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. 2013 Jun 3;123(7):2948–2960. doi: 10.1172/JCI66398

Figure 6. Oral dosing of EPI-002 blocks AR transcriptional program and inhibits growth of VCaP CRPC xenografts that express AR splice variants.

Figure 6

(A) VCaP tumor growth in castrated mice administered EPI-002 (200 mg/kg body weight) or bicalutamide (10 mg/kg body weight) daily by gavage for a total of 28 doses. Tumors were harvested 2 days after the last treatment. (B) Photographs of tumors harvested at day 28 from animals as in A. Scale bars: 10 mm. (C) Body weight change over the duration of the experiment. (D) Transcript levels of FL-AR and AR variants (V7, V567es) normalized to RPL13A using total RNA isolated from VCaP xenografts from castrated hosts treated with bicalutamide (n = 8), EPI-002 (n = 8), or DMSO control (CMC; n = 7) for 28 days. (E) Protein levels of AR and AR variants from harvested xenografts treated with EPI-002 or bicalutamide or vehicle control. Quantification of protein bands (FL-AR and AR variant), normalized to β-actin, is also shown. (F) Transcript levels of UBE2C, AKT1, CDC20, CYCLINA2, PSA, and ERG, normalized to levels of RPL13A. (G) Proliferation (Ki67) and apoptosis (caspase-3) index, measured in harvested VCaP xenografts. Data are mean ± SEM. *P < 0.05; **P < 0.01; #P < 0.001.