SARMs vs Prohormones vs Anabolic Steroids: How They Actually Differ

Across our SARM Showdown series, one question keeps coming up: what actually makes a SARM different from a steroid? On forums and social media the terms are often used as if they mean the same thing. They don't.

This guide explains the three categories: what they are made of, how they act on the body and why "selective" is the key word. It also covers several popular compounds that are usually called SARMs but aren't.

All information is for educational and research purposes only.

The Common Thread: the Androgen Receptor

All three categories involve the androgen receptor (AR). This is a protein inside cells that, when activated, switches on genes involved in muscle growth, bone density, red blood cell production and male sexual characteristics.

The androgen receptor is found throughout the body, including muscle, bone, prostate, skin, hair follicles, liver and brain. That spread is the key to the whole comparison. Activate the receptor everywhere and you get effects everywhere. Activate it in some tissues more than others and the picture changes.

Anabolic-Androgenic Steroids (AAS)

What they are: synthetic versions of testosterone. They share its four-ring steroid structure and are modified to change potency, oral activity or how long they last in the body.

How they work: they activate the androgen receptor in every tissue that has one. Many are also converted by enzymes into other active hormones:

Aromatase converts some steroids into oestrogens.
5α-reductase converts some into more potent androgens such as DHT, which is especially active in the prostate, skin and scalp.

Key point: anabolic steroids are non-selective. Their muscle-building effects come with androgenic effects on other tissues, as well as effects on lipids, the heart and liver, and natural hormone production. They have established medical uses (such as testosterone replacement) and are controlled substances in the UK.

Prohormones

What they are: precursors that aren't very active themselves but are converted by the body's enzymes into active steroid hormones. Androstenedione, which became well known in the late 1990s, is the classic example.

How they work: once swallowed, enzymes in the liver and other tissues convert the precursor into testosterone, nandrolone or other active steroids. The result is essentially a steroid effect, just one step removed.

Key point: prohormones are really steroids in disguise. They were widely sold as supplements until regulators caught up. In the US, the Anabolic Steroid Control Act of 2004 reclassified most of them as controlled substances. Because the active compound is made inside the body, the effects are harder to predict than with the steroid itself.

Selective Androgen Receptor Modulators (SARMs)

What they are: compounds, mostly non-steroidal, designed to bind the androgen receptor. The first non-steroidal SARMs were described in the late 1990s. They were developed as possible treatments for muscle wasting, osteoporosis and other conditions.

How they work: a SARM binds the androgen receptor and changes its shape in a way that differs from testosterone. That changed shape affects which "helper" proteins (coregulators) the receptor recruits. Those proteins vary from tissue to tissue, so the same compound can act strongly in muscle and bone while acting only weakly in the prostate.

Most non-steroidal SARMs are also not processed by aromatase or 5α-reductase. So they don't convert into oestrogens or DHT the way testosterone does.

Key point: SARMs are designed to be tissue-selective, but selectivity is relative, not absolute. Human trials of compounds such as LGD-4033 and Ostarine have consistently shown suppression of natural testosterone and changes to cholesterol. No SARM has yet been approved as a medicine.

One exception worth knowing: YK-11 has a steroidal structure (it is derived from DHT) but is described as a partial androgen receptor agonist. Lab research (Kanno et al., 2013) found that it increased follistatin, a natural myostatin inhibitor, in muscle cells. It is usually grouped with SARMs but doesn't fit the non-steroidal definition.

At a Glance

	Anabolic Steroids	Prohormones	SARMs
Structure	Steroidal	Steroidal	Mostly non-steroidal
Active as taken?	Yes	Mostly converted in the body	Yes
Androgen receptor selectivity	Non-selective	Non-selective (once converted)	Designed to be tissue-selective
Converted to oestrogen / DHT?	Often	Often	Generally no (non-steroidal SARMs)
Hormone suppression	Yes	Yes	Yes, usually milder but documented
Approved medical use	Yes (some)	No	No

"SARMs" That Aren't SARMs

Several of the most popular compounds in this space don't act on the androgen receptor at all:

Cardarine (GW-501516) is a PPARδ agonist. It shifts how the body uses fuel towards burning fat. It is a metabolic compound, not an anabolic one.
Stenabolic (SR9009) is a Rev-Erb agonist. It affects the circadian clock and metabolism.
Ibutamoren (MK-677) is a growth hormone secretagogue. It mimics ghrelin to increase growth hormone and IGF-1 release.

They are often sold alongside SARMs and discussed with them, but their mechanisms, research questions and risk profiles are completely different. That is exactly why our Showdowns compare them on their own terms. See Stenabolic vs Cardarine and Ibutamoren vs Cardarine for more.

The Bottom Line

Steroids activate the androgen receptor everywhere.
Prohormones turn into steroids inside the body.
SARMs aim to activate the androgen receptor in some tissues more than others, but selectivity has limits.
Cardarine, Stenabolic and MK-677 are different classes of compound altogether.

Knowing which category a compound belongs to is the first step in any serious research. The second is knowing that what's in the vial or tablet matches the label. Independent lab reports for our range are on our Independent Analysis page.