For laboratory research use only. Not for human consumption. All compounds referenced in this article are sold by Explicit SARMs solely as reference materials for in-vitro and animal research by qualified professionals. Nothing here is medical advice, and no statement has been evaluated by the FDA. These materials are not intended to diagnose, treat, cure or prevent any disease.
S-23 is a nonsteroidal selective androgen receptor modulator (SARM) from the aryl-propionamide family, the same chemical lineage that produced S4 (Andarine) and Ostarine. It stands out in that family for two reasons: its very high binding affinity for the androgen receptor, and the specific research question it was developed to answer, which was whether a SARM could serve as the androgen component of a reversible hormonal male contraceptive in animal models.
Unlike Ostarine or LGD-4033, S-23 has no published human clinical data. Its literature is preclinical, built mainly on a 2009 rat study from the Dalton laboratory. This review covers what that research reports, how S-23 acts at the androgen receptor, and what laboratories should consider. Explicit SARMs supplies S23 Capsules strictly as laboratory reference material.
What Is S-23?
S-23 is (S)-N-(4-cyano-3-trifluoromethyl-phenyl)-3-(3-fluoro, 4-chlorophenoxy)-2-hydroxy-2-methyl-propanamide. [1] Its structure follows the aryl-propionamide template first explored in the hydroxyflutamide and bicalutamide series of antiandrogens, then modified to produce AR agonists. [3]
- Common names: S-23, S23
- Class: nonsteroidal selective androgen receptor modulator (aryl-propionamide)
- Primary target: androgen receptor
- Research setting: preclinical (rat) studies; no registered human trials
- Regulatory status: not approved by the FDA or any other regulator for any indication
Mechanism of Action
S-23 binds the androgen receptor’s ligand-binding domain and acts as a full agonist in vitro, with an inhibitory constant (Ki) reported at about 1.7 nM, which places it among the higher-affinity compounds in the class. [1] Once bound, the receptor translocates to the nucleus, binds androgen response elements and recruits coregulators.
Like other nonsteroidal SARMs, S-23 is not a substrate for 5-alpha reductase or aromatase, so it is not converted to DHT-like or estrogenic metabolites. Its tissue selectivity in rats was measured in the standard way, by comparing potency in the levator ani muscle against potency in the prostate. In castrated male rats, S-23 was markedly more potent in the levator ani than in the prostate, with an ED50 roughly five-fold lower in muscle. [1]
S-23 also acts strongly at the pituitary. By activating the androgen receptor there, it suppresses luteinizing hormone (LH) and follicle-stimulating hormone (FSH), the signals that drive testicular testosterone production and spermatogenesis. That pituitary activity is the core of its research interest.
Research History
The research group of James Dalton and Duane Miller developed a series of aryl-propionamide SARMs in the 2000s. Some, such as S-4, were characterized for muscle and bone in hormone-deficient rat models. [2] S-23 was designed and characterized with a different goal: a potent, non-injectable androgen that could suppress gonadotropins enough to stop sperm production while maintaining androgen-dependent functions elsewhere.
The key paper, published in Endocrinology in 2009 by Jones and colleagues, remains the primary reference for the compound. [1]
What Published Studies Report
Gonadotropin suppression
In intact male rats treated for 14 days, S-23 alone suppressed LH by more than 50% at higher exposures, with a reduction in prostate size and an increase in levator ani muscle size. [1]
Reversible contraception in rats
In a longer study lasting up to 10 weeks, intact male rats received S-23 together with estradiol benzoate, which the authors used to maintain sexual behavior in the rats. The combination suppressed LH and FSH and spermatogenesis. In one group, four of six animals had no sperm in the testis, and mating trials produced no pregnancies. After treatment stopped, fertility fully recovered, with a 100% pregnancy rate after 100 days of recovery. Estradiol benzoate alone had no effect on spermatogenesis. [1]
Other tissue effects
The same study reported dose-dependent increases in bone mineral density and lean mass, and reductions in fat mass, in the treated rats. [1] These are animal findings from a single laboratory and have not been tested in controlled human studies.
Research Considerations
- Potency. High AR affinity means small mass errors produce large exposure differences. Use calibrated balances and verified stock solutions.
- HPG-axis endpoints. Because pituitary suppression is a central effect, LH, FSH, testosterone, testis histology and sperm counts are the natural endpoints in rodent work.
- Combination designs. The published contraception model relied on estradiol benzoate co-administration. Studies that omit it are not directly comparable.
- Recovery phase. The reversibility finding is one of the most important results; designs that include a washout and recovery period allow direct comparison with the original data.
- Limited replication. With one principal preclinical paper, independent replication is valuable. Validate identity and purity carefully so results can be attributed to S-23 itself.
S-23 in the Context of Male Contraception Research
The idea behind the S-23 work has a long history. Testosterone alone, given at high enough exposure, suppresses LH and FSH and therefore spermatogenesis, and this was explored for decades as a hormonal male contraceptive strategy. Steroidal approaches have practical drawbacks, including the need for injectable formulations and effects on androgen-dependent tissues. [3]
A non-injectable SARM with strong pituitary activity offered a possible alternative, and S-23 was characterized with that question in mind. The rat data showed that the approach could work in principle in that species: gonadotropins were suppressed, sperm production stopped in most animals, and fertility returned after treatment ended. [1]
Two caveats limit interpretation. First, the published regimen depended on estradiol benzoate co-administration to maintain sexual behavior in rats, so the contribution of S-23 alone to that outcome cannot be isolated. Second, the findings come from a single species and have not been followed by registered human studies.
WADA Status
S-23 is named explicitly in WADA section S1.2 (Other Anabolic Agents) and is prohibited at all times. [5] Detection methods for SARMs, including aryl-propionamides, are well established in anti-doping laboratories. [4]
Storage, Purity and COA
- Store capsules sealed, dry, and away from light and heat.
- Label every container and log lot numbers and receipt dates in study records.
- Review the lot-specific Certificate of Analysis. A credible COA reports HPLC purity, confirms identity by mass spectrometry, and lists the lot number and analysis date.
- Because S-23 is a single enantiomer (the S form), chiral purity can matter for receptor activity. Ask whether chiral analysis is available for the lot.
For lot documentation, use the contact page.
Related Research Compounds
- S4 Andarine Capsules, an earlier SARM from the same laboratory and chemical family
- Ostarine MK-2866 Capsules, the aryl-propionamide that progressed furthest in clinical trials
- RAD-140 Testolone Capsules, a high-affinity SARM from a different chemical series
- Class overview: SARMs vs Traditional Research Compounds and the SARMs collection
Frequently Asked Questions
What is S-23 used for in research?
Its primary published use is as a potent androgen receptor agonist in rat models of hormonal male contraception, where it was combined with estradiol benzoate to suppress gonadotropins and spermatogenesis reversibly. [1]
Has S-23 been tested in human clinical trials?
No. There are no registered or published human clinical trials of S-23. Its literature is preclinical.
How does S-23 compare with Ostarine?
Both are aryl-propionamide SARMs. S-23 has higher reported AR affinity and stronger pituitary suppression in rats, while Ostarine has a large clinical trial record.
Is S-23 approved by the FDA?
No. S-23 has never been approved by the FDA or any other regulator.
Is S-23 prohibited in sport?
Yes. It is named in WADA section S1.2 and is prohibited at all times. [5]
Why did the rat study use estradiol benzoate?
The authors added estradiol benzoate to maintain sexual behavior in the rats, because strong suppression of endogenous testosterone and its estrogen metabolite can reduce mating behavior. Estradiol benzoate alone did not affect spermatogenesis. [1]
What makes S-23 useful as a research tool?
Its high AR affinity, full agonist activity in vitro and strong pituitary suppression make it a useful probe for studying androgen receptor control of the HPG axis in rodents. [1]
References
- Jones A, et al. 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. PubMed 18772237
- Gao W, et al. Selective androgen receptor modulator treatment improves muscle strength and body composition and prevents bone loss in orchidectomized rats. Endocrinology. 2005. PubMed 16099859
- Narayanan R, et al. Development of selective androgen receptor modulators (SARMs). Mol Cell Endocrinol. 2018. PubMed 28624515
- Thevis M, Schanzer W. Detection of SARMs in doping control analysis. Mol Cell Endocrinol. 2018. PubMed 28137616
- World Anti-Doping Agency. 2026 Prohibited List. wada-ama.org
For laboratory research use only. Not for human consumption. All compounds referenced in this article are sold by Explicit SARMs solely as reference materials for in-vitro and animal research by qualified professionals. Nothing here is medical advice, and no statement has been evaluated by the FDA. These materials are not intended to diagnose, treat, cure or prevent any disease.