Epistane is the common product name for methylepitiostanol (17α-methylepithiostanol), a designer anabolic steroid. It is a 17α-methylated version of epitiostanol, an older Japanese drug that was studied in breast cancer. Methylepitiostanol itself was never developed as a medicine. By 2009 it had appeared in products sold online as “dietary supplements” (Okano et al., Drug Test Anal 2009).
The single most important fact: there are no controlled human trials of methylepitiostanol. What is known comes from lab analyses of supplement products, cell and horse studies, and case reports of liver injury. In the US it has been a Schedule III controlled substance since the Designer Anabolic Steroid Control Act of 2014, and WADA bans it by name.
This page summarizes what analytical studies, case reports and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Class | Designer 17α-methylated anabolic-androgenic steroid with a 2α,3α-epithio (sulfur-bridged) A-ring |
| Other names | Methylepitiostanol, 17α-methylepithiostanol, hemapolin, Havoc, Epi plex (PubChem synonyms) |
| Formula / weight | C₂₀H₃₂OS; 320.5 g/mol |
| Route | Oral (capsules sold as “supplements”) |
| Medical approval | None found; the parent drugs epitiostanol and mepitiostane were used in Japan |
| Studied human doses | None; no controlled human trials |
| Half-life | Not established in humans; no published human pharmacokinetic data |
| US status | Schedule III anabolic steroid (named in the Designer Anabolic Steroid Control Act, December 18, 2014) |
| WADA status | Prohibited at all times (S1.1 anabolic androgenic steroids), listed as “17α-methylepithiostanol (epistane)” |
What it is
Methylepitiostanol’s chemical name is 2α,3α-epithio-17α-methyl-5α-androstan-17β-ol (PubChem CID 71752521). It is built on a DHT-like (5α-reduced) steroid skeleton with two changes:
| Change | What it does |
|---|---|
| 2α,3α-epithio bridge: a sulfur atom links carbons 2 and 3 of the A-ring, replacing the usual 3-keto group | Inherited from epitiostanol. It makes the steroid “non-ketoic”; doping chemists noted this unusual A-ring could help it slip past standard screens (Waller et al., Drug Test Anal 2020). |
| 17α-methyl group | Makes the steroid orally active. It is the same modification found in oral steroids such as methyltestosterone and Superdrol. |
The non-methylated parent, epitiostanol (C₁₉H₃₀OS), and its oral prodrug mepitiostane were developed in Japan. KEGG classifies both as estrogen receptor antagonists used as antineoplastics, and lists mepitiostane (brand Thioderon) in the Japanese Pharmacopoeia (KEGG D01265; KEGG D01602).
| Compound | Structure | Medical history |
|---|---|---|
| Epitiostanol | 2α,3α-epithio-5α-androstan-17β-ol | Studied in advanced breast cancer by 1973 (Fujimori, Cancer 1973) |
| Mepitiostane | Epitiostanol with a 1-methoxycyclopentyl ether at C17; oral prodrug of epitiostanol | Studied in breast cancer; prescribed in Japan for anemia in dialysis patients (Maeda et al., Clin Nephrol 1989) |
| Methylepitiostanol (Epistane) | Epitiostanol with a 17α-methyl group | No medical use; appeared in online supplements |
Okano and colleagues described methylepitiostanol as either a 17-methylated analogue of epitiostanol or a prodrug of desoxymethyltestosterone (“madol,” 17α-methyl-5α-androst-2-en-17β-ol). In other words, losing the sulfur bridge would give madol, another designer steroid (Okano et al., Drug Test Anal 2009).
About “anti-estrogenic” and “dry” claims. Epistane is often marketed as an anti-estrogenic steroid because its parent, epitiostanol, is classified as an estrogen receptor antagonist. We found no study testing whether methylepitiostanol has anti-estrogenic effects in people. The parent’s profile should not be assumed to carry over.
How it works in the body
No human pharmacokinetic study of methylepitiostanol has been published, so its absorption, peak level and half-life in people are unknown. The evidence that exists is indirect:
- Androgen receptor activity (cell culture). A steroid extracted from a supplement sold as “Hemapolin” activated the human androgen receptor in three lab assays (Akram et al., Anal Chem 2011). Its potency relative to testosterone was 34 in yeast cells, 333 in human kidney cells and 80,000 in human liver cells. The authors traced the huge spread to metabolism inside the cells: when they blocked steroid-metabolizing enzymes, the rankings became consistent. These numbers cannot be translated into human potency.
- Metabolism (horse). After a thoroughbred horse was given synthetic methylepitiostanol, its urine contained madol and several madol derivatives (Waller et al., Drug Test Anal 2020). Methylepitiostanol and many of these metabolites strongly activated the equine androgen receptor in a yeast assay. This supports the prodrug idea, but it is animal data.
- Androgen receptor activity in liver cells. In cultured human liver cells, methylepitiostanol activated the androgen receptor at 0.01 μM (Petrov et al., Arch Toxicol 2020).
For the non-methylated relatives, there is some human data. After a single oral 10 mg dose of mepitiostane, its metabolites epitiostanol sulfoxide and epitiostanol were detectable in urine for up to 48 h and 24 h, respectively (Okano et al., J Pharm Biomed Anal 2015). In rats, mepitiostane was absorbed largely through the intestinal lymph, which let it bypass first-pass metabolism in the liver (Ichihashi et al., Xenobiotica 1991). Neither finding tells us how the 17α-methylated compound behaves.
Regulatory status
| Jurisdiction | Status |
|---|---|
| United States | Named in the Designer Anabolic Steroid Control Act of 2014, signed December 18, 2014, as “2α,3α-epithio-17α-methyl-5α-androstan-17β-ol” (Public Law 113-260). It is now listed among the Schedule III anabolic steroids (21 CFR 1308.13). The same law requires anabolic steroid products to carry IUPAC chemical names on the label. |
| Spain | In December 2013 the Spanish medicines agency (AEMPS) banned sale of the product “Epistane 18” and ordered its withdrawal after identifying methylepitiostanol in it. AEMPS cited risks including serious liver injury, stroke, kidney failure and pulmonary embolism (AEMPS 2013). |
| Sport (WADA) | Prohibited at all times under S1.1 anabolic androgenic steroids; non-specified substance (WADA 2026 Prohibited List). |
Epistane was marketed as a supplement, but a 2015 review notes that designer steroids in over-the-counter supplements have been linked to serious harms, including cholestasis, kidney failure, hypogonadism, gynecomastia and infertility (Rahnema et al., Andrology 2015).
What the research shows
No human efficacy data
No randomized or controlled trial has tested methylepitiostanol for muscle mass, strength, body composition or any medical condition. Claims about how much muscle it builds, or how “dry” those gains are, come from marketing and user reports, not from studies.
What the parent drug did in patients
The closest human evidence comes from mepitiostane, the non-methylated oral prodrug of epitiostanol. It was studied mainly as a hormonal treatment for advanced breast cancer:
| Trial | Design and n | Mepitiostane dose | Result |
|---|---|---|---|
| Japanese Cooperative Group, Cancer 1978 | Randomized, double-blind; 50 vs 48 patients | 10 mg twice daily vs fluoxymesterone 10 mg twice daily | Tumor regression in 17 of 50 (34%) vs 20 of 48 on fluoxymesterone; not significantly different. Liver toxicity significantly less common with mepitiostane. |
| Inoue et al., Cancer Treat Rep 1978 | Uncontrolled; 45 patients | 20 mg/day | Regression in 14 of 45 (31.1%). Virilizing effects (hoarseness, hirsutism, acne) seen relatively often. |
| Izuo et al., Cancer 1985 | Randomized phase III; 40 vs 47 postmenopausal patients | 10 mg twice daily vs high-dose medroxyprogesterone acetate | Response in 14 of 40 (35.0%) vs 19 of 47 (40.4%) |
The fluoxymesterone comparator is Halotestin. These results describe a different molecule without the 17α-methyl group, so they say nothing about the efficacy or liver safety of Epistane.
What is actually in “Epistane” products
When Japanese anti-doping chemists analyzed a product called EPISTANE bought online, the label claimed only the 2α,3α form of methylepitiostanol. The capsules also contained its 2β,3β isomer and desoxymethyltestosterone (madol) (Okano et al., Drug Test Anal 2009). A second product in the same study, P-PLEX, contained madol and an isomer of it. A buyer of such a product cannot know what, or how much, they are taking.
Side effects and risks
Cholestatic liver injury
Cholestasis means bile flow out of the liver is blocked, which causes jaundice, intense itching and dark urine. It is the best-documented harm of methylepitiostanol.
Researchers in Valencia, Spain, identified four people who developed long-lasting cholestasis after taking Epistane (Petrov et al., Arch Toxicol 2020). In the three patients whose bile acids were profiled:
- the total serum bile acid pool was 14 to 61 times higher than normal;
- the rise was driven mainly by primary conjugated bile acids (cholic acid conjugates), while secondary bile acids were very low.
In cultured human liver cells, the same group found that methylepitiostanol:
- at concentrations as low as 0.01 μM, raised expression of two key bile acid synthesis genes, CYP7A1 (by 65%) and CYP8B1 (by 67%);
- increased the uptake and accumulation of a fluorescent bile acid analogue by 50–70%;
- at 0.01 μM, activated the androgen receptor, which in turn raised CYP8B1.
The authors proposed that people differ widely in these bile acid enzymes and transporters, which could explain why only some users develop cholestasis. A later metabolomics analysis by the same group found that Epistane produced a consistent cholestatic pattern in all exposed patients they studied, unlike drugs whose injury pattern varied from person to person (Moreno-Torres et al., Int J Mol Sci 2024).
The 17α-methyl group is the structural feature it shares with other oral steroids linked to cholestasis. In the 1978 breast cancer trial, the non-methylated parent mepitiostane caused significantly less liver toxicity than 17α-methylated fluoxymesterone. That comparison is consistent with, but does not prove, the role of 17α-methylation.
Suppression of natural testosterone
No study has measured hormone suppression with methylepitiostanol. It activates the androgen receptor, and androgens generally suppress the body’s own testosterone production. The parent class offers a signal: among male hemodialysis patients in Japan, 23 men taking mepitiostane or nandrolone decanoate had mean testosterone of 205.2 ng/dL vs 449.7 ng/dL in men not taking them (Maeda et al., Clin Nephrol 1989). Testosterone rose in three men after they stopped mepitiostane. One man with no sperm recovered sperm production after stopping mepitiostane and receiving hCG.
Virilization
In women treated with mepitiostane for breast cancer, virilizing effects (hoarseness, hirsutism and acne) were reported relatively often (Inoue et al., Cancer Treat Rep 1978). Whether methylepitiostanol causes the same effects at the same rate is unknown.
Unknown and unstudied risks
Lipid changes, blood pressure, heart effects and long-term safety have not been studied for methylepitiostanol. Because products have been found to contain other steroids than the label states, any harm in a user cannot be cleanly attributed to methylepitiostanol alone.
Key takeaways
- A designer steroid, not a medicine. Epistane is 17α-methylated epitiostanol; the parent drug was used in Japan, but methylepitiostanol was never approved anywhere we could find.
- No human trials. Its potency, effective dose and half-life in people are unknown. Cell-assay potency figures varied more than 2,000-fold depending on the cell type.
- Cholestatic liver injury is documented. Four users in Spain developed long-lasting cholestasis with serum bile acids up to 61 times normal, and lab work points to an androgen-receptor-driven rise in bile acid synthesis.
- Labels are unreliable. An analyzed Epistane product also contained an isomer and the designer steroid madol.
- Controlled and banned. Schedule III in the US since 2014, withdrawn from the Spanish market in 2013, and prohibited at all times by WADA.
Sources
- National Center for Biotechnology Information. 2,3-Thioepoxy madol (methylepitiostanol), PubChem CID 71752521. PubChem.
- Okano M, Sato M, Ikekita A, Kageyama S. Analysis of non-ketoic steroids 17alpha-methylepithiostanol and desoxymethyl- testosterone in dietary supplements. Drug Test Anal. 2009;1(11-12):518–525. PubMed.
- Akram ON, Bursill C, Desai R, et al. Evaluation of androgenic activity of nutraceutical-derived steroids using mammalian and yeast in vitro androgen bioassays. Anal Chem. 2011;83(6):2065–2074. PubMed.
- Waller CC, Weththasinghe SA, McClure L, et al. In vivo metabolism of the designer anabolic steroid hemapolin in the thoroughbred horse. Drug Test Anal. 2020;12(6):752–762. PubMed.
- Petrov PD, Fernández-Murga L, Conde I, et al. Epistane, an anabolic steroid used for recreational purposes, causes cholestasis with elevated levels of cholic acid conjugates, by upregulating bile acid synthesis (CYP8B1) and cross-talking with nuclear receptors in human hepatocytes. Arch Toxicol. 2020;94(2):589–607. PubMed.
- Moreno-Torres M, Quintás G, Martínez-Sena T, Jover R, Castell JV. Exploring individual variability in drug-induced liver injury (DILI) responses through metabolomic analysis. Int J Mol Sci. 2024;25(5):3003. PubMed.
- Rahnema CD, Crosnoe LE, Kim ED. Designer steroids - over-the-counter supplements and their androgenic component: review of an increasing problem. Andrology. 2015;3(2):150–155. PubMed.
- Kanehisa Laboratories. KEGG DRUG: Epitiostanol (D01265) and Mepitiostane (D01602). KEGG D01265; KEGG D01602.
- Fujimori M. 2α,3α-Epithio-5α-androstan-17β-ol in the treatment of advanced breast cancer. Cancer. 1973;31(4):789–792. PubMed.
- Japanese Cooperative Group of Hormonal Treatment for Breast Cancer. 2alpha, 3alpha-epithio-5alpha-androstan-17beta-yl 1-methoxycyclopentyl ether in the treatment of advanced breast cancer. Cancer. 1978;41(2):758–760. PubMed.
- Inoue K, Okazaki K, Morimoto T, et al. Therapeutic value of mepitiostane in the treatment of advanced breast cancer. Cancer Treat Rep. 1978;62(5):743–745. PubMed.
- Izuo M, Yoshida M, Tominaga T, et al. A phase III trial of oral high-dose medroxyprogesterone acetate (MPA) versus mepitiostane in advanced postmenopausal breast cancer. Cancer. 1985;56(11):2576–2579. PubMed.
- Okano M, Sato M, Kojima A, Kageyama S. Determination of mepitiostane metabolites in human urine by liquid chromatography/tandem mass spectrometry for sports drug testing. J Pharm Biomed Anal. 2015;115:236–244. PubMed.
- Ichihashi T, Kinoshita H, Yamada H. Absorption and disposition of epithiosteroids in rats (2): avoidance of first-pass metabolism of mepitiostane by lymphatic absorption. Xenobiotica. 1991;21(7):873–880. PubMed.
- Maeda Y, Nakanishi T, Ozawa K, et al. Anabolic steroid-associated hypogonadism in male hemodialysis patients. Clin Nephrol. 1989;32(4):198–201. PubMed.
- Designer Anabolic Steroid Control Act of 2014. Public Law 113-260, 128 Stat. 2929 (December 18, 2014). govinfo.
- Drug Enforcement Administration. Schedule III, 21 CFR 1308.13. 21 CFR 1308.13.
- Agencia Española de Medicamentos y Productos Sanitarios. Retirada del producto Epistane 18 (ICM-MI 15/2013). December 20, 2013. AEMPS.
- World Anti-Doping Agency. The 2026 Prohibited List. WADA 2026 Prohibited List.