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Ginsenoside Rh2 is a major metabolite from ginseng that has antitumor activity. Previously, we reported that Rh2-O, an octyl ester derivative of ginsenoside Rh2, had a higher anti-cancer activity than Rh2 in human HepG2 cells. The aim of the present study was to compare the antitumor and immunomodulatory effects of ginsenoside Rh2 and Rh2-O using an animal model. Experiments using H22 tumor-bearing mice demonstrated that the antitumor effect of Rh2-O (10 mg/kg) was better than that of Rh2 (10 mg/kg) with inhibitory rates of 50.6% and 28.2%, respectively (p < 0.05). Both Rh2 and Rh2-O induced tumor cells apoptosis by regulating the expression of the Bcl-2 family proteins and the activation of the caspase family proteins. Additionally, Rh2 and Rh2-O treatment increased the serum IL-2 levels, TNF-α production, T lymphocyte counts, CD4+/CD8+ ratio, and NK cell levels. Furthermore, immune-histochemical and western blot analyses demonstrated that Rh2 and Rh2-O inhibited vascular endothelial growth factor (VEGF) production. These results showed that inducing tumor cell apoptosis, modulating the immune response, and down-regulating VEGF expression may be involved in Rh2- and Rh2-O-inhibited tumor growth in H22-tumor bearing mice.