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AC-262 (Accadrine), (10mg/capsule) 60 Capsules

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AC-262 (Accadrine) is a selective androgen receptor modulator (SARM) characterised by tissue-selective binding at the androgen receptor (AR). Research interest centers on its differential activation profile across musculoskeletal versus other AR-expressing tissue models, distinguishing it from non-selective steroidal AR ligands. Research applications include AR binding-affinity assays, tissue-selectivity comparison studies, and SARM structure-activity relationship investigation.

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3D Molecular Structure

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Chemical Formula C18H18N2O
Synonyms AC-262536, 870888-46-3, UNII-U8VS41J5O6, U8VS41J5O6
Molar Mass 278.3 g/mol
CAS Number 870888-46-3
PubChem CID 44512434
Total Compound Content 600mg (10mg per capsule)
Shelf Life 36 months
AC-262 (Accadrine) is a non-steroidal SARM compound that engages the androgen receptor with a tissue-selective activation pattern distinct from testosterone and other endogenous androgens. In vitro receptor-binding assays characterise its AR affinity and partial agonist behaviour relative to full agonists such as DHT, while comparative tissue-culture models (musculoskeletal versus other AR-bearing cell lines) are used to investigate the molecular basis of its selectivity. Structure-activity relationship studies position AC-262 within a broader class of arylpropionamide-derived AR ligands under investigation for receptor-selective pharmacology. Independently third-party HPLC-tested; COA available per batch.

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What distinguishes AC-262 from steroidal androgen receptor agonists in receptor-binding research?

AC-262 is a non-steroidal arylpropionamide-derived androgen receptor (AR) ligand that differs structurally from steroid-based AR agonists. This distinct chemical scaffold produces unique receptor conformations upon binding, influencing co-regulator recruitment and downstream transcriptional activity. As a result, AC-262 is frequently used in comparative receptor pharmacology and structure-activity relationship (SAR) studies investigating how ligand architecture affects AR activation, signalling bias, and gene-expression outcomes.

How is AC-262's tissue selectivity evaluated in research models?

Tissue selectivity is typically assessed by comparing AR-mediated transcriptional activity across multiple AR-expressing experimental systems using reporter-gene assays, gene-expression profiling, and pathway-activation studies. Differences in potency, efficacy, and transcriptional output between model systems provide insight into selective AR modulation. Combining these functional measurements with receptor-binding data helps distinguish effects related to receptor affinity from those arising through downstream signalling and co-regulator interactions.

What assay formats are commonly used to evaluate AC-262 androgen receptor activity?

Standard approaches include competitive receptor-binding assays to determine relative AR affinity and cell-based transactivation assays utilizing AR-responsive reporter constructs to quantify functional activity. Additional studies often incorporate co-activator recruitment assays, gene-expression analysis, and comparative ligand profiling to characterize receptor activation patterns. Together, these methods provide a comprehensive assessment of receptor binding, signalling efficacy, and selective androgen receptor modulation.

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