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In short: SARMs are small, non-steroidal molecules that bind the androgen receptor and behave differently depending on the tissue they act in. In laboratory models, the better-characterised compounds show anabolic activity in muscle and bone with comparatively weak activity in reproductive tissue. None are approved as medicines, and they are supplied strictly as research reference materials.
- SARM stands for selective androgen receptor modulator — three words that each describe part of how the class behaves.
- They are not steroids. They share a target (the androgen receptor) but not a chemical backbone, and they are not substrates for aromatase or 5α-reductase.
- They are not peptides either. SARMs are small molecules acting on an intracellular receptor; peptides are amino acid chains that typically act at cell-surface receptors.
- Research interest has centred on muscle wasting, bone density, hypogonadism models and androgen-receptor-positive cancers.
- Several compounds sold alongside SARMs — including MK-677 and SR-9009 — are not SARMs at all and act through entirely different receptors.
- Independent purity testing matters: published market analyses have repeatedly found mislabelled research chemicals.
What does "selective androgen receptor modulator" mean?
The name is a description of the mechanism, and it is worth unpacking one word at a time. Each part of the acronym answers a different question about how the class was designed to behave.
Androgen receptor
The androgen receptor (AR) is a nuclear hormone receptor found in muscle, bone, prostate, skin, the central nervous system and elsewhere. Under normal physiology it is activated by testosterone and dihydrotestosterone. Once activated, the receptor moves to the cell nucleus, binds specific DNA sequences and changes which genes are transcribed. The receptor is the target; every compound in this class is defined by its relationship to it.
Modulator
A modulator is not simply an on/off switch. Depending on the compound and the tissue, a modulator can act as a full agonist, a partial agonist, or even an antagonist at the same receptor. This is the same principle behind selective oestrogen receptor modulators (SERMs) such as tamoxifen, which blocks the oestrogen receptor in breast tissue while behaving as an agonist in bone — an established precedent that directly inspired androgen receptor work in the late 1990s.
Selective
Selectivity is the design goal that gives the class its research interest. The aim has been to produce compounds with a favourable ratio of anabolic activity (muscle, bone) to androgenic activity (prostate, seminal vesicles, skin, hair). In animal models this ratio is often reported by comparing the weight of the levator ani muscle against the weight of the prostate and seminal vesicles after treatment — the classic Hershberger assay readout.
How SARMs work at the androgen receptor
All AR ligands begin the same way: the compound diffuses into the cell and binds the receptor's ligand-binding domain. What happens next is where selectivity is thought to originate.
Binding induces a conformational change in the receptor. That shape determines which coregulator proteins — coactivators and corepressors — can dock with the receptor complex. Because different tissues express different coregulators in different proportions, the same compound-receptor complex can drive strong transcription in one tissue and weak transcription in another. Non-steroidal ligands adopt binding poses that differ from testosterone's, and the prevailing explanation for tissue selectivity is that these poses recruit a different coregulator profile.
A second, more concrete mechanism concerns metabolism. In prostate tissue, testosterone is converted by 5α-reductase into dihydrotestosterone, a considerably more potent AR agonist — an amplification step specific to androgen-sensitive tissue. Non-steroidal SARMs are not substrates for 5α-reductase, so this amplification does not occur. They are likewise not substrates for aromatase, the enzyme that converts testosterone into oestradiol, which is why oestrogenic activity is not a feature of the class in the way it is for many steroidal androgens.
The practical consequences that follow from the chemistry are worth noting for anyone designing an experiment: most SARMs in the literature are orally bioavailable in animal models, have short-to-moderate half-lives, and — being small molecules rather than proteins — are considerably more stable in solution than the peptides they are often shelved beside.
"SARM" is used loosely in retail listings and forums, where it often means "any research compound taken orally that is not a steroid". In the scientific literature the term is narrower: a non-steroidal ligand of the androgen receptor with demonstrated tissue-selective activity. This guide uses the narrower definition, and the section on commonly confused compounds covers the ones that get grouped in incorrectly.
How SARMs differ from anabolic-androgenic steroids
This is the most common point of confusion, and the answer is more nuanced than "SARMs are weaker steroids". The two classes share a receptor but differ in chemistry, metabolism and selectivity.
| Property | SARMs | Anabolic-androgenic steroids |
|---|---|---|
| Chemical class | Non-steroidal small molecules — aryl-propionamide, quinolinone, hydantoin and related scaffolds | Derivatives of the four-ring steroid nucleus of testosterone |
| Molecular target | Androgen receptor | Androgen receptor |
| Tissue selectivity | Central design goal; anabolic-to-androgenic ratios in animal models are typically far higher | Limited; anabolic and androgenic effects are difficult to separate |
| Aromatisation to oestradiol | Not a substrate for aromatase | Many aromatise, producing oestrogenic activity |
| 5α-reduction in prostate | Not a substrate — no local amplification | Testosterone is amplified to DHT in androgen-sensitive tissue |
| Oral activity | Generally orally bioavailable without 17α-alkylation | Oral forms typically require 17α-alkylation, associated with hepatic strain |
| Regulatory status | No compound approved as a medicine in any major jurisdiction | Several approved medicines exist; most are controlled substances |
| Anti-doping | Prohibited by WADA at all times, listed under "other anabolic agents" since 2008 | Prohibited by WADA at all times |
The short version: the difference is not potency but architecture. A steroid is a modified hormone that goes wherever the hormone goes and does much of what the hormone does. A SARM is a purpose-built molecule that engages the same receptor while deliberately avoiding some of the downstream chemistry.
How SARMs differ from research peptides
Because both appear in the same catalogues, SARMs and peptides are often treated as variations on a theme. Mechanistically they have almost nothing in common, and the practical handling requirements are different enough to matter in the lab.
| Property | SARMs | Research peptides |
|---|---|---|
| Structure | Small synthetic molecules, typically under 500 Da | Chains of amino acids, commonly 3–50 residues |
| Receptor location | Intracellular — the ligand must cross the cell membrane | Usually cell-surface receptors, triggering second-messenger cascades |
| Mode of action | Direct modulation of gene transcription | Signalling cascades; some act on tissue repair or hormone release pathways |
| Typical format | Solutions or capsules; stable at room temperature in the short term | Lyophilised powder requiring reconstitution and cold storage |
| Stability | Robust; degradation is slow under normal storage | Sensitive to heat, light, agitation and repeated freeze-thaw cycles |
| Examples in this catalogue | RAD-140, LGD-4033, MK-2866 | BPC-157, TB-500, Ipamorelin |
Our companion guide on research peptides covers that class in the same depth. The handling difference is the one researchers notice first. Lyophilised peptides in our aminos range require reconstitution — usually with bacteriostatic water — and careful cold storage thereafter. The compounds in the liquids range arrive in solution and are comparatively forgiving.
Compounds often grouped with SARMs — but chemically distinct
Several widely researched compounds are routinely filed under "SARMs" by retailers and search engines despite acting on entirely unrelated receptors. Getting this right matters: the mechanism determines what a compound is a useful reference material for.
| Compound | Actual class | Molecular target |
|---|---|---|
| MK-677 (Ibutamoren) | Growth hormone secretagogue | Ghrelin receptor (GHS-R1a) — no androgen receptor activity whatsoever |
| SR-9009 (Stenabolic) | Rev-erb agonist | Rev-erbα/β nuclear receptors, studied in circadian and metabolic research |
| SLU-PP-332 | ERR agonist | Oestrogen-related receptors (ERRα/β/γ), studied in mitochondrial metabolism |
| 5-Amino-1MQ | Enzyme inhibitor | Nicotinamide N-methyltransferase (NNMT) |
| GW501516 (Cardarine) | PPAR agonist | PPARδ, studied in fatty acid oxidation research |
MK-677 is the clearest example. It is frequently listed beside SARMs and researched alongside them, but it works by stimulating the ghrelin receptor to increase endogenous growth hormone release — our review of the MK-677 research covers what the trials found. If an experiment is designed around androgen receptor signalling, MK-677 is not a comparator — it belongs to a different pathway entirely.
What SARMs are studied for
The research programme behind this class began with a clear clinical problem: testosterone therapy improves lean mass and bone density, but its effects on the prostate and its delivery limitations constrain its use. A compound with the anabolic profile and less of the androgenic activity would, in principle, open several indications. The following are the areas the published literature has concentrated on. None of these represent approved uses.
Muscle wasting and cancer cachexia
The most developed line of research. Enobosarm (also known as ostarine or MK-2866) progressed furthest, with trials in cancer-related muscle loss reporting increases in lean body mass. Notably, improvements in lean mass did not consistently translate into improvements in measured physical function — a distinction that shaped how endpoints in subsequent studies were designed, and a useful cautionary result for anyone reading this literature.
Bone density and osteoporosis models
Androgen signalling contributes to bone maintenance in both sexes. Preclinical work has examined whether AR-selective compounds can increase bone mineral density and mechanical strength in ovariectomised and orchidectomised animal models, sometimes in comparison with, or combination with, bisphosphonates.
Hypogonadism and androgen deficiency models
Because SARMs activate the same receptor as testosterone, they have been investigated as candidates for age-related functional decline and androgen deficiency — the "function-promoting therapies" framing found in the geriatric medicine literature. Phase I work with LGD-4033 in healthy men reported dose-dependent increases in lean mass alongside dose-dependent suppression of endogenous testosterone.
Androgen-receptor-positive cancers
A subset of breast cancers express the androgen receptor, and AR agonism has been explored as a treatment strategy in that setting. RAD-140 entered clinical study in AR-positive, ER-positive metastatic breast cancer, and enobosarm has continued into later-stage oncology trials in a similar population. This is the area where the class remains most active clinically.
Benign prostatic hyperplasia and stress urinary incontinence
Andarine (S-4) was studied preclinically in BPH models, on the reasoning that a partial agonist could compete with dihydrotestosterone in prostate tissue while maintaining anabolic activity elsewhere. Pelvic floor muscle work has also attracted interest in stress urinary incontinence research.
| Compound | Also known as | Primary focus in the literature |
|---|---|---|
| MK-2866 | Ostarine, enobosarm, GTx-024 | Muscle wasting, cachexia, AR-positive breast cancer |
| LGD-4033 | Ligandrol, VK5211 | Lean mass and bone in hypogonadism and hip fracture recovery models |
| RAD-140 | Testolone | Neuroprotection models and AR-positive breast cancer |
| S-4 | Andarine | BPH and osteoporosis models; preclinical only |
| S-23 | — | Preclinical work including male contraception models in rodents |
What the research does not show
An honest guide has to cover the gaps, and they are substantial. Anyone citing this literature should be clear about what has and has not been established.
- No long-term safety data. Most human studies have run for weeks to months in modest cohorts. Multi-year data does not exist for any compound in the class.
- Suppression of endogenous androgen production. Trials have consistently reported dose-dependent suppression of testosterone, LH and FSH, alongside reductions in HDL cholesterol.
- Hepatic signals. Case reports of drug-induced liver injury associated with products marketed as SARMs appear in the clinical literature, though the contribution of mislabelled or contaminated products is difficult to separate from the compounds themselves.
- Selectivity is relative, not absolute. Tissue selectivity is a ratio observed in models, not a guarantee of inactivity in non-target tissue.
- Product quality is a genuine confounder. A 2017 analysis published in JAMA purchased products sold online as SARMs and found roughly half contained the compound named on the label; a quarter contained substances not listed at all, and some contained no active compound whatsoever.
That last point is a methodological problem as much as a safety one. An experiment run on an unverified compound produces unverifiable data, which is why independent analysis of every batch is a baseline requirement rather than a marketing feature. Our own third-party lab reports are published in full for exactly this reason.
Regulatory and legal status
No selective androgen receptor modulator has been approved as a medicine by the FDA, EMA, MHRA or TGA. That fact defines how the class is supplied and how it must be described.
- Not approved for human use. These compounds are supplied as laboratory reference materials, not as therapeutics, supplements or dietary ingredients.
- Marketed products draw enforcement. Regulators have issued warning letters to companies marketing SARMs as bodybuilding or dietary supplements, and several jurisdictions restrict their sale for human consumption.
- Prohibited in sport. The World Anti-Doping Agency has listed SARMs since 2008, under section S1.2 of the Prohibited List, banned at all times in and out of competition.
- Research supply is distinct. Supply for in-vitro and laboratory research purposes, correctly labelled and not marketed for human consumption, is the basis on which reference materials like ours are sold — consistent with 21 C.F.R. §§ 312.2(b)(3) and 312.160.
Requirements vary by jurisdiction and change over time. Institutions should confirm their own local position before ordering.
Working with SARMs in the laboratory
Practical considerations, assuming a properly equipped research setting.
Verify identity and purity before you begin
Ask for a certificate of analysis tied to the specific lot you have received, not a generic document for the compound. HPLC establishes purity; mass spectrometry confirms identity. Both should be present, and the report should be unredacted — a supplier unwilling to publish full results is telling you something useful.
Understand the format you are handling
Compounds supplied as solutions carry a stated concentration in mg/mL and a defined solvent system; capsules carry a stated mass per unit. Neither is interchangeable with raw powder in an experimental protocol, and the solvent matters for anything downstream — particularly cell culture work, where carrier tolerance limits the usable concentration range.
Store and document sensibly
Keep solutions away from direct light and extremes of temperature, keep containers sealed, and record lot numbers against every experiment. Lot-level traceability is what allows an anomalous result to be investigated rather than merely discarded.
All compounds discussed in this guide are supplied strictly for laboratory and in-vitro research. They are not medicines, are not for human or veterinary use, and are not intended to diagnose, treat, cure or prevent any disease. Nothing here is medical advice or a protocol for administration.
Frequently asked questions
What does SARM stand for?
Selective androgen receptor modulator. The name describes a compound that binds the androgen receptor and modulates its activity differently depending on the tissue, rather than switching it on uniformly throughout the body.
Are SARMs steroids?
No. SARMs and anabolic-androgenic steroids act on the same receptor, but SARMs are non-steroidal small molecules built on entirely different chemical scaffolds. They are not substrates for aromatase or 5α-reductase, so the downstream oestrogenic and prostate-amplification chemistry associated with steroidal androgens does not apply.
Is MK-677 a SARM?
No. MK-677 (Ibutamoren) is a growth hormone secretagogue that acts on the ghrelin receptor, GHS-R1a. It has no activity at the androgen receptor and is only grouped with SARMs by retail convention.
What are SARMs studied for?
The main research areas are muscle wasting and cancer cachexia, bone density and osteoporosis models, androgen deficiency and function-promoting therapy in ageing, and androgen-receptor-positive breast cancer. None of these are approved indications; all remain research contexts.
How do SARMs differ from peptides?
SARMs are small molecules that cross the cell membrane to act on an intracellular receptor and change gene transcription directly. Peptides are amino acid chains that usually act on cell-surface receptors and trigger signalling cascades. They also differ practically: peptides normally arrive lyophilised and need reconstitution and cold storage, while SARMs are supplied ready to use in solution or capsule form.
How is the purity of a research SARM verified?
Through independent third-party analysis of the specific lot, typically HPLC for purity and mass spectrometry for identity, documented in a certificate of analysis. Published market analyses have found a high rate of mislabelling among products sold online, which makes lot-level verification a prerequisite for reproducible data rather than an optional extra.
Selected reading
Starting points in the primary literature — each title links to its record on PubMed. These are provided for reference and are not endorsements of any particular finding.
- Narayanan R, Coss CC, Dalton JT. Development of selective androgen receptor modulators (SARMs). Molecular and Cellular Endocrinology, 2018.
- Bhasin S, Jasuja R. Selective androgen receptor modulators as function promoting therapies. Current Opinion in Clinical Nutrition and Metabolic Care, 2009.
- Dalton JT, et al. The selective androgen receptor modulator GTx-024 (enobosarm) improves lean body mass and physical function in healthy elderly men and postmenopausal women. Journal of Cachexia, Sarcopenia and Muscle, 2011.
- Basaria S, et al. The safety, pharmacokinetics, and effects of LGD-4033, a novel non-steroidal oral SARM, in healthy young men. Journals of Gerontology Series A, 2013.
- Dobs AS, et al. Effects of enobosarm on muscle wasting and physical function in patients with cancer: a double-blind, randomised controlled phase 2 trial. Lancet Oncology, 2013.
- Van Wagoner RM, et al. Chemical composition and labeling of substances marketed as selective androgen receptor modulators and sold via the internet. JAMA, 2017.
- Solomon ZJ, et al. Selective androgen receptor modulators: current knowledge and clinical applications. Sexual Medicine Reviews, 2019.
- World Anti-Doping Agency. Prohibited List, section S1.2, Other Anabolic Agents.
Continue reading
Every batch is independently tested and individually lot-tracked, with the full report published before listing.
This guide is provided for educational and informational purposes only and is based on published research. Core Labs supplies research chemicals for laboratory use exclusively. Products are not approved for human consumption, nor for medical, veterinary or household use.