Supplementary Figures S1-S13 from Selectively Targeting STAT3 Using a Small Molecule Inhibitor is a Potential Therapeutic Strategy for Pancreatic Cancer

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Fig. S1. Structure-based ligand discovery of STAT3 inhibitorsFig. S2. Surface plasmon resonance analysis of interactions between WB436B to STATfamily proteinsFig. S3. The biology evaluation of WB436B inactive analogue WB345Fig. S4. The mutation in STAT3 SH2 domain directly inhibited STAT3 transcriptionalactivitiesFig. S5. WB436B induced pancreatic cancer cells apoptosisFig. S6. STAT3 knockdown reduced PDAC cells growth and colony formationFig. S7. WB436B displayed little cytotoxicity to STAT3 stable knockdown PDAC cells.Fig. S8. STAT3 depletion inhibited the growth of PDAC cellsFig. S9. WB436B suppressed STAT3 nuclear translocation and the binding to the targetgenes in pancreatic cancer cellsFig. S10. WB436B was well-tolerated in vivoFig. S11. WB436B was well-tolerated in pancreatic cancer metastatic mouse model.Fig. S12. WB436B inhibited PDAC tumor metastasis in vivoFig. S13. WB436B decreased PDAC tumors angiogenesis, inhibited tumor-associatedmacrophage infiltration and induced apoptosis in vivo

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