Half-life is one of the first figures a researcher looks up for any compound. It describes how quickly the concentration of a substance in the blood falls by half, and it shapes almost every part of how a pharmacokinetic study is designed: how often samples are taken, how long a study runs before measurements are stable, and how long a washout period needs to be before follow up readings are taken. This guide sets out the half-lives that have been measured or estimated for the common SARMs and related compounds, explains where each figure comes from, and describes how the published trials were designed around them. It is a reference for reading the research. It is not a usage guide and contains no timing, dosing or cycle information.
What half-life means
Half-life is the time it takes for the plasma concentration of a compound to fall by 50 percent once it has been absorbed and distributed.
After four to five half-lives, roughly 94 to 97 percent of a compound has been cleared. The figure is not a fixed property of the molecule. It depends on the species studied, the formulation, the route of administration and the assay used to measure it, so a half-life measured in rats can differ widely from one measured in people. That is why the source of each figure in the table below matters as much as the number itself.
Why half-life matters in study design
Researchers use half-life to plan three parts of a study: the sampling schedule, the time to steady state and the washout period.
In a pharmacokinetic study, blood samples are clustered early, when concentrations change fastest, and spaced further apart later on. Steady state is the point where intake and clearance balance, so that measurements taken at different visits can be compared fairly; for most compounds it takes about four to five half-lives to reach. The washout period is the gap left after the last exposure before baseline measurements are repeated or a crossover arm begins. A compound with a long half-life needs a longer washout, and its effects on hormones or blood lipids can outlast the compound itself.
The measured half-lives
Only a few of these compounds have human pharmacokinetic data; the rest rely on animal studies or have no published figure at all.
| Compound | Half-life | Source of the figure |
|---|---|---|
| Ostarine (MK-2866) | About 24 hours | Human phase I and II data (GTx) |
| Ligandrol (LGD-4033) | 24 to 36 hours | Human phase I (Basaria 2013) |
| Testolone (RAD-140) | About 60 hours (preclinical) | Rodent and primate data; no human figure |
| Ibutamoren (MK-677) | 4 to 6 hours, with GH effects lasting 24 hours | Human studies (Chapman 1996) |
| Cardarine (GW-501516) | Estimated 12 to 24 hours | Human phase I lipid studies |
| Stenabolic (SR-9009) | Under 4 hours (rodent) | Rodent pharmacokinetics; poor oral bioavailability |
| Andarine (S-4) | About 4 hours | Preclinical data (Kearbey 2004) |
| YK-11 and S-23 | Not established in humans | In vitro and rodent work only |
How the published trials were designed
The human studies behind these figures follow the standard clinical sequence: small phase I studies to measure pharmacokinetics and safety, then larger placebo controlled phase II trials to measure clinical endpoints.
Phase I studies enrol small groups of healthy volunteers, take blood at fixed intervals and report the peak concentration, the time to peak and the elimination half-life. The LGD-4033 phase I study (Basaria 2013) followed this pattern over three weeks in healthy young men and kept measuring hormones and lipids after the last exposure.
Phase II studies run for longer, randomise participants to the compound or a placebo, and measure outcomes that matter clinically. The Ostarine (enobosarm) trial reported by Dalton and colleagues in 2011 measured lean body mass by DEXA scan, stair climb power, and changes in blood lipids and hormones in older men and postmenopausal women.
The MK-677 work shows a different design problem. Chapman and colleagues (1996) measured growth hormone across 24 hour sampling windows and IGF-1 alongside it, because the hormone response lasts much longer than the compound stays in circulation; Nass and colleagues (2008) then followed body composition in a randomised, placebo controlled trial lasting up to two years. That gap between a short plasma half-life and a long biological effect is a good example of why half-life alone does not describe what a compound does.
The exact protocol of each study is set out in the original paper, linked in the sources below. We do not summarise or adapt those protocols here: they were designed for supervised clinical research and are not guidance of any kind.
Short half-life compounds and their limits
Stenabolic (SR-9009) and Andarine (S-4) have the shortest reported half-lives in this group, and both have known pharmacokinetic limits.
SR-9009 was characterised in mice by Solt and colleagues in 2012, and its oral bioavailability was so low that its usefulness by mouth has been questioned in the literature since. Andarine cleared quickly in rat pharmacokinetic work (Kearbey 2004), and its early development also reported a visual disturbance that resolved once the compound had cleared. Our guides on SR-9009 and S-4 go into both points.
Study length and follow up
Published trial lengths range from three weeks for the LGD-4033 phase I study to twelve weeks for the Ostarine phase II trial, and up to two years for MK-677.
Longer studies recorded larger changes in lean mass, but also larger changes in testosterone and HDL cholesterol, which is why the better designed trials kept measuring hormones and lipids after the last exposure. In the LGD-4033 study those markers moved back towards baseline during follow up. Our guide on hormone recovery after SARM studies covers what those follow up samples showed.
What half-life data does and does not tell you
A half-life describes how a compound was cleared in the population that was studied, and nothing more.
It says nothing about safety or effectiveness, and it is not a guide to how any product should be handled outside a laboratory. Several of the figures above come from animals only, and YK-11 and S-23 have no published human pharmacokinetic data at all. When you read a claim about any of these compounds, check which species, which formulation and which assay the figure came from. If you are new to the topic, start with The ultimate guide to SARMs and what the safety data shows, then read the compound guide for whichever you are researching. All of our SARMs are batch tested, with certificates on the lab results page.
Sources
- Basaria S et al. (2013). The safety, pharmacokinetics, and effects of LGD-4033, a novel nonsteroidal oral, selective androgen receptor modulator, in healthy young men. J Gerontol A Biol Sci Med Sci. PubMed 22459616
- Dalton JT et al. (2011). The selective androgen receptor modulator GTx-024 (enobosarm) improves lean body mass and physical function in healthy elderly men and postmenopausal women. J Cachexia Sarcopenia Muscle. PubMed 22031847
- Chapman IM et al. (1996). Stimulation of the growth hormone (GH)-insulin-like growth factor I axis by daily oral administration of a GH secretogogue (MK-677) in healthy elderly subjects. J Clin Endocrinol Metab. PubMed 8954023
- Nass R et al. (2008). Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial. Ann Intern Med. PubMed 18981485
- Sprecher DL et al. (2007). Triglyceride:high-density lipoprotein cholesterol effects in healthy subjects administered a peroxisome proliferator activated receptor delta agonist. Arterioscler Thromb Vasc Biol. PubMed 17110604
- Miller CP et al. (2011). Design, synthesis, and preclinical characterization of the selective androgen receptor modulator (SARM) RAD140. ACS Med Chem Lett. PubMed 24900290
- Solt LA et al. (2012). Regulation of circadian behaviour and metabolism by synthetic REV-ERB agonists. Nature. PubMed 22460951
- Kearbey JD et al. (2004). Pharmacokinetics of S-3-(4-acetylamino-phenoxy)-2-hydroxy-2-methyl-N-(4-nitro-3-trifluoromethyl-phenyl)-propionamide in rats, a non-steroidal selective androgen receptor modulator. Xenobiotica. PubMed 15204699
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