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. 2019 Sep 26;2(6):453–467. doi: 10.1021/acsptsci.9b00065

Figure 2.

Figure 2

LNCaP-RALR xenografts retain biological resistance to ralaniten and sensitivity to enzalutamide in vivo. (A) LNCaP and LNCaP-RALR tumor growth in castrated mice treated daily with ralaniten (200 mg/kg), enzalutamide (10 mg/kg), or vehicle by oral gavage. Tumors were harvested 2 days after last treatment. Data presented as mean ± SEM and analyzed by two-way ANOVA with Sidak’s test applied post hoc. (B) Representative photographs of LNCaP-RALR tumors. Scale bars: 10 mm. (C) Body weight change over the course of the experiment. Data presented as mean ± SEM and analyzed by two-way ANOVA with Dunnett’s test applied post hoc (n = 5 mice per group). (D) Representative examples of immunohistochemistry (IHC) from LNCaP-RALR tumors showing AR and PSA expression levels (n = 2 tumors per group). (E) Real-time PCR of AR, FKBP5, RHOU, and PSA transcript normalized to SDHA harvested from LNCaP-RALR tumors (n = 8 tumors/sample for all genes except FKBP5, n = 6 for RAL). *p < 0.05; **p < 0.01; ***p < 0.001; #p < 0.0001; n.s., not significant: RAL, ralaniten; ENZ, enzalutamide; VEH, vehicle.