Novel FLT3/AURK multikinase inhibitor is efficacious against sorafenib-refractory and sorafenib-resistant hepatocellular carcinoma

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
Cell line	Histopathology	DBPR114	Sorafenib	DBPR114	Sorafenib
HA22T/VGH	HCC, p53^MT, poorly differentiated, HBV⁺/HCV⁻	54.8 ± 3.8, *	27.2 ± 2.3	3.9 ± 1	− 1.6 ± 1.2
Huh7	HCC, p53^MT, moderately differentiated, HBV⁻/HCV⁻	86.7 ± 3.2*	50.6 ± 10.2*	0.7 ± 0.9	− 3.8 ± 0.9
PLC/PRF/5	HCC, p53^MT, moderately differentiated, HBV⁺/HCV⁻	25.7 ± 13.3**	85.5 ± 1.8*	− 9.4 ± 2.8	− 22.2 ± 2.1
Hep3B	HCC, p53^null, 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

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