SARMs, suppression and what is in the bottle

The six half-lives, plus one number the internet cannot agree on Mixed

Start with the arithmetic, because it decides dosing frequency and it decides how long anything takes to build up or leave. These are the values in OptiPin's pharmacokinetic database, with the plateau column derived at roughly 4.3 half-lives.

RAD-140 is where this gets interesting. Most pages selling it quote a half-life of 16 to 20 hours. Others quote 44.7 hours from a phase I clinical dataset. Our figure is 2.2 days, so about 53 hours, which sits close to the clinical end rather than the retail end. The lower numbers appear to descend from preclinical work; the higher ones from human data. It is a large practical difference: at 16 hours a compound is gone in three or four days, at 53 hours it is still accumulating into the second week. Anyone confidently telling you the daily schedule is reasoning from a number they have not checked.

You can put any of these on a curve with the half-life calculator, or drop them into a stack alongside anabolics in the cycle calculator, which added all six in September 2026.

Selective means tissue, not pituitary Strong evidence

The selling proposition is in the name. Selective androgen receptor modulators were designed to act on muscle and bone while sparing prostate and skin, which is a real pharmacological goal and to a degree a real achievement. What the word never meant was selective about your hormonal axis.

The trial data is unambiguous on this. In the clinical program for ostarine, doses of 1 mg and upward significantly lowered both sex hormone-binding globulin and total testosterone, with the effect scaling by dose. SARMs suppress luteinizing hormone and follicle-stimulating hormone through the same hypothalamic-pituitary feedback loop that testosterone does, because as far as that loop is concerned an androgen receptor agonist is an androgen receptor agonist. There is nothing exotic happening.

That makes the most repeated claim in this category, that SARMs do not require post-cycle consideration, not a nuanced position but a contradiction of the trial data. Suppression is measured, dose-dependent and expected. Whether any specific post-cycle protocol helps is a separate and much weaker question, which the restart and PCT guide covers honestly. The point here is narrower: if you were told there was nothing to suppress, you were told something the manufacturer's own trials disprove.

The practical consequence is that LH, FSH and total testosterone belong on a baseline panel before starting rather than after something feels wrong. Without a personal baseline there is no way to tell recovery from a value you always had.

Cardarine is not a SARM at all Strong evidence

GW-501516 is sold alongside these compounds, listed on the same product pages, discussed in the same threads. It is a different class of molecule entirely. It is a PPAR-delta agonist. It has no androgenic activity, does not touch the androgen receptor, does not suppress the axis and does not belong to any of the arithmetic above.

It matters because its risk profile is also different. Development was abandoned after rodent carcinogenicity studies produced tumors across multiple organ systems at a range of doses. That is not an internet rumor with a citation bolted on afterwards; it is why a pharmaceutical company stopped work on a compound it had spent money developing. Our cycle calculator flags it separately for that reason.

What is actually in the bottle Strong evidence

Everything above assumes you took the compound on the label. A 2017 investigation published in JAMA tested that assumption directly. It is the single most useful thing to know about this category.

Van Wagoner and colleagues searched for SARM suppliers online, found more than 210 products, then purchased the 44 that were actually available. On analysis, only 52% contained the SARM named on the label. A further 39% contained a different unapproved substance that was not disclosed. Some contained none of the labeled compound at all. Labels listed ostarine, andarine, RAD-140, ibutamoren, GW-501516 and SR9009, which is very close to the product list you would see today.

Read against everything else on this page, that is the finding that reframes the rest. A half-life table is only useful if the substance is what the bottle says. A dose is only meaningful if the concentration is real. And a person who reacts badly cannot know whether they reacted to the compound they intended to take, to an undisclosed one, or to a dose several times what they measured. Roughly half the time, the answer to "what did you take" is genuinely unknown.

The liver signal nobody was expecting Strong evidence

SARMs are frequently marketed on being easier on the liver than oral steroids, since they are not 17-alpha-alkylated. The case literature does not support the comfortable version of that claim.

Fewer than 20 cases of SARM-associated drug-induced liver injury have been published since 2020, involving ligandrol, testolone, ostarine and YK-11. The number is small, as is the number of people who present to hepatology and get written up. What is notable is the pattern: with one exception, the reported injuries were cholestatic or mixed, which is the same picture the alkylated orals produce. One RAD-140 case was assessed as probable causality with severe injury and biopsy-confirmed canalicular cholestasis. In the reported cases, injury resolved after stopping.

So the honest statement is not that SARMs are hepatotoxic like Anadrol. It is that "not alkylated" was assumed to mean "no hepatic risk". The published cases show that assumption was too strong. If you are running one, GGT and bilirubin belong on the panel alongside AST and ALT, for the reasons that page explains.

Why none of them became a drug Strong evidence

The last thing worth knowing is that these compounds were not abandoned because they failed to work. Enobosarm, which is ostarine, reached two identically designed phase 3 trials for muscle wasting in lung cancer patients, each randomizing 150 people to 3 mg daily against 150 on placebo for 147 days. It increased lean mass. It missed the co-primary endpoints, which paired lean body mass with physical function. Physical function is where it fell down.

That is a genuinely informative failure. It says the compound does what the mechanism predicts to the tissue, while translating tissue change into function is harder than the mechanism suggests. It is also the closest thing this category has to a large, controlled, long-duration human safety dataset, which is worth remembering when someone describes SARMs as understudied. Ostarine is not understudied. The rest largely are.