Table 1.

Anticancer activities of commonly studied relevant ginsenosides [5, 8, 11–14].

Ginsenoside	Anticancer activity	Molecular mechanism
Rb1	Weakly antiproliferative; antiangiogenic	(i) Inhibit capillary genesis (ii) Inhibit TNF-a release (iii) Protect against oxidative stress (iv) Inhibit tube-like structure formation of endothelial cells by regulating pigment epithelium-derived factor (PEDF) through estrogen receptor-β [13, 14]
Rb3	No antiproliferative activity	Inhibit TNF-α release
Rg1	Antiproliferative	(i) Inhibit oncogenes c-myc, c-fos (ii) Downregulate nucleophosmin.
Rg3	Antiproliferative, apoptotic, antiangiogenic, antimetastatic, anti-invasive, and cell cycle regulation, [8, 11, 12]	(i) Regulate mitochondrial cytochrome C, poly ADP ribose polymerase (PARP) and C9 (ii) Inhibit MMP-2 and 9 (iii) Inhibit adhesion of metastatic cells to basement membrane (iv) Inhibit MDR (most potent among all ginsenosides)
Rh1	Causes differentiation of teratocarcinoma cells, strongly apoptotic	(i) Bind to steroid receptor (ii) Inhibit TNF-α  (iii) Inhibit phosphorylation of JAK1, STAT1, STAT3, and ERK