
AC-262536 | Pen
AC-262536 is a SARM positioned for controlled research settings where androgen receptor–selective anabolic signaling is being studied in relation to lean mass preservation, muscle strength/function endpoints, and tissue-selective androgenic load (e.g., prostate-associated markers).
Supports
- Androgen receptor (AR) partial-agonist signaling with tissue selectivity (model-dependent)
- Lean tissue maintenance markers during catabolic or immobilization paradigms
- Strength and functional performance readouts in skeletal muscle models
- Lower relative androgenic signaling in non-target tissues (prostate/seminal vesicle endpoints)
- Endocrine-axis feedback markers (LH/FSH/testosterone panels) in controlled studies
Description
AC-262536 is a non-steroidal selective androgen receptor modulator (SARM) investigated for anabolic-biased signaling in skeletal muscle with reduced relative androgenic activity in other androgen-sensitive tissues. In experimental pharmacology, it is commonly characterized as a potent AR ligand with partial agonist behavior compared with testosterone, allowing research designs to probe “anabolic vs androgenic” separation using standardized tissue readouts.
Preclinical work has evaluated AC-262536 in androgen-deprived and castrated animal models to quantify muscle-associated outcomes (e.g., levator ani or other anabolic proxies) alongside prostate/seminal vesicle endpoints used as androgenic surrogates. This framework is frequently used to test whether a candidate modulator can support muscle-directed signaling while limiting off-target androgenic effects.
AC-262536 is presented for research positioning only. Findings depend on dose, duration, species, baseline androgen status, and endpoint choice, and should be interpreted within controlled experimental protocols.
Clinical Status
AC-262536 is primarily supported by preclinical pharmacology and mechanistic assays (in vitro and animal studies) describing AR binding, tissue-selective activity profiles, and anabolic/androgenic endpoint separation. Human clinical trial evidence specific to AC-262536 is not established as a primary basis for interpretation.
Evidence type:
Human RCT ☐ | Observational ☐ | Animal ✔ | In vitro ✔ | Regulatory approval ☐
Mechanism of Action
AC-262536 selectively binds the androgen receptor and is described as a partial agonist in functional assays. In research models, AR activation can drive anabolic transcriptional programs in skeletal muscle (protein synthesis and myofiber remodeling pathways), while tissue-selective modulators are evaluated for comparatively reduced activation of androgen-responsive programs in prostate-associated tissues.
In vivo, SARM profiling often includes measurement of anabolic proxies (e.g., levator ani growth in androgen-deprived models) alongside androgenic proxies (e.g., prostate and seminal vesicle weights). AC-262536 has been reported to produce substantial anabolic effects relative to testosterone with a lower relative androgenic signal in these surrogate endpoints, though outcomes remain model-dependent.
Benefits
-
Muscle-directed anabolic signaling:
Studied for increasing anabolic endpoints in skeletal muscle models using standard SARM profiling readouts. -
Tissue-selective androgenic load:
Evaluated for reduced relative androgenic effects in prostate-associated surrogate endpoints compared with testosterone in controlled animal studies. -
Lean mass preservation paradigms:
Positioned for research on maintaining lean tissue markers during catabolic stress, reduced activity, or deficit-like models. -
Strength/function endpoints:
Used in experimental designs that track functional performance markers alongside tissue and biomarker outcomes. -
Limited steroid-like conversions:
As a non-steroidal AR ligand, it is studied without assuming classic steroid conversion pathways, supporting mechanistic separation studies. -
Comparative SARM benchmarking:
Frequently contextualized alongside other SARMs (e.g., ostarine, ACP-105, LGD-class ligands) to compare potency and selectivity profiles under matched assays.
Research Data
| Study/model | Reported effect |
| AR functional cell-based assays (in vitro) | Potent AR binding with partial agonist activity relative to testosterone; minimal activity across non-AR panels reported in select screens |
| Castrated male rat SARM profiling (2-week study) | Increased anabolic proxies (e.g., levator ani growth) with weaker androgenic surrogate effects (prostate/seminal vesicle endpoints) versus testosterone |
| Androgen-deprivation endocrine readouts (animal) | Suppression of elevated LH in castrated models reported in certain designs, consistent with AR-axis engagement |
| Tissue selectivity comparison (animal) | Reported anabolic effect magnitude around ~60–70% of testosterone in muscle readouts with substantially lower prostate effect in the same paradigm (endpoint-dependent) |
| Gene expression profiling approaches (androgen-responsive tissues) | Comparative transcriptional signatures used to differentiate SARM vs testosterone pathway activation profiles in controlled studies |
| Analytical anti-doping detection (human urine methods) | LC–MS/MS panels include AC-262536 for detection/verification workflows; informs exposure confirmation rather than efficacy |
| Metabolism characterization (animal/veterinary models) | Metabolite profiling in plasma/urine/hair reported in controlled administration studies (PK/exposure mapping) |
| SARM safety signal reviews (literature synthesis) | Broader SARM class reviews discuss endocrine suppression risk signals and liver-related monitoring in misuse contexts; interpretation is compound- and protocol-dependent |
Stack Suggestions
In extended experimental designs, AC-262536 is sometimes paired with:
- Ibutamoren (MK-677) → to co-study GH/IGF-axis signaling markers alongside AR-driven anabolic endpoints
- Cardarine (GW-501516) → to compare endurance/metabolic readouts with muscle maintenance outcomes (distinct receptor systems)
- SS-31 (Elamipretide) → to explore mitochondrial stress markers in parallel with training- or disuse-related muscle models
Stacks discussed are for experimental design only, not safety/efficacy guidance.
Possible Side Effects
Although AC-262536 is considered one of the safer compounds among SARMs, there are observations of some side effects, especially with prolonged use or higher doses:
• Temporary suppression of testosterone production, depending on the duration of intake;
• Individual sensitivity to androgen stimulation, especially in more sensitive models;
• Limited long-term data.
Compliance with the optimal dosage and control over the duration of the application play a key role in limiting the manifestation of side effects.
Scientific References
- Pharmacological characterization of AC-262536, a novel selective androgen receptor modulator — Animal/In vitro
- Discovery of potent and muscle selective androgen receptor modulators (medicinal chemistry series) — In vitro
- AC-262536 related compound record (chemical identity and annotations) — Database
- AC-262536 (DrugBank) — Database
- Deciphering the selective androgen receptor modulators paradigm — Review
- Considerations, possible contraindications, and potential mechanisms for deleterious effect in recreational and athletic use of SARMs: a narrative review — Review
- Selective Androgen Receptor Modulators (LiverTox) — Review
- Equine metabolism of the selective androgen receptor modulator AC-262536 in vitro and in urine, plasma and hair following oral administration — Animal
- Monitoring of selective androgen receptor modulators in dietary supplements and related analytical workflows — In vitro
- Selective Androgen Receptor Modulators (SARMs): effects on performance/body and safety profile (systematic review) — Review
Cautions
- For educational and scientific context only; not intended to diagnose, treat, cure, or prevent any disease.
- If you are pregnant, nursing, have a medical condition, or use prescription medication, consult a qualified professional.
- Discontinue use if sensitivity occurs.
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AC-262536 | Pen
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