This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.

High-risk compound

Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.

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DHT

Extensively Studied

Dihydrotestosterone | Endogenous most-potent natural androgen + transdermal Andractim (EU-approved, no US FDA pathway) | WADA S1 prohibited

Aliases (9)

dihydrotestosterone · 5α-dihydrotestosterone · 5alpha-DHT · stanolone · androstanolone · Andractim · DHT gel · 5α-androstan-17β-ol-3-one · 17β-hydroxy-5α-androstan-3-one

TYPICAL DOSE

Endogenous: ~30-85 ng/dL serum (men) | Andracti…

Daily transdermal (Andractim) | endogenous biosynthesis continuous

ROUTE

Transdermal gel (Andractim, EU only); endogenou…

Transdermal gel (Andractim 2.5%, EU only); endogenous T → DHT via SRD5A1/2

CYCLE

Andractim: 3-12 months per indication | Endogen…

Per indication (3-12 mo); endogenous lifelong

STORAGE

Andractim gel: room temperature; original tube

Room temp; original tube; do not refrigerate (Andractim hydroalcoholic gel)

Overview

What is DHT?

DHT (dihydrotestosterone, 5α-DHT, androstanolone, stanolone) is a C19 steroid androgen and the most potent natural ligand at the human androgen receptor — binding with ~2-3x the affinity of testosterone and dissociating ~5x more slowly. Endogenously, DHT is biosynthesized from testosterone by 5α-reductase Type 1 (skin, sebaceous glands, scalp, liver) and Type 2 (prostate, genital skin, CNS), or via the 'backdoor pathway' from 17-OH-progesterone (relevant in congenital adrenal hyperplasia, polycystic ovary syndrome, castration-resistant prostate cancer). Exogenously, transdermal DHT exists as Andractim 2.5% gel — approved in France/Belgium/Netherlands for male hypogonadism, idiopathic gynecomastia, and pediatric micropenis. NOT FDA-approved in the US. DEA Schedule III. WADA S1 prohibited (exogenous DHT detectable via mass spectrometry). Crucially: DHT cannot be aromatized to estradiol — this is the entire pharmacological rationale for choosing DHT over testosterone in clinical contexts where E2 elevation is undesirable.

Key Benefits

Endogenous: obligate for fetal external genitalia formation, prostate development, pubertal virilization (facial/body hair, voice), and adult male phenotype. Exogenous Andractim: AR signaling without aromatization (Kunelius 2002 PMID 11932266: improved erections, no PSA change, hematocrit rise); paradoxical resolution of idiopathic + hypogonadal gynecomastia (PMID 6354523, 6220269); pediatric micropenis correction (Karrou 2023, PMC10619192) without bone-age advancement risk. Bone density association: each SD DHT → 26% lower hip fracture risk in older men (LeBlanc Metabolism 2021, PMID 33058848). Lower SHBG-binding-displacement effects on free T similar to other DHT-class compounds.

Mechanism of Action

5α-reductase converts testosterone → DHT in target tissues (Type 1: skin/sebaceous/scalp/liver; Type 2: prostate/genital skin/CNS). DHT binds androgen receptor (AR) with ~2-3x higher affinity than T and dissociates ~5x slower (Saartok 1984, PMID 6539197) — net AR signaling per molecule is ~5-10x stronger than T. Cannot be aromatized to estradiol (lacks the C4-C5 double bond that aromatase requires). Mediates: in utero male external genitalia formation, prostate development, pubertal virilization, adult male sebaceous/follicular androgen phenotype (acne, MPB), prostate hypertrophy (BPH driver). Inactivated in skeletal muscle by 3α-HSD (3α-hydroxysteroid dehydrogenase) into the much weaker 3α-androstanediol — this is why raw DHT is not used as a muscle-building AAS, and why DHT-derivative AAS (drostanolone, oxandrolone, methenolone, stanozolol) all carry ring modifications that block 3α-HSD inactivation.

Pharmacokinetics

PeakHalf-life

Approximate curve — visual aid only, not data-precise PK

Research Indications

Most Effective

Structural identity

DHT is (5α,17β)-17-hydroxyandrostan-3-one (C19H30O2; MW 290.44 g/mol; CAS 521-18-6). It is the 5α-reduced metabolite of testosterone — th…

Effective

Receptor pharmacology — the most potent endogenous androgen

[Saartok 1984 (PMID 6539197)](https://pubmed.ncbi.nlm.nih.gov/6539197/) established the foundational AR + SHBG binding affinities across …

Investigational

Cannot aromatize — pharmacologically definitive

DHT lacks the C4-C5 double bond and the 3-keto-Δ4 structure that aromatase (CYP19) requires for the first oxidation step of estrogen bios…

Investigational

Skeletal muscle inactivation by 3α-HSD

Native DHT, despite being a potent AR ligand, is rapidly inactivated in skeletal muscle by 3α-hydroxysteroid dehydrogenase (3α-HSD) into …

Investigational

5α-reductase isoenzymes

Three isoenzymes exist; two clinically relevant: - SRD5A1 (Type 1): Skin, sebaceous glands, scalp, liver. Inhibited modestly by finasteri…

Investigational

Backdoor pathway

[Auchus 2004 (PMID 15519890)](https://pubmed.ncbi.nlm.nih.gov/15519890/) characterized the alternative DHT biosynthesis route bypassing t…

Peptide Interactions

[Finasteride](finasteride.md) / [dutasteride](dutasteride.md):

Avoid

Mechanistic opposites. Finasteride/dutasteride suppress endogenous DHT by blocking T → DHT conversion; exogenous DHT bypasses this entirely. Combining is con…

[Testosterone](testosterone.md) (TRT):

Avoid

Most TRT effects are AR-mediated (DHT downstream of T) or E2-mediated (aromatization). DHT delivers AR signaling alone. Stacking is rare; usually one or the …

[Anastrozole](anastrozole.md) / letrozole (aromatase inhibitors):

Avoid

DHT cannot aromatize. AI on top of DHT has nothing to inhibit (other than residual endogenous T → E2). Crashes E2 too low → joint pain, mood issues, lipid wo…

DHT-derivative AAS ([Masteron](masteron.md), [Anavar](anavar.md), [Primobolan](primobolan.md), Winstrol):

Avoid

All DHT-derivatives stabilize against muscle 3α-HSD inactivation via various ring modifications. Stacking with raw DHT compounds androgenic side effects (hai…

Oral 17α-alkylated AAS (methyltestosterone, oxymetholone):

Avoid

Hepatotoxic + redundant. Combining strictly dominated by transdermal-only.

Hair-loss treatments (oral finasteride/dutasteride, topical RU58841, minoxidil):

Avoid

Conflicting goals. Using minoxidil to mitigate damage from a compound you're voluntarily taking is unusual.

Quality Indicators

✓

Andractim 2.5% gel — pharmacy-dispensed (EU only)

Sealed 80 g tube with manufacturer markings (Besins Healthcare / Laboratoires Besins-Iscovesco), graduated dosing applicator showing 2.5 g and 5 g markings (= 62.5 mg / 125 mg DHT), prescription label, lot number, expiration date. EU pharmacy chain of custody. Not legally importable to US without IND.

✓

Clear, faintly viscous gel — characteristic mild ethanol scent

Andractim is hydroalcoholic gel (ethanol/water vehicle). Should be clear to slightly translucent, no clumping, no separation, no discoloration. Mild ethanol smell on opening. Stable at room temperature; do not refrigerate.

US gray-market 'DHT cream' / research chem suppliers

Online 'transdermal DHT' or 'androstanolone gel' from research-chem vendors is unregulated. Active concentration may differ from labeled, transdermal absorption variable, contamination possible. Independent third-party HPLC + mass-spec verification recommended if pursued. The economic incentive to substitute cheaper compounds (mesterolone, methyltestosterone) is real.

✗

Cloudy gel, separation, color change

Cloudiness, phase separation, yellowing, or any unusual coloration suggests degradation, contamination, or counterfeit product. Do not apply transdermally.

✗

Oral 'DHT pill' or sublingual claims

Oral DHT undergoes near-complete first-pass hepatic inactivation (back to 5α-androstanediol) — bioavailability is essentially zero. Any product marketed as 'oral DHT' is either mislabeled (likely mesterolone, oxandrolone, or methyltestosterone) or pharmacologically inert. Sublingual claims are similarly unsubstantiated.

What to Expect

Day 1-7
Establishing topical application technique. Subtle initial effects: morning erections may improve subtly; mood/drive shifts minimal at this stage.
Week 1-4
First subjective signals — gradual erection quality improvement (the Kunelius 2002 signal at week 12 emerges around here), libido shifts subtle but present.…
Week 4-12
Peak effects: stable AR-mediated phenotype — modestly elevated drive, erection quality, lean tissue tone in low-BF states. Hair shedding may emerge in genet…
Month 3-6
Full hematologic + lipid response. HDL drop typical (DHT-class non-aromatizing → no E2 HDL preservation, drops more than T at equivalent androgenic exposure…
Off-cycle
Gel washout fast — apparent serum t½ 24-48h means DHT clears within ~7 days of last application. HPG axis suppression usually milder than T-class (no E2 con…

Side Effects & Safety 12

Side Effects

1Hematocrit elevation — Kunelius 2002 (PMID 11932266) documented Hct 43.5→45.8% (p<0.001) over 6 months; Idan 2010 noted Hct >50% as primary discontinuation reason. Class-typical androgenic erythropoiesis.
2Acne / oily skin — DHT-class AR activation at sebaceous glands; DHT is the dominant androgen at sebaceous glands; effect more pronounced than equivalent T exposure.
3Hair shedding / accelerated androgenic alopecia in genetically predisposed users — DHT is the proximate molecular driver (not metabolic intermediate). Finasteride / dutasteride cannot rescue because they block T → DHT conversion, which exogenous DHT bypasses. This makes exogenous DHT among the worst possible compound choices for hair-loss-predisposed users.
4HDL decline — DHT-class non-aromatizing → no E2 HDL preservation; HDL drops more than at equivalent T exposure.
5HPG axis suppression — measurable LH/FSH drop within weeks; less severe than T-class at equivalent androgenic exposure (no E2 contribution to feedback) but not zero.
6Mild blood pressure elevation — class-typical at supraphysiologic exposure; less pronounced at Andractim clinical doses.
7Sleep disturbance in some users.
8Libido shifts — initially up via SHBG displacement / free-T elevation, course variable as HPG suppression takes hold.
9Prostate effects — Idan 2010 showed no volume change at 70 mg/d × 24 mo, but higher doses and longer durations may differ; PSA monitoring relevant >40 yo.
10Skin reactions at application site — gel vehicle (ethanol/water) can cause local erythema, dryness, itching in sensitive users.
11Mild aggression / drive elevation / mood lability (DHT-class CNS effects).
12Forearm / bicep "pumps" — transient, dehydration-related, typical of DHT-derived AAS at supraphysiologic doses.

When to Stop

Severe atherogenic dyslipidemia leading to accelerated CVD with cumulative chronic exposure — comparable to other DHT-class profiles, possibly worse on HDL specifically due to non-aromatization. [Baggish 2017 (PMID 28533317)](https://pubmed.ncbi.nlm.nih.gov/28533317/) cohort data shows accelerated coronary atherosclerosis tracking cumulative AAS exposure.
Persistent post-cycle hypogonadism — documented in young AAS users with otherwise healthy HPG axes ([Rasmussen 2016 PMID 27536957](https://pubmed.ncbi.nlm.nih.gov/27536957/)); risk likely higher when HPG axis is still maturing (late teens / early 20s).
Severe androgenic alopecia / accelerated MPB in predisposed users — can be irreversible; DHT-specific risk higher than other AAS due to proximate-driver role.
Polycythemia with thromboembolic events at supraphysiologic doses — class-typical androgenic erythropoiesis exaggerated by chronic exposure.
Skin transfer to female partners or children — virilization risk in women (clitoral hypertrophy, hirsutism, voice deepening), virilization or premature puberty in children. Andractim labeling specifically warns about this.
At age 20: HPG axis is still consolidating final adult set-point. Suppression at this age has higher theoretical risk of permanent change vs same suppression at 30. Same-family AAS skip-at-20 logic applies.
Week 4-8 of any course: ALT/AST (less relevant for transdermal — minimal hepatic exposure), full lipid panel, blood pressure, hematocrit, hair photos. Flag if HDL drops >50%, BP >140/90, or visible hairline recession.
End of course: Full HPG panel (T, LH, FSH, E2, DHT) to quantify suppression.
Week 4-8 post-cycle: HPG recovery check; if still suppressed, formal endocrinology consult.
PSA monitoring: Required >40 yo and at any age with family history of prostate cancer.

References

Imperato-McGinley J et al. (1996). "5α-reductase-2 gene mutations in the Dominican Republic." J Clin Endocrinol Metab 81(11):4116-4120. PMID: 8626825.

pubmed.ncbi.nlm.nih.gov · 1996

Foundational SRD5A2 kindred study; molecular basis of guevedoces.

DHT

Overview

What is DHT?

Key Benefits

Mechanism of Action

Pharmacokinetics

Research Indications

Structural identity

Receptor pharmacology — the most potent endogenous androgen

Cannot aromatize — pharmacologically definitive

Skeletal muscle inactivation by 3α-HSD

5α-reductase isoenzymes

Backdoor pathway

Peptide Interactions

Quality Indicators

Andractim 2.5% gel — pharmacy-dispensed (EU only)

Clear, faintly viscous gel — characteristic mild ethanol scent

US gray-market 'DHT cream' / research chem suppliers

Cloudy gel, separation, color change

Oral 'DHT pill' or sublingual claims

What to Expect

Side Effects & Safety 12

Side Effects

When to Stop

References

Imperato-McGinley J et al. (1996). "5α-reductase-2 gene mutations in the Dominican Republic." *J Clin Endocrinol Metab* 81(11):4116-4120. PMID: 8626825.

Kunelius P et al. (2002). "The effects of transdermal dihydrotestosterone in the aging male: a prospective, randomized, double blind study." *J Clin Endocrinol Metab* 87(4):1467-1472. PMID: 11932266.

Idan A, Griffiths KA, Harwood DT et al. (2010). "Long-term effects of dihydrotestosterone treatment on prostate growth in healthy, middle-aged men without prostate disease: a randomized, placebo-controlled trial." *Annals of Internal Medicine* 153(10):621-632. PMID: 21079217.

Page ST et al. (2011). "Dihydrotestosterone administration does not increase intraprostatic androgen concentrations or alter prostate androgen action in healthy men: a randomized-controlled trial." *J Clin Endocrinol Metab* 96(2):430-437.

Sartorius GA et al. (2014). "Male sexual function can be maintained without aromatization: randomized placebo-controlled trial of dihydrotestosterone (DHT) in healthy, older men for 24 months." *J Sex Med* 11(10):2562-2570. PMID: 24521101.

LeBlanc ES et al. (2021). "Testosterone, dihydrotestosterone, bone density, and hip fracture risk among older men: The Cardiovascular Health Study." *Metabolism* 114:154399. PMID: 33058848.

Eberle J et al. (1982). "Gynecomastia: effect of prolonged treatment with dihydrotestosterone by the percutaneous route." *Schweiz Med Wochenschr* 112(23):873-876. PMID: 6220269.

Wickramatunga MN et al. (1983). "Studies on the treatment of idiopathic gynaecomastia with percutaneous dihydrotestosterone." *Clin Endocrinol* 19(4):461-468. PMID: 6354523.

Karrou M et al. (2023). "Efficacy of transdermal dihydrotestosterone and testosterone enanthate for penile augmentation in patients with idiopathic micropenis: a comparative randomized study." *Clin Med Insights Endocrinol Diabetes* 16:11795514231208328.

Auchus RJ. (2004). "The backdoor pathway to dihydrotestosterone." *Trends Endocrinol Metab* 15(9):432-438. PMID: 15519890.

Marchetti PM, Barth JH. (2013). "Clinical biochemistry of dihydrotestosterone." *Ann Clin Biochem* 50(2):95-107. PMID: 23440717.

Swerdloff RS et al. (2017). "Dihydrotestosterone: biochemistry, physiology, and clinical implications of elevated blood levels." *Endocr Rev* 38(3):220-254.

Saartok T, Dahlberg E, Gustafsson JA. (1984). "Relative binding affinity of anabolic-androgenic steroids: comparison of binding to androgen receptors in skeletal muscle and prostate, as well as to sex hormone-binding globulin." *Endocrinology* 114(6):2100-2106. PMID: 6539197.

Rasmussen JJ et al. (2016). "Former Abusers of Anabolic Androgenic Steroids Exhibit Decreased Testosterone Levels and Hypogonadal Symptoms Years after Cessation." *PLoS One* 11(8):e0161208. PMID: 27536957.

Baggish AL et al. (2017). "Cardiovascular toxicity of illicit anabolic-androgenic steroid use." *Circulation* 135(21):1991-2002. PMID: 28533317.

Pope HG Jr et al. (2014). "Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement." *Endocrine Reviews* 35(3):341-375. PMID: 24423981.

StatPearls — Biochemistry, Dihydrotestosterone (NBK557634)

Androstanolone — Wikipedia

WADA Prohibited List 2026 (S1.1)

Dihydrotestosterone — DrugBank DB02901

See something off?

Related compounds

Imperato-McGinley J et al. (1996). "5α-reductase-2 gene mutations in the Dominican Republic." J Clin Endocrinol Metab 81(11):4116-4120. PMID: 8626825.

Kunelius P et al. (2002). "The effects of transdermal dihydrotestosterone in the aging male: a prospective, randomized, double blind study." J Clin Endocrinol Metab 87(4):1467-1472. PMID: 11932266.

Idan A, Griffiths KA, Harwood DT et al. (2010). "Long-term effects of dihydrotestosterone treatment on prostate growth in healthy, middle-aged men without prostate disease: a randomized, placebo-controlled trial." Annals of Internal Medicine 153(10):621-632. PMID: 21079217.

Page ST et al. (2011). "Dihydrotestosterone administration does not increase intraprostatic androgen concentrations or alter prostate androgen action in healthy men: a randomized-controlled trial." J Clin Endocrinol Metab 96(2):430-437.

Sartorius GA et al. (2014). "Male sexual function can be maintained without aromatization: randomized placebo-controlled trial of dihydrotestosterone (DHT) in healthy, older men for 24 months." J Sex Med 11(10):2562-2570. PMID: 24521101.

LeBlanc ES et al. (2021). "Testosterone, dihydrotestosterone, bone density, and hip fracture risk among older men: The Cardiovascular Health Study." Metabolism 114:154399. PMID: 33058848.

Eberle J et al. (1982). "Gynecomastia: effect of prolonged treatment with dihydrotestosterone by the percutaneous route." Schweiz Med Wochenschr 112(23):873-876. PMID: 6220269.

Wickramatunga MN et al. (1983). "Studies on the treatment of idiopathic gynaecomastia with percutaneous dihydrotestosterone." Clin Endocrinol 19(4):461-468. PMID: 6354523.

Karrou M et al. (2023). "Efficacy of transdermal dihydrotestosterone and testosterone enanthate for penile augmentation in patients with idiopathic micropenis: a comparative randomized study." Clin Med Insights Endocrinol Diabetes 16:11795514231208328.

Auchus RJ. (2004). "The backdoor pathway to dihydrotestosterone." Trends Endocrinol Metab 15(9):432-438. PMID: 15519890.

Marchetti PM, Barth JH. (2013). "Clinical biochemistry of dihydrotestosterone." Ann Clin Biochem 50(2):95-107. PMID: 23440717.

Swerdloff RS et al. (2017). "Dihydrotestosterone: biochemistry, physiology, and clinical implications of elevated blood levels." Endocr Rev 38(3):220-254.

Saartok T, Dahlberg E, Gustafsson JA. (1984). "Relative binding affinity of anabolic-androgenic steroids: comparison of binding to androgen receptors in skeletal muscle and prostate, as well as to sex hormone-binding globulin." Endocrinology 114(6):2100-2106. PMID: 6539197.

Rasmussen JJ et al. (2016). "Former Abusers of Anabolic Androgenic Steroids Exhibit Decreased Testosterone Levels and Hypogonadal Symptoms Years after Cessation." PLoS One 11(8):e0161208. PMID: 27536957.

Baggish AL et al. (2017). "Cardiovascular toxicity of illicit anabolic-androgenic steroid use." Circulation 135(21):1991-2002. PMID: 28533317.

Pope HG Jr et al. (2014). "Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement." Endocrine Reviews 35(3):341-375. PMID: 24423981.