Selective androgen receptor modulators (SARMs) are a class of synthetic compounds studied in the laboratory for their ability to bind the androgen receptor (AR) with apparent tissue selectivity. In preclinical research they are of interest because they appear to favour anabolic signalling in muscle and bone while showing weaker activity in tissues such as the prostate. This article explains, for educational and research-reference purposes, how SARMs are understood to act at the androgen receptor, why tissue selectivity arises, and what the published literature does and does not establish. It is written as laboratory information only and is not guidance for human use.

What are SARMs?

SARMs are synthetic molecules designed in drug-discovery research to bind the androgen receptor, the same nuclear receptor activated by testosterone and dihydrotestosterone. Most well-characterised SARMs are nonsteroidal, meaning their chemical scaffold differs from the steroid ring system of testosterone. In experimental models they behave as receptor agonists or partial agonists. They are investigational research compounds: none has been approved as a medicine by the FDA, EMA, or MHRA, and they are studied here strictly as laboratory reference materials, not as products for human consumption.

How do SARMs work at the androgen receptor?

In laboratory models, a SARM molecule binds the ligand-binding domain of the androgen receptor. This binding induces a conformational change in the receptor that influences which regulatory proteins, called coactivators and corepressors, can dock onto it. The receptor-ligand complex then interacts with androgen-response elements on DNA and modulates transcription of androgen-responsive genes. Because different ligands stabilise slightly different receptor shapes, they can recruit different sets of coregulators, which is one proposed basis for the distinct gene-expression patterns observed with SARMs compared with classical androgens in cell and animal studies.

What does tissue selectivity actually mean?

Tissue selectivity refers to the observation, in animal and cell research, that some SARMs produce stronger anabolic responses in muscle and bone than androgenic responses in tissues such as the prostate. The androgen receptor protein itself is the same throughout the body, so the receptor is not the source of selectivity. Instead, researchers attribute differences to the mix of coregulatory proteins present in each tissue and to ligand-specific receptor conformations. Selectivity in published studies is relative and context-dependent, not absolute, and is typically described using an "anabolic-to-androgenic" ratio derived from animal assays.

Why are SARMs different from anabolic steroids?

A key structural distinction is that many SARMs are nonsteroidal. Because they are not built on the testosterone scaffold, they are generally not substrates for the enzymes 5-alpha-reductase or aromatase, which convert testosterone into dihydrotestosterone or estradiol respectively. In research interpretations, this lack of steroidal metabolism may explain part of the apparent selectivity: classical steroids are amplified into more potent androgens in some tissues, whereas nonsteroidal SARMs are not. A 2025 critical appraisal argues that much of the observed selectivity may stem from these metabolic differences rather than from a wholly novel receptor mechanism.

How do SARMs compare with anabolic-androgenic steroids?

The table below summarises commonly described research-level differences between nonsteroidal SARMs and anabolic-androgenic steroids. These are generalisations drawn from preclinical and early clinical literature and do not apply uniformly to every compound.

Which SARMs appear most often in research?

Several SARMs recur throughout the scientific literature as reference compounds. The most studied include the following:

• Ostarine (enobosarm, MK-2866, GTx-024)
• Ligandrol (LGD-4033)
• Andarine (S-4)
• Testolone (RAD140)
• S23
• YK-11

What is Ostarine (enobosarm) known for in studies?

Ostarine is among the most extensively investigated SARMs. In published research it has acted as a partial agonist at the androgen receptor with a preference for skeletal muscle and bone in animal models. It has been examined in clinical trials for muscle-wasting conditions; a phase 2 study in patients with cancer reported increases in lean body mass relative to placebo. It remains investigational and is not an approved medicine in the UK, EU, or US.

What about Ligandrol, Andarine, Testolone, and others?

Ligandrol (LGD-4033) is frequently described in research as a relatively potent nonsteroidal agonist. Andarine (S-4) has been noted in early studies for muscle and bone activity, with reports of visual side effects in some contexts. Testolone (RAD140) appears in preclinical work as a high-affinity AR ligand. Compounds such as S23 and YK-11 are far less characterised; YK-11 is sometimes discussed in relation to myostatin pathways, but human data are very limited. All are research compounds only.

What does the published research show overall?

Across the literature, SARMs consistently demonstrate anabolic effects on muscle and bone in animal models, and some early clinical trials report measurable gains in lean body mass. However, evidence for improvements in physical strength and function is mixed, and long-term safety in humans has not been established. Reported research findings include androgen suppression, changes in liver-associated blood markers, and lipid changes. Reviewers caution that the marketed image of SARMs as side-effect-free anabolics is not supported by the current evidence base.

What is the legal and regulatory status of SARMs in the UK?

SARMs are not licensed medicines in the United Kingdom and have not been evaluated or approved by the MHRA, nor by the EMA in the EU or the FDA in the US. They cannot lawfully be sold or marketed as dietary supplements or for human consumption, and regulators including the FDA have issued public safety warnings. They are also prohibited in sport at all times by the World Anti-Doping Agency (WADA). In legitimate settings they are handled only as laboratory research chemicals by qualified personnel.

Summary

SARMs are investigational compounds that bind the androgen receptor and, in preclinical research, show a relative preference for anabolic activity in muscle and bone. Their apparent tissue selectivity is linked to ligand-specific receptor conformations, tissue-specific coregulator proteins, and, for nonsteroidal SARMs, the absence of steroidal metabolism. While early clinical work is promising for conditions such as muscle wasting, robust long-term human safety and efficacy data are lacking, and no SARM is an approved medicine. The information here is provided for scientific and educational reference only.

Research references

• Bond P, Smit DL, Verdegaal T, de Ronde W. Selective androgen receptor modulators: a critical appraisal. Frontiers in Endocrinology. 2025;16:1634799. DOI: 10.3389/fendo.2025.1634799
• Bhasin S, Jasuja R. Selective androgen receptor modulators as function promoting therapies. Current Opinion in Clinical Nutrition and Metabolic Care. 2009;12(3):232-240. DOI: 10.1097/MCO.0b013e32832a3d79
• Dobs AS, Boccia RV, Croot CC, et al. Effects of enobosarm on muscle wasting and physical function in patients with cancer: a double-blind, randomised controlled phase 2 trial. The Lancet Oncology. 2013;14(4):335-345. DOI: 10.1016/S1470-2045(13)70055-X
• LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Selective Androgen Receptor Modulators. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases. NCBI Bookshelf NBK619971

Disclaimer: This article is provided for laboratory and educational research purposes only. SARMs are not approved medicines and are not intended for human consumption, diagnosis, treatment, or to prevent any disease. Nothing here is medical advice or a recommendation of use.