AC-262536
Also known as: AC-262536, AC262536, Accadine
A weak partial agonist — meaning it can activate the androgen receptor and block stronger androgens from it at the same time.
Substance family
Non-steroidal compounds binding the same androgen receptor as testosterone, but favouring muscle and bone over prostate and hair. The selectivity is real; the suppression of the body's own production is not avoided by it. None is approved anywhere.
Effects on
Which outcomes this substance acts on — descriptive, not a recommendation.
Strain profile
Where this substance is most likely to hit — a rough orientation, individually dependent on dose, duration and predisposition.
This substance causes
Dosing & protocols by goal
Rough orientation ranges as reported in harm-reduction literature — not an individual treatment plan. Doses are individual and open-ended; frequency depends on the ester or half-life.
Human clinical data
MedicalDose
Does not exist
Frequency
—
Cycle length
—
Developed within the same programme that produced ostarine. Rat studies only; no human trial was conducted.
Grey market practice
Not a recommendationDose
10–25 mg / day reported
Frequency
1–2× daily
Cycle length
6–8 weeks reported
Figures from user reports without research basis. The effect is consistently described as weak, which is what a partial agonist would predict.
Side effect & countermeasure
Typical problems and what you can do to reduce harm — at a glance. Does not replace medical monitoring.
Problem
A partial agonist can work against stronger androgens
Countermeasure
This is the property worth understanding. A partial agonist activates the receptor weakly — but while it occupies the receptor, a stronger androgen cannot. Taken alongside testosterone or a potent compound, it can therefore compete with them and reduce their effect. That makes it a poor choice to stack, which is exactly how people tend to use it.
Problem
Weak effect, real suppression
Countermeasure
The muscle-building effect is modest even by SARMSARMA non-steroidal compound that binds the androgen receptor with claimed tissue selectivity. standards, but the suppressionsuppressionThe body shutting down its own testosterone production because an external source is present. is not proportionally modest. That is the worst combination in this category: little to gain, and the same recovery problem afterwards. Bloodwork and a PCTPCTThe protocol after a cycle intended to restart the body's own testosterone production. plan still apply.
Problem
Falling HDL
Countermeasure
As with the other oral SARMsSARMsA non-steroidal compound that binds the androgen receptor with claimed tissue selectivity.. Cardio, omega-3 and citrus bergamot help at the margin; a lipid panel decides whether to continue.
Problem
No manufacturing oversight
Countermeasure
Sold as a research chemical, with the usual contamination and mislabelling problems of that market.
Overview
AC-262536, sometimes called accadine, came out of the same research programme that produced ostarine. Like most of the second tier, it stopped at rat studies.
Its distinguishing feature is not potency but the opposite — it is a notably weak partial agonist, and that has a consequence people generally do not anticipate.
Mechanism of Action
Most SARMs are full or near-full agonists: they bind the androgen receptor and activate it strongly. AC-262536 binds it and activates it only weakly.
The important part is that binding and activating are separate things. While AC-262536 occupies a receptor, that receptor is unavailable to anything else. So in a system with strong androgens present, a weak partial agonist can lower the overall effect by displacing them.
In practice: taken alone, it produces a mild anabolic effect. Taken alongside testosterone or a potent SARM, it can compete with them and blunt what they would otherwise do.
That inverts the usual stacking logic, and it is the main reason this page exists.
Where It Sits
Among SARMs it is at the weak end, weaker than ostarine in reported effect. The suppression, however, is not correspondingly mild — users report measurable drops in testosterone.
Little benefit with a normal recovery cost is the least favourable trade in this category. The rat data also showed some effect on behaviour and cognition, which occasionally gets framed as a nootropic angle; that is a rodent finding and nothing more.
Side Effects & Risks
- Suppression of the body's own production, disproportionate to the weak anabolic effect
- Falling HDL, rising LDL
- Fatigue and low mood, largely downstream of suppression
- Can reduce the effect of stronger androgens taken alongside
- No manufacturing oversight; contamination and mislabelling are common
Blood Work & Monitoring
- Total and free testosterone, LH, FSH — before, during and after
- Lipid profile (LDL, HDL, triglycerides)
- Liver values (ALT, AST, GGT)
- Estradiol (sensitive assay)
Legal status by region
Regulation differs considerably between jurisdictions and changes over time. This is a rough orientation, not legal advice — check the rules that apply where you are.
| Region | Regulatory status |
|---|---|
| United States | Not approved; FDA warning issued |
| EU / UK | No marketing authorisationNeither a medicine nor a supplement — no legal route for human use. |
| Most other jurisdictions | Unregulated grey area |
| Competitive sport | Prohibited at all timesListed by WADA under S1.2. |