S-23 is an experimental nonsteroidal selective androgen receptor modulator (SARM). It was developed in the 2000s by researchers at the Ohio State University, the University of Tennessee and the company GTx, and was first described in 2008 as a candidate for an oral hormonal male contraceptive (Jones et al., Endocrinology 2009).
The single most important fact is that S-23 has never been tested in a clinical trial and has never been approved as a medicine. Its effects on muscle, fat, bone and fertility are known only from rat studies. Everything known about S-23 in people comes from anti-doping metabolism studies in a handful of volunteers, one case report and analyses of products sold online. Unlike some other SARMs, S-23 was a full androgen in the rat prostate, not a “prostate-sparing” compound, and it strongly suppressed the hormones that drive sperm production.
This page summarizes what the rat studies, anti-doping research and product analyses report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Nonsteroidal SARM (aryl-propionamide type) |
| Chemical name | (2S)-3-(4-chloro-3-fluorophenoxy)-N-[4-cyano-3-(trifluoromethyl)phenyl]-2-hydroxy-2-methylpropanamide |
| Formula and weight | C₁₈H₁₃ClF₄N₂O₃, 416.8 g/mol |
| Approval status | Never approved; never entered a clinical trial |
| Routes studied | Oral and intravenous (rat kinetics); daily subcutaneous injection in rat efficacy studies |
| Half-life | Rat data only: 10.9 h (IV) and 11.9 h (oral); no human half-life published |
| Oral bioavailability | 96% in rats |
| Key mechanism fact | Full androgen receptor agonist; strongly suppressed LH and FSH in rats |
| US status | Not FDA approved; not named as a Schedule III anabolic steroid |
| WADA status | Prohibited at all times, named in class S1.2 (other anabolic agents) |
What it is
S-23 is not a steroid. It belongs to the aryl-propionamide family of SARMs, the same chemical family as ostarine (enobosarm) and andarine (S-4) (PubChem). A SARM binds the androgen receptor, the same receptor that testosterone and dihydrotestosterone (DHT) act on. The aim of SARM design is full activity in muscle and bone with weaker activity in the prostate and other “androgenic” tissues.
S-23 differs from its close relatives only in the substituents on its rings:
| Compound | A-ring group (para position) | B-ring (phenoxy) group | Source |
|---|---|---|---|
| S-23 | Cyano | 4-chloro-3-fluoro | PubChem |
| C-6 (earlier research compound) | Nitro | 4-chloro-3-fluoro | Jones et al., Endocrinology 2009 |
| Ostarine (enobosarm) | Cyano | 4-cyano | PubChem |
The developers made S-23 by swapping the nitro group of C-6 for a cyano group. This roughly doubled binding strength and doubled potency in rats (Jones et al., Endocrinology 2009). Key laboratory findings:
- Receptor binding. S-23 bound the rat androgen receptor with a Ki (a measure of binding strength; lower is stronger) of 1.7 nM, compared with 0.45 nM for DHT. A later paper put its binding at 26.5% of DHT’s, the highest in a series of related compounds (Jones et al., JPET 2010).
- Full agonist. In cell assays, S-23 at 100 nM activated the androgen receptor to 101% of the response to 1 nM DHT. Its mirror-image form (R-23) barely bound the receptor and had no activity in rats.
- Estrogen receptors. S-23 showed weak partial activity at estrogen receptor alpha in cell assays (≈25% of estradiol’s response). It is not a steroid and was described as nonaromatizable, meaning it is not converted to estradiol.
About “tissue selectivity.” S-23 is often grouped with SARMs that are said to spare the prostate. In the developers’ own comparison of nine related compounds in castrated rats, S-23 was the exception: it showed “full agonist activity in androgenic and anabolic tissues,” keeping the prostate at 110% and the levator ani muscle at 136% of intact levels, while the other compounds were prostate-sparing (Jones et al., JPET 2010).
Pharmacokinetics
In rats
The only formal pharmacokinetic study gave male rats a single 10 mg/kg dose by vein or by mouth (Jones et al., Endocrinology 2009):
| Parameter | 10 mg/kg IV (n = 4) | 10 mg/kg oral (n = 5) |
|---|---|---|
| Terminal half-life | 10.9 h | 11.9 h |
| Oral bioavailability | Not applicable | 96% |
| Time to peak | Not applicable | Plateau 6–10 h after the dose (mean Tmax 252 min) |
| Clearance | 0.87 mL/min/kg | 0.90 mL/min/kg (CL/F) |
| Volume of distribution (steady state) | 655 mL/kg | 649 mL/kg (Vss/F) |
These are rat values. Drug handling can differ greatly between species, and no human pharmacokinetic study has been published.
In people (anti-doping studies)
Three small administration studies were run by anti-doping and forensic laboratories to learn how long S-23 stays detectable in urine. They did not measure a half-life, effects or safety:
| Study | Who and what | Main finding |
|---|---|---|
| Ameline et al., J Pharm Biomed Anal 2022 | 1 volunteer, single oral dose of ≈8 mg | S-23 detectable in urine from 2 h to 28 days (0.5–93 ng/mL); hair taken one month later was negative |
| Alhalabi et al., Biomed Chromatogr 2025 | 5 healthy men per dose; single and repeated oral microdoses of 1, 10 and 50 µg | 18 metabolites found; a single 1 µg dose was detectable for up to 253 h on average, a single 50 µg dose for up to 544 h |
| Korsmeier et al., J Anal Toxicol 2025 | 5 volunteers per dose; 10 or 50 µg applied to the forearm skin | S-23 crossed the skin and was traceable in urine for up to 16 and 24 days |
S-23 is broken down in the liver mainly by hydroxylation (adding an -OH group), loss of the B-ring and glucuronidation (attachment of a sugar acid that helps excretion), according to studies with human liver enzymes (Thevis et al., Drug Test Anal 2010; Ameline et al., 2022). The long detection windows, even after microgram doses, mean that a contaminated supplement can cause a positive doping test.
Regulatory status
- No approval and no clinical trials. S-23 has never been approved by the FDA or any other regulator. A 2025 anti-doping paper states that S-23 “never became subject of a clinical trial” (Alhalabi et al., 2025). Italian regulators testing SARM products noted that no SARM is approved for human consumption (Maccelli et al., Anal Methods 2024).
- Not on the DEA’s anabolic steroid list. S-23 is not among the substances named in the federal Schedule III list (21 CFR 1308.13). That does not make it an approved or legal drug for human use.
- Banned in sport. The WADA list names S-23 under S1.2 “other anabolic agents,” prohibited at all times (in and out of competition) and classed as a non-specified substance (WADA 2026 Prohibited List). WADA reported 1 adverse analytical finding (a positive test) for S-23 in 2019, none in 2020, 2 in 2021 and 5 in 2022 (Alhalabi et al., 2025).
What the research shows
All efficacy data below come from rats. Doses are in mg per day or mg/kg of rat body weight, usually given by injection, and they cannot be converted into human doses.
Muscle and prostate in castrated rats
Castrated rats were given daily injections of S-23 (0.01–3 mg/day, n = 5 per group) for 14 days (Jones et al., Endocrinology 2009):
| Tissue | ED50 (dose giving half the maximum effect) | Maximum effect (% of intact rats) |
|---|---|---|
| Levator ani muscle | 0.079 mg/day | 129% |
| Prostate | 0.43 mg/day | 138% |
| Seminal vesicles | 0.41 mg/day | 144% |
At 0.1 mg/day, S-23 kept the levator ani muscle (a standard rat measure of anabolic effect) at intact levels while the prostate and seminal vesicles stayed under 30% of normal. At 1 mg/day, the prostate and seminal vesicles were kept at or above normal size. In other words, selectivity was seen only at low doses.
Hormone suppression and male fertility in rats
In 14-day studies, S-23 lowered LH (luteinizing hormone, the pituitary signal that tells the testes to make testosterone) in a dose-dependent way. In intact rats, LH fell from 0.58 ng/mL in controls to 0.25 ng/mL at 0.1 mg/day, 0.08 ng/mL at 0.3 mg/day and below the assay limit at 0.75 mg/day and above (Jones et al., Endocrinology 2009).
The main study treated intact male rats for 70 days with S-23 plus a small dose of estradiol benzoate (EB, 5 µg/day). The EB was added because male rats need estrogen to keep normal mating behavior; it is not part of how S-23 would act in people:
| Group (70 days) | Testis weight (% of control) | Levator ani (% of control) | Males fertile in mating trial | Pregnancies |
|---|---|---|---|---|
| Vehicle | 100% | 100% | All | 12/12 |
| EB alone | 94% | 62% | 4 of 5 | 8/10 |
| EB + S-23 0.1 mg/day | 34% | 97% | 0 of 6 | 0/12 |
| EB + S-23 0.3 mg/day | 45% | 100% | 1 of 6 | 2/12 |
- Sperm. At 0.1 mg/day, 4 of 6 rats had no sperm in the testis and the other 2 had very low counts. Higher doses (up to 0.75 mg/day) restored sperm production, a biphasic effect the authors attributed to S-23 itself acting on the testis at high doses.
- Reversibility. In a separate recovery group, 83% fertility returned 70 days after stopping, and the authors reported full recovery by about 100 days.
- Body composition. Fat mass fell and fat-free mass rose in a dose-dependent way. Bone mineral density did not change dose-dependently with S-23 on top of EB.
Female rats
In ovariectomized female rats (a model of menopause), S-23 increased sexual motivation in a partner-preference test at most doses from 0.05 mg/day to 3 mg/kg/day. It was also the most uterus-stimulating compound in the series: at 3 mg/kg/day it kept the uterus at 98.9% of intact size, and it drove LH below the assay limit (Jones et al., JPET 2010).
Muscle wasting
The same group reported in 2010 that “a novel SARM” blocked muscle atrophy caused by the steroid dexamethasone or by castration in rats (Jones et al., Endocrinology 2010). A 2025 paper cites this study as S-23 research (Alhalabi et al., 2025), but the abstract does not name the compound.
Humans
No randomized or controlled human study of S-23 exists. The only human exposures in the literature are the anti-doping administration studies above (which reported detection, not effects) and one case report.
Side effects and risks
With no human trials, there are no measured side-effect rates for S-23. The concerns below come from rat pharmacology, from the SARM class and from one case report.
Hormonal suppression
About the “mild” or “non-suppressive” claim. In the rat studies, S-23 was designed to shut down the hormonal signals for sperm production, and it did: LH fell by more than 50% at doses over 0.1 mg/day in 14 days, and LH was undetectable in females given 3 mg/kg/day (Jones et al., 2009; Jones et al., 2010). Testis size fell in every S-23 group. These are rat findings, but they point toward suppression of the body’s own testosterone and sperm production rather than away from it.
Liver, lipids and the one case report
A 27-year-old weightlifter who reported taking S-23 together with LGD-4033 was found on a routine check-up to have an abnormal lipid panel, raised liver enzymes suggesting hepatocellular (liver-cell) injury and suppression of the pituitary–gonadal axis. He had no symptoms, and all values returned to baseline after he stopped (Malave, Bull Natl Res Cent 2023). A review tabulated his peak ALT at 144 IU/L and AST at 75 IU/L after 8 weeks of use, and noted that the products were not tested in the lab (Leciejewska et al., Eur J Clin Pharmacol 2024). Because two drugs were involved, the case cannot be attributed to S-23 alone.
Across the SARM class, a 2023 systematic review counted 15 case reports of drug-induced liver injury and found raised ALT in a mean of 7.1% of SARM-treated trial participants. None of these involved S-23 (Vignali et al., J Xenobiot 2023). One rodent and cell study, which used S-23, found that androgens raise the ALT2 enzyme in muscle and prostate, so part of an ALT rise during androgen use may come from outside the liver (Coss et al., Pharm Res 2012). This does not rule out true liver injury.
Who should not use it
As an unapproved compound with no human safety data, S-23 has no established safe dose for anyone. In rats it suppressed fertility, so effects on sperm production are a specific concern. Competitive athletes face an anti-doping violation, and the human studies show that microgram amounts, swallowed or rubbed on the skin, can be detected for weeks.
Quality and contamination
Products sold as S-23 do not reliably contain it:
- Italy, 2024. Italy’s national health institute (ISS) tested 13 SARM products bought online, including two labeled S-23. One contained S-23 but was contaminated with ligandrol, ostarine and ibutamoren. The other contained no S-23; it had traces of cardarine plus the steroid epimethandienone and the erectile-dysfunction drug tadalafil (Gaudiano et al., Sex Med 2024).
- Supplement contamination. Anti-doping researchers ran their microdose studies specifically because contaminated supplements are a recognized cause of positive SARM tests (Alhalabi et al., 2025).
Key takeaways
- An experimental SARM that never reached trials. S-23 is a nonsteroidal androgen receptor agonist from the ostarine chemical family, developed as a possible male contraceptive. It has never been approved or tested in a clinical trial.
- Potent and less selective than its reputation. In castrated rats it built muscle at low doses but fully stimulated the prostate at higher doses, unlike most related compounds.
- Strongly suppressive in rats. It lowered LH and FSH, shrank the testes and made male rats infertile at 0.1 mg/day, with fertility returning within about 100 days.
- Long-acting in rats, long-detectable in people. The rat half-life was about 11–12 hours with 96% oral absorption. In people, microgram doses stayed detectable in urine for weeks.
- Very little human safety data. The only clinical report describes liver enzyme, lipid and hormone changes in a man also taking LGD-4033.
- Unreliable products and banned in sport. Products labeled S-23 have contained other drugs or none at all, and WADA prohibits it at all times.
Sources
- Jones A, Chen J, Hwang DJ, Miller DD, Dalton JT. Preclinical characterization of a (S)-N-(4-cyano-3-trifluoromethyl-phenyl)-3-(3-fluoro, 4-chlorophenoxy)-2-hydroxy-2-methyl-propanamide: a selective androgen receptor modulator for hormonal male contraception. Endocrinology. 2009;150(1):385–395. PubMed.
- Jones A, Hwang DJ, Duke CB 3rd, et al. Nonsteroidal selective androgen receptor modulators enhance female sexual motivation. J Pharmacol Exp Ther. 2010;334(2):439–448. PubMed.
- Jones A, Hwang DJ, Narayanan R, et al. Effects of a novel selective androgen receptor modulator on dexamethasone-induced and hypogonadism-induced muscle atrophy. Endocrinology. 2010;151(8):3706–3719. PubMed.
- Thevis M, Gerace E, Thomas A, et al. Characterization of in vitro generated metabolites of the selective androgen receptor modulators S-22 and S-23 and in vivo comparison to post-administration canine urine specimens. Drug Test Anal. 2010;2(11-12):589–598. PubMed.
- Coss CC, Bauler M, Narayanan R, et al. Alanine aminotransferase regulation by androgens in non-hepatic tissues. Pharm Res. 2012;29(4):1046–1056. PubMed.
- Ameline A, Gheddar L, Raul JS, Kintz P. In vitro characterization of S-23 metabolites produced by human liver microsomes, and subsequent application to urine after a controlled oral administration. J Pharm Biomed Anal. 2022;212:114660. PubMed.
- Alhalabi H, Korsmeier L, Thomas A, Thevis M. Investigations into the urinary metabolite elimination profile of the selective androgen receptor modulator S-23 in studies mimicking contaminated product ingestion for doping control purposes. Biomed Chromatogr. 2025;39(6):e70090. PubMed.
- Korsmeier L, Krombholz S, Alhalabi H, et al. Exploring transdermal SARMs exposure: analysis of the elimination profiles and metabolism for doping control purposes. J Anal Toxicol. 2025;49(9):681–690. PubMed.
- Malave B. Metabolic and hormonal dysfunction in asymptomatic patient using selective androgen receptor modulators: a case report. Bull Natl Res Cent. 2023;47:11. DOI.
- Leciejewska N, Jędrejko K, Gómez-Renaud VM, et al. Selective androgen receptor modulator use and related adverse events including drug-induced liver injury: analysis of suspected cases. Eur J Clin Pharmacol. 2024;80(2):185–202. PubMed.
- Vignali JD, Pak KC, Beverley HR, et al. Systematic review of safety of selective androgen receptor modulators in healthy adults: implications for recreational users. J Xenobiot. 2023;13(2):218–236. PubMed.
- Gaudiano MC, Aureli F, Manna L, et al. Illegal products containing selective androgen receptor modulators purchased online from Italy: health risks for consumers. Sex Med. 2024;12(2):qfae018. PubMed.
- Maccelli A, Borioni A, Aureli F, et al. A screening method for the quantitative determination of selective androgen receptor modulators (SARMs) in capsules by high resolution (19)F- and (1)H-NMR spectroscopy. Anal Methods. 2024;16(14):2135–2146. PubMed.
- National Center for Biotechnology Information. PubChem Compound Summary for CID 24892822, S-23. PubChem.
- National Center for Biotechnology Information. PubChem Compound Summary for CID 11326715, Enobosarm. PubChem.
- World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA 2026 Prohibited List.
- Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.