Tetrahydrogestrinone (THG) is a synthetic anabolic-androgenic steroid that was never developed or sold as a medicine. It is a lightly modified form of gestrinone, a marketed progestin, and was apparently made to escape the doping tests used in sport at the time (Handelsman, Sci STKE 2004). In 2003 the UCLA Olympic Analytical Laboratory identified it in the residue of a used syringe (Catlin et al., Rapid Commun Mass Spectrom 2004; Malvey and Armsey, Curr Sports Med Rep 2005). Handelsman called it the first true “designer androgen” found in sport. It was the steroid behind the BALCO case and the product coded “The Clear” (Kicman, Br J Pharmacol 2008).

The single most important fact: THG has never been tested in a controlled human study. Because it was never approved, no legitimate human dosing or excretion studies have been done (Lévesque et al., Anal Chem 2005). What is known comes from receptor assays, cell culture, rodent and horse studies, and doping-control chemistry. In the US it is a named Schedule III controlled substance, and WADA bans it at all times.

This page summarizes what laboratory studies, doping-control research and regulators report. It is for education only and is not medical advice.

Property	Detail
Class	Designer 19-nor anabolic-androgenic steroid with a 4,9,11-triene structure (like trenbolone)
Other names	Tetrahydrogestrinone, THG, “The Clear” (BALCO code name)
Formula / weight	C₂₁H₂₈O₂; 312.4 g/mol (PubChem)
Origin	Made by hydrogenating gestrinone; identified by UCLA in 2003
Medical approval	None; FDA called it an unapproved new drug in 2003
Studied human doses	None; no controlled human trials
Half-life	Not established in humans; 1.9 h in horses after an oral dose
Receptor profile	Strong androgen and progestin in vitro; also binds glucocorticoid and mineralocorticoid receptors
US status	Schedule III anabolic steroid, named in the Anabolic Steroid Control Act of 2004
WADA status	Prohibited at all times (S1.1 anabolic androgenic steroids), listed by name

What it is

THG’s US legal chemical name is 13β,17α-diethyl-17β-hydroxygon-4,9,11-trien-3-one (21 CFR 1308.13). WADA lists it as 17-hydroxy-18a-homo-19-nor-17α-pregna-4,9,11-trien-3-one (WADA 2026 Prohibited List). PubChem gives the formula C₂₁H₂₈O₂ and a molecular weight of 312.4 g/mol (PubChem CID 6857686).

The UCLA laboratory made reference THG by hydrogenating gestrinone (Catlin et al., 2004). The reaction reduces the triple bond of gestrinone’s 17α-ethynyl group to an ethyl group and leaves the ring double bonds intact (Salvador et al., Anal Chem 2007). Gestrinone is C₂₁H₂₄O₂ (PubChem CID 27812), so the step adds four hydrogen atoms. That is where the “tetrahydro” in the name comes from.

Steroid	Relationship to THG	Status
Gestrinone	Parent compound; has a 17α-ethynyl group where THG has a 17α-ethyl group	Marketed progestin
Trenbolone	Shares the 4,9,11-triene ring system (the conjugated “ketotrienyl” structure)	Animal growth promoter; Schedule III
Methyltrienolone (metribolone, R1881)	Same ring system; THG carries two extra methyl groups (ethyl in place of methyl at C-13 and C-17)	Potent synthetic androgen; Schedule III

Sources for the table: Kicman 2008, Dorn et al., Arch Toxicol 2008, Marques et al., J Chromatogr A 2007, Pereira de Jésus-Tran et al., Protein Sci 2006 and 21 CFR 1308.13. For the related veterinary steroid, see Trenbolone Acetate.

Why the 17α change matters

Progestins and androgens act on closely related receptors. In a yeast assay that screened many marketed progestins, the 17α-ethynyl progestins (gestrinone, ethisterone, norethisterone, norgestrel) had the most built-in androgenic activity. Turning that ethynyl group into a methyl, ethyl or allyl group, as in THG and norbolethone, raised androgenic activity further (McRobb et al., J Steroid Biochem Mol Biol 2008). Kicman notes that this simple step “hides the thinking” behind THG’s design (Kicman 2008).

History in doping

2003, discovery. UCLA identified THG in a spent syringe said to contain a steroid that urine tests could not detect, and built new LC/MS/MS and GC/HRMS tests for it (Catlin et al., 2004). THG did not show up on the routine gas chromatography–mass spectrometry screen used by accredited laboratories (Kicman 2008).
BALCO. The Bay Area Laboratory Co-operative supplied a preparation coded “The Clear,” which was identified as THG. Norbolethone was reputedly its active ingredient before THG replaced it. It was supplied as a liquid for use under the tongue (Kicman 2008).
October 28, 2003, FDA. FDA declared THG an unapproved new drug and said it does not meet the definition of a dietary supplement (FDA statement, 2003).
2004, US law. Congress named THG as an anabolic steroid in the Anabolic Steroid Control Act of 2004 (Public Law 108-358).

The case pushed anti-doping laboratories toward screening methods that can catch steroids nobody has seen before, such as androgen bioassays combined with mass spectrometry (Handelsman, Sci STKE 2004). Madol, another designer steroid found by the same laboratory, is covered on the Madol (DMT) page.

How it works in the body

Receptor activity

THG acts on the androgen receptor (AR), the same receptor testosterone and dihydrotestosterone (DHT) use. The studies agree that it is a strong AR binder. They disagree on how strongly it switches the receptor on:

Study	Model	Main finding
Death et al., JCEM 2004	Yeast cells expressing human receptors	Highly potent androgen and progestin; no estrogenic activity; no antagonism at any of the three receptor classes tested
Jasuja et al., Endocrinology 2005	Recombinant AR; mouse mesenchymal cells	Bound AR with affinity similar to DHT; promoted muscle-cell (myotube) formation in culture
Pereira de Jésus-Tran et al., Protein Sci 2006	Crystal structure of human AR binding domain	About twofold higher AR affinity than DHT (EC50 1.86 nM vs 2.8 nM for metribolone); more contacts with the receptor than DHT or testosterone
Friedel et al., Toxicol Lett 2006	Reporter-gene assay; receptor binding	AR activation two orders of magnitude weaker than DHT; high but unselective binding to androgen, progesterone, glucocorticoid and mineralocorticoid receptors, highest to the glucocorticoid receptor

Binding strength and activation strength are not the same thing, and results also depend on the assay. The safest summary is that THG is a potent androgen and progestin that is not selective for the androgen receptor.

Pharmacokinetics

No human pharmacokinetic data have been published, so THG’s half-life in people is unknown. The available data come from animals and human liver cells:

Model	Finding
Horses, single oral dose of 25 µg/kg (n = 10)	Peak plasma level 1.5–4.8 ng/mL; back to baseline by 24 h; detectable in urine for 36 h; plasma half-life 1.9 h (Machnik et al., J Vet Pharmacol Ther 2009)
Baboon administration study	THG is excreted in urine (Catlin et al., 2004)
Human liver cells (hepatocytes) in vitro	Hydroxylation and glucuronidation at C-18, the same pathway as gestrinone; a second glucuronide oxidized most likely at C-16 (Lévesque et al., 2005)

Horse data do not translate directly to people. They are listed here because they are the only published in vivo half-life.

Regulatory status

FDA: an unapproved new drug that cannot be legally marketed; not a dietary supplement (FDA statement, 2003).
US controlled-substance law: the Anabolic Steroid Control Act of 2004, approved October 22, 2004, added THG to the statutory list of anabolic steroids; those amendments took effect 90 days after enactment (Public Law 108-358). DEA lists it by name in Schedule III, along with its salts, esters and ethers (21 CFR 1308.13).
Sport: WADA lists THG by name under S1.1 anabolic androgenic steroids. It is prohibited in and out of competition, and all S1 substances are non-Specified Substances (WADA 2026 Prohibited List). Sport federations also ban it in horse sports (Machnik et al., 2009).

What the research shows

There are no human trials of THG for any outcome: not muscle, strength, performance or safety. The evidence that it is anabolic comes from rodents.

Animal studies

Three groups tested THG in male rodents, measuring the weight of the prostate and seminal vesicles (androgenic effect) and the levator ani, a muscle used to gauge anabolic effect:

Study	Animal	Finding
Jasuja et al., 2005	Castrated rats	Prevented castration-induced shrinkage of levator ani, prostate and seminal vesicles, and prevented loss of fat-free mass
Labrie et al., J Endocrinol 2005	Mice	About 20% of DHT’s potency in increasing prostate, seminal vesicle and levator ani weight; gene-expression changes in muscle and prostate largely overlapped with DHT (671 shared genes in levator ani, 95 in gastrocnemius, 939 in prostate)
Friedel et al., 2006	Castrated rats	Stimulated prostate, seminal vesicle and levator ani; lowered a glucocorticoid-controlled liver gene (tyrosine aminotransferase), unlike testosterone propionate

About “anabolic without androgenic” claims. Reviewing these three studies, Kicman found little separation between THG’s muscle-building and androgenic effects in the animal tests (Kicman 2008). There is no published evidence that THG is more “selective” for muscle than other anabolic steroids.

Side effects and risks

No human safety data exist. FDA said in 2003 that little was formally known about THG’s safety, but that its structure and relationship to known steroids suggested its use may pose considerable health risks (FDA statement, 2003). Handelsman described its use at high doses, with unknown contaminants and no prior biological or toxicological testing, as a significant health risk (Handelsman 2004).

Findings from animal and cell studies

Glucocorticoid interference (in rats). THG bound the glucocorticoid receptor most strongly of all receptors tested and suppressed a glucocorticoid-dependent liver gene. The authors concluded that adverse effects from this are conceivable (Friedel et al., 2006).
Chromosome damage (in hamster cell culture). THG and trenbolone up to doubled the rate of micronuclei (small fragments of chromosomes, a marker of genetic damage) in V79 cells; testosterone did not. The pattern pointed to errors in chromosome distribution (an aneugenic effect), with the peak at 3 µM for THG. The authors could not rule out a genotoxic hazard in people using it (Dorn et al., Arch Toxicol 2008).
Dioxin-like signalling (in cell culture). THG activated the aryl hydrocarbon receptor and raised CYP1A1 enzyme levels, the same pathway dioxins act through (Moon et al., Toxicol In Vitro 2012).
Progestin activity. THG is a potent progestin as well as an androgen (Death et al., 2004). The effects of combining both actions in humans have not been studied.

Expected class effects

As a potent androgen, THG would be expected to share the risks of the anabolic steroid class, but none has been measured for THG itself. Kicman notes that no anabolic steroid has achieved full separation of muscle effects from androgenic effects, and that strongly anabolic steroids still cause excess hair growth and, eventually, virilization in women and children (Kicman 2008).

What has not been studied

There are no human data on THG’s effects on the liver, blood lipids, heart, blood pressure, hormone suppression, fertility or mood, and no data on a safe or effective dose.

Detection

THG did not appear on the routine GC-MS screen of the time (Kicman 2008). Its triene structure is also labile, which causes problems with the derivatization step of classical GC-MS (Marques et al., 2007). After the discovery, laboratories added:

LC/MS/MS of unaltered THG and a GC/HRMS method using a stable derivative (Catlin et al., 2004);
a GC-MS method able to confirm THG, gestrinone and trenbolone below 2 ng/mL in urine (Marques et al., 2007);
an antibody test (ELISA) with a detection limit of 0.25 µg/L in human urine (Salvador et al., 2007).

Key takeaways

A designer steroid, never a medicine. THG is gestrinone with its 17α-ethynyl group reduced to ethyl, made to evade doping tests and exposed in 2003 through the BALCO case.
No human trials. There are no controlled human data on its effects, dose, half-life or safety. The only in vivo half-life (1.9 h) comes from horses.
Potent but not selective. It binds the androgen receptor at least as strongly as DHT, but also acts as a progestin and binds glucocorticoid and mineralocorticoid receptors.
Anabolic in rodents. It restored muscle and sex-organ weight in castrated rats and mice, with little separation between anabolic and androgenic effects.
Lab safety signals. Cell studies found chromosome damage and dioxin-like signalling, and rat studies found glucocorticoid interference in the liver.
Banned and controlled. FDA calls it an unapproved new drug; it is Schedule III in the US and prohibited at all times by WADA.

Sources

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Malvey TC, Armsey TD 2nd. Tetrahydrogestrinone: the discovery of a designer steroid. Curr Sports Med Rep. 2005;4(4):227–230. PubMed.
Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol. 2008;154(3):502–521. PMC.
Lévesque JF, Templeton E, Trimble L, et al. Discovery, biosynthesis, and structure elucidation of metabolites of a doping agent and a direct analogue, tetrahydrogestrinone and gestrinone, using human hepatocytes. Anal Chem. 2005;77(10):3164–3172. PubMed.
Food and Drug Administration. FDA statement on THG. October 28, 2003. FDA (archived).
Anabolic Steroid Control Act of 2004. Public Law 108-358, 118 Stat. 1661. October 22, 2004. govinfo.
Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
World Anti-Doping Agency. The 2026 Prohibited List: International Standard. In effect January 1, 2026. WADA 2026 Prohibited List.
National Center for Biotechnology Information. PubChem Compound Summary for CID 6857686, Tetrahydrogestrinone. PubChem.
National Center for Biotechnology Information. PubChem Compound Summary for CID 27812, Gestrinone. PubChem.
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Dorn SB, Bolt HM, Thevis M, et al. Induction of micronuclei in V79 cells by the anabolic doping steroids tetrahydrogestrinone and trenbolone. Arch Toxicol. 2008;82(4):257–263. PubMed.
Moon HY, Kim SH, Ryu SH, Suh PG. The androgenic anabolic steroid tetrahydrogestrinone produces dioxin-like effects via the aryl hydrocarbon receptor. Toxicol In Vitro. 2012;26(7):1129–1133. PubMed.

THG (Tetrahydrogestrinone)