Table 13.

P-gp-resistance reversal properties of triterpene derivatives 112–114 [131,132].

Compound	R1	R2	R3	Cells/In Vivo Models	Biological Activity
112	OH		OH	HepG2/ADM	At 5 µM reduced the GI50 1 of vincristine 132-fold and paclitaxel 79-fold. Suppressed P-gp efflux function. Inhibition of ERK1/2 and AKT phosphorylation.
				MCF-7/ADR	At 5 µM reduced the GI50 1 of vincristine 151.04-fold and paclitaxel 151.07-fold.
				KB-C2 cell xenografts in nude mice model	At 15 mg/kg significantly enhanced the anticancer activity of paclitaxel (18 mg/kg), with no significant change in the body weight (Reduced toxicity).
113	OH	OH		HepG2/ADM	At 4 µM reduced the GI50 1 of vincristine 48.03–fold and paclitaxel 82-fold. Inhibited P-gp ATP-ase activity and suppress its efflux function
				MCF-7/ADR	At 4 µM reduced the GI50 1 of vincristine 29-fold and paclitaxel 47-fold.
114	OAc	OAc		HepG2/ADM	At 4 µM reduced the GI50 1 of vincristine 232-fold and paclitaxel 282-fold. Inhibited P-gp ATP-ase activity and suppress its efflux function.
				MCF-7/ADR	At 4 µM reduced the GI50 1 of vincristine 183-fold and paclitaxel 59-fold.
verapamil (1)2	-	-	-	HepG2/ADM	At 5 µM reduced the GI50 1 of vincristine 22-fold and paclitaxel 11-fold.
				MCF-7/ADR	At 5 µM reduced the GI50 1 of vincristine 29-fold and paclitaxel 59-fold.

¹ GI₅₀—Defined as the concentration of compound that inhibited cell growth by 50%. Lower GI₅₀ values mean higher intrinsic toxicity; ² verapamil (1) was used as positive control.