AC-262536 SARM Overview – What To Expect (Based On Clinical Studies)

What Is AC-262536?

This is another SARM that has no clinical studies on human subjects; consequently any conclusions or theories we develop around the compound have to be taken with a grain of salt.

How Strong Is AC-262536?

AC-262536 exerted up to 66% of the anabolic benefits of Testosterone, while simultaneously only exerting 27% as much Androgenic activity.

From this we can conclude that AC-262536 has an anabolic:androgenic rating/ratio of 2.45:1

For the record, none of the SARMs that have been developed are entirely selective for anabolic effects in muscle and bone without producing some trace androgenic effects in tissues.

The most notable being the prostate gland, which we can use as a gauge to assess how androgenic a SARM is based on its’ effect on the prostate gland to some extent.

There are several SARMs that have anabolic:androgenic ratios of 3:1 and up though, and those are fairly typical.

The highest ratio among the mainstream SARMs we are aware of is currently RAD-140 with an anabolic:androgenic ratio of 90:1.

This doesn’t mean that RAD-140 will significantly outperform AC-262536 in all aspects, but it does shed some light on what we can expect as we increase the dosage of AC-262536 in our research (the higher the dose, the more androgenic side effects we can expect to start cropping up, as opposed to RAD-140 where you can expect significantly more anabolic activity than androgenic activity each time the dosage increases).

The point being, the further you can get away from androgenic side effects via a more favorable ratio (and other factors), the more viable the SARM becomes for actual clinical application in the future (e.g. for treating women with Osteoporosis and other muscle and bone wasting conditions).

The baseline hormone we typically compare ratios to is Testosterone, which has a ratio of 1:1.

How Suppressive Is AC-262536 (and touching further on the strength of it)?

The binding affinity of AC-262536 is Ki of 5nM.

To put this into perspective, LGD-4033 features a binding affinity of Ki of ~1nM.

Consequently, through mild broscience we can assume that it takes about 5x more AC-262536 to achieve the same extent of binding affinity as LGD-4033 at the androgen receptor.

Meanwhile, this figure would put AC-262536 into the same general range of binding affinity as Ostarine and S4.

One thing to note is that binding affinity isn’t necessarily the best/only indicator of how strong or suppressive a SARM is (although it should still be strongly considered).

Another commonly overlooked trait is the literal interaction with the androgen receptor.

AC-262536 is a partial agonist; meanwhile LGD-4033 is a full agonist (using this comparison as LGD-4033 has a lot of supporting data to compare to).

Full agonists induce greater levels of suppression, but are more potent (based on the information presented).

With AC-262536 in particular, being a partial agonist it would result in less suppression, although it will also likely be weaker than LGD-4033 on a mg:mg comparison.

Raising the dose could make it formidable to heavy hitters like LGD-4033, but referring back to the anabolic:androgenic rating of AC-262536 (2.45:1), we can assume that the higher the dose, the greater the chance of suppression and androgenic side effects.

However, AC-262536 had minimal effects on the prostate size.

It was actually 14x less potent compared to Testosterone in terms of affecting prostate size.

Consequently, we can assume that a higher dose of AC-262536 may yield effects formidable to that of Testosterone, with a very minimal presence of negative androgenic side effects.

At the end of the day though, there is very minimal research done on this compound and megadosing it in hopes of replicating a near side effect free version of Testosterone could result in unforeseen side effects cropping up.

Dosage

The studies done on AC-262536 went as high as 10mg/kg and 30mg/kg on the rat subjects.

Obviously equating this to some efficacious dosage where there would be minimal/no side effects for human use is impossible to do without some sort of experimentation being done, and as of now there are no clinical trials done on humans.

Typically, researchers have reported that 10mg-30mg of AC-262536 is effective, however, this remains to be seen, as there is EXTREMELY limited data, even anecdotally.

Does AC-262536 Require PCT?

Anything that suppresses your natural endocrine function may warrant PCT.

Conclusion

This SARM seems relatively weak from the data we have gathered, but the main appeal of it is that there should be significantly less suppression than many of the more mainstream SARMs, and supposedly this SARM is still undetectable (so I’ve heard), so any drug-tested athlete would hypothetically be able to get a sizeable edge from AC-262536.