Fig. 5
a–f RBGO1 ADCs preferentially target endometrial cancer cells and increase drug sensitivity by up to 200-fold. Normal endometrial, HEC1A cancer or Ishikawa cancer cells were incubated with control medium or medium containing vcE (a–c; 0.01 to 100 μM) or mcF (d–f; 0.01 to 100 μM), or RBGO1 (a–f), RBGO1 -vcE (a–c) or RBGO1 -mcF (d–f; 0.01 to 100 μg/ml) for 96 h. Cell viability was determined by RealTime-Glo™ MT Cell Viability Assay and lethal dose 50 (LD50) values determined following curve fitting using a 4-parameter logistic model. Drug equivalencies were calculated based on an average DAR of 3. Data are expressed as mean (SD) from 4 independent experiments and normalized to the untreated control to account for cell growth during the period of the experiment. (g–j) RBGO1 ADC is more efficacious in HEC1A EC cells than HER2 ADC. HEC1A EC cells were treated with RBGO1 ADC (g; 0.1 to 5 μg/ml), HER2 ADC (h; 0.1 to 5 μg/ml), or RBGO1 ADC and HER2 ADC (i; 0.1 to 5 μg/ml) for 96 h and cell viability determined at 0, 24, 48, 72 and 96 h using the RealTime-Glo™ MT Cell Viability Assay. Heat map color intensities were based on percent cell viability compared to the untreated control (g–i; see scale in figure). Relative cell viability plots were fitted using a 4-parameter logistic model (j). Data displayed are means of three independent experiments. Data were analyzed by ANOVA and Dunnett’s multiple comparison test. ADCs differs from each other within the same dose, *p < 0.05, **p < 0.01