Testosterone acetate is testosterone with acetic acid attached at the 17β position. Acetate is the shortest of the testosterone esters, just two carbon atoms, so it is the closest ester to plain testosterone. Like other esters, it is a prodrug: the body has to cut the ester off before the hormone can act.

It was used as a medicine in Europe in the mid-20th century. A 1946 French case report describes 50 injections, and a 1957 Hungarian paper refers to a product called Androfort. Today there is no FDA-approved testosterone acetate product, and we found no published study of how it behaves in people. Its half-life in humans has not been measured. Most recent research on it comes from doping-control and food-safety labs, which use it as a target when testing for steroid esters.

This page summarizes what the chemistry databases, laboratory and animal studies, and regulators report, and what is known about testosterone itself. It is for education only and is not medical advice.

Property	Detail
Drug class	Androgen; anabolic-androgenic steroid (testosterone ester)
Chemistry	Testosterone 17β-acetate, C₂₁H₃₀O₃, 330.5 g/mol (PubChem CID 92145)
Testosterone content	≈87% of the ester’s weight (100 mg ester ≈ 87 mg testosterone)
Approved products	None found in FDA’s Drugs@FDA or NDC Directory databases
Route in published studies	Injection in older human reports; subcutaneous, intraperitoneal and buccal in animal studies
Half-life in humans	Not established; no human pharmacokinetic study found
Active form	Testosterone, released when esterases cut off the acetate
US status	Schedule III; the listing for testosterone covers its esters
WADA status	Prohibited at all times (S1.1 anabolic androgenic steroids)

What it is

Testosterone acetate is a small modification of testosterone (C₁₉H₂₈O₂, 288.4 g/mol). The acetate group adds 42 g/mol, so it makes up about 13% of the molecule’s weight (PubChem: testosterone acetate; PubChem: testosterone). That is less than any other common ester:

Ester	Formula	Molecular weight	Carbons in ester chain	Testosterone share of weight	XLogP3 (fat-solubility index)
None (testosterone)	C₁₉H₂₈O₂	288.4	0	100%	3.3
Acetate	C₂₁H₃₀O₃	330.5	2	≈87%	3.9
Propionate	C₂₂H₃₂O₃	344.5	3	≈84%	4.4
Enanthate	C₂₆H₄₀O₃	400.6	7	≈72%	6.3
Cypionate	C₂₇H₄₀O₃	412.6	8	≈70%	6.4
Undecanoate	C₃₀H₄₈O₃	456.7	11	≈63%	8.5

Molecular weights and XLogP3 values are PubChem computed properties; the testosterone share is testosterone’s weight divided by the ester’s weight.

Steroid esters often lack affinity for their receptor and show little direct hormonal activity. A food-safety lab that screens animal feed made this point and used testosterone acetate as a model ester, activating it by hydrolysis (cutting the ester off) before testing it in a yeast androgen bioassay (Rijk et al., Anal Chim Acta 2011).

Once the acetate is removed, what remains is ordinary testosterone. It then acts like testosterone from any source: directly on the androgen receptor, and after conversion to dihydrotestosterone (DHT) or estradiol. In an enzyme study using human placental tissue, labeled testosterone acetate was first hydrolyzed to testosterone, and that testosterone was then converted to estradiol. Almost no estradiol acetate formed, so the ester does not seem to be aromatized directly (Larner et al., Steroids 1992).

How it behaves in the body

Why the ester matters

The ester’s only job is to change how fast testosterone is released. The Depo-Testosterone label explains the general principle: testosterone esters are less polar than free testosterone, and when injected in oil they are absorbed slowly from the oil depot (FDA label). Longer ester chains make the molecule less water-soluble, and that is linked to a longer effect (Bellmann et al., Acta Endocrinol 1976).

Acetate is the least fat-soluble of the esters in the table above. That fits the common description of it as a short-acting ester. But we found no human study that measured how long testosterone acetate raises blood testosterone, so no reliable half-life or dosing interval can be given. The sibling page on testosterone propionate, a one-carbon-longer ester with human data, is the closest documented comparison.

Ester cleavage in human tissue

One in-vitro study compared how quickly samples of female human tissue cleave testosterone acetate versus testosterone enanthate (Bellmann et al., Acta Endocrinol 1976):

Human tissue (in vitro)	Faster cleavage of
Subcutaneous fat	Long-chain esters (enanthate)
Myometrium and endometrium	Long-chain esters
Gastric mucosa, rectus muscle, placenta, vaginal mucosa	Short-chain esters (acetate)

The authors concluded that short- and long-chain steroid esters are probably cleaved by different enzymes. These are test-tube results and do not give a half-life in the body.

Animal data

The few in-vivo studies of testosterone acetate were done in animals:

Buccal tablets in dogs. In castrated male dogs, a bioadhesive tablet placed in the cheek delivered testosterone better than tablets containing its acetate, propionate, enanthate or decanoate esters. The authors attributed this to the esters’ lower solubility (Voorspoels et al., Pharm Res 1996).
Hair testing in rats. Rats given 10 mg/kg/day testosterone acetate by intraperitoneal injection for 5 days had no detectable testosterone or testosterone acetate in their hair (Höld et al., J Anal Toxicol 1999).

Regulatory status

United States. We found no testosterone acetate product in FDA’s Drugs@FDA or National Drug Code (NDC) Directory databases (openFDA). It is still a controlled substance: Schedule III lists testosterone “including its salts, esters and ethers” (21 CFR 1308.13).
Sport. Testosterone is an anabolic androgenic steroid under section S1.1 of the WADA list, prohibited in and out of competition. The list extends to substances with similar structure or effects “including their esters” (WADA 2026 Prohibited List).
Not in Sustanon 250. The multi-ester product Sustanon 250 contains testosterone propionate, phenylpropionate, isocaproate and decanoate, not acetate (Forsdahl et al., Drug Test Anal 2015). See Sustanon 250.

Former medical use

The record of medical use is thin. The PubMed record of a 1946 French case report describes improvement of kraurosis penis (a hardening, scarring condition of the foreskin) after 50 injections of testosterone acetate (Degos et al., Ann Dermatol Syphiligr 1946). A 1957 Hungarian paper on the carcinogenic effect of “Androfort (testosterone acetate)” shows that a product was available there (Kendrey et al., Kiserl Orvostud 1957). Neither paper has an abstract in PubMed, so their doses and results cannot be summarized here.

What the research shows

No controlled human trials

We found no randomized or controlled human trial of testosterone acetate for any outcome, including muscle, strength or hypogonadism. Any claim about how its effects differ from other testosterone esters in people is not backed by published data.

Testosterone itself

Because testosterone acetate releases testosterone, its effects should depend on the amount of testosterone delivered and the blood levels reached, not on the ester. The best human dose-response data come from testosterone enanthate. In a 20-week trial, 61 healthy young men had their own testosterone suppressed and received 25–600 mg/week testosterone enanthate (Bhasin et al., Am J Physiol Endocrinol Metab 2001):

Weekly dose (enanthate)	Mean nadir testosterone	Fat-free mass change
25 mg	253 ng/dL	Gain not reported
50 mg	306 ng/dL	Gain not reported
125 mg	542 ng/dL	+3.4 kg
300 mg	1,345 ng/dL	+5.2 kg
600 mg	2,370 ng/dL	+7.9 kg

The abstract reports fat-free mass gains only for the three higher doses. Gains tracked the logarithm of the testosterone level (r = 0.73). Hemoglobin rose and HDL cholesterol fell as testosterone levels rose. These results are for enanthate; no equivalent data exist for acetate.

Animal muscle data

In female rats, testosterone acetate at 40 mg/kg/day under the skin for 12 days made the gastrocnemius (calf) muscle 8% heavier than in controls. It did not prevent muscle loss from cortisol: rats given both steroids had muscles 18% lighter than controls, versus 20% lighter with cortisol alone (Capaccio et al., J Appl Physiol 1987). These are rat results and should not be applied to people.

Side effects and risks

No safety study of testosterone acetate itself exists. Its risks are expected to be those of testosterone and other anabolic steroids. The points below come from the testosterone cypionate label and human testosterone studies.

Effects shared by testosterone products

The Depo-Testosterone label lists, among others (FDA label):

Polycythemia (too many red blood cells). The label says hemoglobin and hematocrit should be checked periodically during long-term use.
Blood pressure. Testosterone can raise blood pressure, which can increase cardiovascular risk over time.
Blood clots. Postmarketing reports describe deep vein thrombosis and pulmonary embolism.
Cardiovascular events. Some studies, but not all, have linked testosterone therapy to a higher risk of heart attack, stroke and cardiovascular death.
Liver. Cholestatic jaundice, abnormal liver tests and, rarely, liver tumors and peliosis hepatis (blood-filled liver cysts).
Anticoagulants. Androgens may increase sensitivity to oral anticoagulants.

Fertility and hormone suppression

Outside testosterone shuts down the body’s own production through feedback on the pituitary. The label states that this lowers LH. At large doses it can also suppress sperm production by lowering FSH (FDA label). Testicular atrophy, subfertility and infertility are listed among reactions reported with abuse.

Lipids

A meta-analysis of 19 studies in 272 hypogonadal men on injected testosterone esters found small average decreases: HDL cholesterol −4 mg/dL (95% CI −5 to −2) and LDL cholesterol −5 mg/dL (95% CI −8 to −1) (Whitsel et al., Am J Med 2001). Those were replacement doses. In the dose-response trial above, HDL fell further as testosterone levels rose.

Abuse at high doses

The label lists serious reactions reported in people who abuse anabolic steroids, including (FDA label):

cardiac arrest, heart attack, hypertrophic cardiomyopathy and heart failure;
stroke;
liver toxicity;
major depression, mania, paranoia, psychosis, hallucinations and aggression.

In women, reported effects include facial and body hair growth, voice deepening, clitoral enlargement, male-pattern baldness and menstrual changes. In adolescents, early closure of the growth plates can stop growth.

Who should not use testosterone

The label’s contraindications are men with breast or known or suspected prostate cancer, pregnant women, people with serious heart, liver or kidney disease, and known hypersensitivity (FDA label).

Unregulated products

Since no approved product exists, any testosterone acetate in circulation is made outside the regulated drug supply. Its dose, purity and sterility are not checked by a regulator.

Detection in sport

Doping labs treat an intact testosterone ester found in blood as unequivocal proof that testosterone was given from outside the body (Forsdahl et al., Drug Test Anal 2015). Testosterone acetate is one of the target esters in published doping-control methods:

Mass spectrometry of plasma. It was among nine testosterone esters characterized for detection in blood plasma (Shackleton et al., Steroids 1997).
Dried blood spots. A 2014 screening assay for eight steroid esters in finger-prick dried blood spots included it (Tretzel et al., J Pharm Biomed Anal 2014).
Blood tubes matter. In a study of six participants given injected esters (not acetate), measured blood levels of short-chain esters in particular depended on the type of collection tube. The detection window was similar across tube types (Forsdahl et al., Drug Test Anal 2015).

Key takeaways

The shortest testosterone ester. Acetate adds only two carbons, so about 87% of each milligram is testosterone.
A prodrug for ordinary testosterone. The ester must be cut off before the hormone acts, and the testosterone released then converts to DHT and estradiol as usual.
No human pharmacokinetic data. Its half-life in people has not been measured, so quoted half-lives and dosing intervals are not supported by published studies.
No approved product. We found no FDA-listed testosterone acetate. It remains Schedule III in the US and is prohibited by WADA.
Risks are those of testosterone. Expect red-cell increases, lower HDL, suppressed fertility and the cardiovascular and psychiatric risks the label lists for steroid abuse.

Sources

National Center for Biotechnology Information. Testosterone acetate, PubChem CID 92145. PubChem.
National Center for Biotechnology Information. Testosterone, PubChem CID 6013. PubChem.
Pfizer. Depo-Testosterone (testosterone cypionate) injection, prescribing information. DailyMed.
U.S. Food and Drug Administration. Drugs@FDA and NDC Directory datasets, searched for “testosterone acetate” on October 11, 2026. openFDA.
Rijk JC, Ashwin H, van Kuijk SJ, et al. Bioassay based screening of steroid derivatives in animal feed and supplements. Anal Chim Acta. 2011;700(1-2):183–188. PubMed.
Larner JM, Pahuja SL, Brown VM, Hochberg RB. Aromatase and testosterone fatty acid esters: the search for a cryptic biosynthetic pathway to estradiol esters. Steroids. 1992;57(10):475–479. PubMed.
Bellmann O, Duhme HJ, Gerhards E. In vitro studies on enzymatic cleavage of steroid esters in the female organism. Acta Endocrinol (Copenh). 1976;81(4):839–853. PubMed.
Voorspoels J, Remon JP, Eechaute W, De Sy W. Buccal absorption of testosterone and its esters using a bioadhesive tablet in dogs. Pharm Res. 1996;13(8):1228–1232. PubMed.
Höld KM, Borges CR, Wilkins DG, et al. Detection of nandrolone, testosterone, and their esters in rat and human hair samples. J Anal Toxicol. 1999;23(6):416–423. PubMed.
U.S. Drug Enforcement Administration. Schedules of controlled substances: Schedule III. 21 CFR 1308.13. eCFR.
World Anti-Doping Agency. The 2026 Prohibited List: International Standard. In effect January 1, 2026. WADA.
Forsdahl G, Erceg D, Geisendorfer T, et al. Detection of testosterone esters in blood. Drug Test Anal. 2015;7(11-12):983–989. PubMed.
Degos R, Delort J, Hewitt J. Kraurosis penis; considerable improvement in the sclerosis of the preputial ring after 50 injections of testosterone acetate [in French]. Ann Dermatol Syphiligr (Paris). 1946;6:127. PubMed.
Kendrey G, Balo J, Juhasz J. Carcinogenic effect of androfort (testosterone acetate) [in Hungarian]. Kiserl Orvostud. 1957;9(5-6):531–536. PubMed.
Bhasin S, Woodhouse L, Casaburi R, et al. Testosterone dose-response relationships in healthy young men. Am J Physiol Endocrinol Metab. 2001;281(6):E1172–E1181. PubMed.
Capaccio JA, Kurowski TT, Czerwinski SM, Chatterton RT Jr, Hickson RC. Testosterone fails to prevent skeletal muscle atrophy from glucocorticoids. J Appl Physiol. 1987;63(1):328–334. PubMed.
Whitsel EA, Boyko EJ, Matsumoto AM, Anawalt BD, Siscovick DS. Intramuscular testosterone esters and plasma lipids in hypogonadal men: a meta-analysis. Am J Med. 2001;111(4):261–269. PubMed.
Shackleton CH, Chuang H, Kim J, de la Torre X, Segura J. Electrospray mass spectrometry of testosterone esters: potential for use in doping control. Steroids. 1997;62(7):523–529. PubMed.
Tretzel L, Thomas A, Geyer H, et al. Use of dried blood spots in doping control analysis of anabolic steroid esters. J Pharm Biomed Anal. 2014;96:21–30. PubMed.

Testosterone Acetate