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LB-100 is a protein phosphatase 2A (PP2A) inhibitor, with IC₅₀ of 0.85 μM and 3.87 μM in BxPc-3 and Panc-1 cells.

LB-100 inhibits cell growth with IC50 values of 2.3 μM (BxPc-3) and 1.7 μM (Panc-1), respectively. LB-100 can reduce PP2A activity by 30-50% in BxPc-3, Panc-1, and SW1990 cells. LB-100 increased the intracellular concentration of doxorubicin (2.5 times the control) and made tumor cells sensitive to the cytotoxicity of doxorubicin. LB-100 increases VEGF secretion, thereby enhancing HIF-1 α - VEGF mediated angiogenesis. LB-100 alters the integrity of ve cadherin between endothelial cells. The pre-treatment results of LB-100 increased the dye content through HUVECs monolayers by nearly 40%. LB-100 induces an increase in paracellular permeability of vascular endothelial cells, which may be the reason for LB-100 increasing the concentration of doxorubicin in tumor cells. LB-100 downregulates Bcl-2 expression and enhances sorafenib induced apoptosis in HCC cells.

LB-100 (2 mg/kg, intraperitoneal injection) reduced the activity of PP2A in nude mouse xenografts and liver in a time-dependent manner. Immunoblotting confirmed that LB-100 does not alter the expression of the three PP2A subunits (PP2A_S, PP2A-B, and PP2A_C) in cell lines, xenografts, or liver. The combination therapy of amphotericin B (1.5 kg/mL, every other day) and LB-100 (2 mg/kg, every other day) significantly slowed down tumor growth and reduced tumor volume in both animals, while monotherapy had no effect on tumor growth in animals.

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