context; the cell-line data does not directly translate to follicular efficacy in vivo.
Evidence Index
Quantitative claims trace to these source studies. Population, dose, and study type matter — claims from HIV-lipodystrophy trials don't transfer cleanly to healthy adults; data from supraphysiologic doses doesn't apply at TRT.
Anagen-to-telogen ratio improved from ~76% to ~87% with topilutamide
Czech Republic double-blind placebo-controlled trial. Only published clinical trial for topilutamide in AGA. Too small for definitive efficacy conclusions. Full text not publicly accessible; data sourced from hairlosscure2020.com summary.
BP-766 achieved 95.9% AR suppression vs 11% for bicalutamide at 10 μM in LNCaP cells
Cell-line assay. Does not directly translate to follicular efficacy in vivo. Wikipedia explicitly notes 'more research is required to validate.' The 9–15x affinity advantage is a pharmacological observation, not a clinical efficacy comparison.
Serum half-life ~6 hours at 37°C; undetectable below 5 ng/mL at 48 hours; metabolites inactive
Confirms rapid serum hydrolysis. BP-34 metabolite confirmed devoid of antiandrogenic activity. This PK profile underpins the systemic safety claim.
Flutamide (oral NSAA) over 20 years: ~50% improvement in mFG hirsutism score, 91% satisfaction, 54.2% adverse effect incidence; 11 cases mild hypertransaminasemia; 1 acute fatty liver
Class-level data only. Illustrates the systemic side effect burden of oral NSAAs that topilutamide's topical-hydrolysis design was engineered to avoid. Do not attribute flutamide side effect rates to topilutamide.
Dutasteride achieves ~60% scalp DHT inhibition despite near-zero serum DHT
Not a controlled trial citation — community and educational content. The serum-vs-scalp DHT gap is a well-established concept; the ~60% figure is the community's working estimate for scalp DHT suppression, not a specific published trial number.
Not medical advice. PepTutor summarizes fallible research and community signal for trained practitioners; some compounds are research-only, unapproved, controlled, jurisdiction-dependent, or labeled not for human consumption.