Table 2.
Antitumor activity of DBPR114 and sorafenib in human HCC xenograft tumors
| Cell line | Histopathology | Tumor growth inhibition, (TGI), % of vehicle control group | Body weight change, % of initial weight | ||
|---|---|---|---|---|---|
| DBPR114 | Sorafenib | DBPR114 | Sorafenib | ||
| HA22T/VGH | HCC, p53MT, poorly differentiated, HBV+/HCV− | 54.8 ± 3.8*, ** | 27.2 ± 2.3 | 3.9 ± 1 | − 1.6 ± 1.2 |
| Huh7 | HCC, p53MT, moderately differentiated, HBV−/HCV− | 86.7 ± 3.2* | 50.6 ± 10.2* | 0.7 ± 0.9 | − 3.8 ± 0.9 |
| PLC/PRF/5 | HCC, p53MT, moderately differentiated, HBV+/HCV− | 25.7 ± 13.3** | 85.5 ± 1.8* | − 9.4 ± 2.8 | − 22.2 ± 2.1 |
| Hep3B | HCC, p53null, well differentiated, HBV+/HCV− | 40 ± 6.9* | 58.8 ± 4.2* | − 0.7 ± 1.0 | − 8.8 ± 1.2 |
HCC xenograft tumors were treated with DBPR114 (40 mg/kg) once a week intravenously or sorafenib (30 mg/kg) once a day, 5 days per week orally for 3–6 weeks. Mean ± SEM, n = 7–12 mice per group
*p < 0.05 vs. vehicle control, **p < 0.05 vs. sorafenib, measured using one-way ANOVA and Bonferroni posttest comparison