Fig. 7.

(A) Schematic shows that cancer cells exploit CSF1R signaling to polarize macrophages to the immunosuppressive M2 phenotype and SIRPα–CD47 interactions to inhibit phagocytosis. (B) Schematic illustration of efficient repolarization of an M2 macrophage to the effector M1 phenotype by dual-function supramolecular therapeutic mediated sustained inhibition of CSF1R signaling and enhanced phagocytosis of cancer cells following inhibition of SIRPα. (C) Representation of the quantum mechanical-optimized structure of the molecular subunit of the supramolecular nanostructure. (D) Snapshot of an all-atomistic simulation. Reproduced with permission from [174]. Copyright 2018 Macmillan Publishers Limited, part of Springer Nature.