Competitive AR binding
Biochemical assay · Recombinant human wild-type androgen-receptor ligand-binding domain [1]
Clascoterone displaced fluorescent DHT; its binding IC50 exceeded that of DHT.
Literature-Reported Treatment Conditions
- Method
- Fluorescence-polarization competitive binding assay
- Co-treatment
- Fluorescent DHT tracer; unlabeled DHT and DDE controls.
- Reported limits
- Ten concentrations tested; exact series, incubation duration and vehicle were not specified in the read binding methods. IC50 is an assay measurement, not a dosing recommendation.
Methods and source locations
Compound reported in the paper: Clascoterone
Evidence applies to literature clascoterone, not to validation of this supplier’s batch or a formulated clinical product.
p. 413, Clascoterone Binding to the AR In Vitro and binding Results; p. 414, Figure 1B caption
Displacement of fluorescent DHT from AR: Two independent assays, each in triplicate. — p. 413, Clascoterone Binding to the AR In Vitro and binding Results; p. 414, Figure 1B caption
AR-dependent transcription
Cell-based study · Mammalian reporter cells expressing full-length human AR and an AR-responsive luciferase reporter [1]
Clascoterone inhibited testosterone-stimulated reporter activity, with a higher IC50 than enzalutamide.
Literature-Reported Treatment Conditions
- Exposure duration
- 24 hours
- Method
- Luciferase reporter assay
- Vehicle
- DMSO control; percentage not specified for this assay.
- Co-treatment
- 400 pM testosterone; enzalutamide comparator; no-cell and DMSO negative controls.
- Reported limits
- Exact clascoterone concentration series not transcribed from the figure; reporter host cell lineage not specified in the read methods.
Methods and source locations
Compound reported in the paper: Clascoterone
Evidence applies to literature clascoterone, not to validation of this supplier’s batch or a formulated clinical product.
p. 413, AR Activity Assay; p. 414, Results and Figure 1C caption
Inhibition of testosterone-stimulated AR transcription: Luciferase response; three independent experiments; plotted points described as mean + SD. — p. 413, AR Activity Assay; p. 414, Results and Figure 1C caption
Lipid accumulation in primary sebocytes
Cell-based study · Primary human sebocytes from seven donors [1]
Clascoterone reduced DHT-induced lipid accumulation, with substantial donor variability.
Literature-Reported Treatment Conditions
- Treatment concentration
- 50 µM clascoterone
- Exposure duration
- 7 days
- Method
- Nile Red staining and flow cytometry; repeated treatments described on the first day and 2 and 4 days later.
- Vehicle
- 0.1% DMSO no-compound control
- Co-treatment
- 10 µM DHT stimulation; comparison against DHT plus DMSO.
- Reported limits
- Raw donor-level fluorescence and numeric variance for this range are not supplied in the read prose. The staining endpoint does not distinguish lipid species.
Methods and source locations
Compound reported in the paper: Clascoterone
Evidence applies to literature clascoterone, not to validation of this supplier’s batch or a formulated clinical product.
p. 413, DHT-Stimulated Lipid Accumulation in Human Sebocytes; pp. 415–416, donor experiment Results and Figure 3C caption; p. 417, Discussion
Inhibition of DHT-induced lipid accumulation across donors: Figure 3C defines inhibition relative to the percentage of Nile Red-positive cells in the DHT + 0.1% DMSO control. — p. 413, DHT-Stimulated Lipid Accumulation in Human Sebocytes; pp. 415–416, donor experiment Results and Figure 3C caption; p. 417, Discussion
