. Author manuscript; available in PMC: 2015 Aug 15.

Published in final edited form as: Biochem Pharmacol. 2014 Jun 14;90(4):367–378. doi: 10.1016/j.bcp.2014.06.006

Table 3.

Motesanib does not show any effect on the ABCC1-and ABCC10-mediated multidrug resistance.

Treatment	HEK293/pcDNA3.1		HEK/ABCC1

	IC₅₀ ± SD^a (µM)	FR^b	IC₅₀ ± SD (µM)	FR

Vincristine	0.021 ± 0.002	[1.0]	0.582 ± 0.027	[27.7]
+#28 (1.5 µM)	0.021 ± 0.002	[1.0]	0.569 ± 0.019	[27.1]
+PAK-104P (2.5 µM)	0.020 ± 0.002	[1.0]	0.112 ± 0.008^*	[5.3]

Treatment	HEK293/pcDNA3.1		HEK/ABCC10

	IC₅₀ ± SD^a (µM)	FR^b	IC₅₀ ± SD(µM)	FR

Paclitaxel	0.0082 ± 0.0007	[1.0]	0.0754 ± 0.0052	[9.2]
+Motesanib (1.5 µM)	0.0077 ± 0.0008	[0.9]	0.0719 ± 0.0051	[8.8]
+Cepharanthine (2.5 µM)	0.0066 ± 0.0007	[0.8]	0.0091 ± 0.0006^*	[1.1]

IC₅₀ values are represented as mean ± SD of at least three independent experiments performed in triplicate.

Values represent the resistance fold (RF) obtained by dividing IC₅₀ value of antineoplastic drugs in HEK293/pcDNA3.1, HEK/ABCC1 and HEK/ABCC10 cells with or without reversal agent divided by the IC₅₀ value of respective antineoplastic drug in HEK293/pcDNA3.1 cells without reversal agent. Cell survival assay was determined by the MTT assay as described in Section 2. PAK-104P was used as a positive control of ABCC1 inhibitor. Cepharanthine was used as a positive control of ABCC10 inhibitor.

P < 0.01 versus the control group without reversal agent.