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Photoactuators based on liquid crystal elastomers or networks are smart materials that show photoinduced motions. However, their crosslinked networks make their repair or reprocessing difficult. Here, a healable and reprocessable photoactuator is fabricated using entangled high‐molecular‐weight azobenzene‐containing polymers (azopolymers) that are non‐crosslinked. A series of linear liquid crystal azopolymers with different molecular weights are synthesized. The low‐molecular‐weight azopolymers (5–53 kg mol−1) cannot form freestanding photoactuators because their polymer chains lack entanglements, which makes them hard and brittle. In contrast, flexible and stretchable actuators are fabricated using high‐molecular‐weight azopolymers (80–100 kg mol−1) that exhibit good processability because of the polymer chain entanglements. The azopolymer photoactuators show photoinduced bending based on photoinduced trans–cis isomerization of the azopolymers on the irradiated side. The experiments show not only photoinduced phase transitions or changes in the order parameters but also photoinduced solid‐to‐liquid transition of the azopolymers resulting in shape changes and mechanical responses. Thus, photoinduced solid‐to‐liquid transition is a new mechanism for the design of photoactuators. Moreover, the azopolymer photoactuators are healable and reprocessable via solution processing or light irradiation. Healability and reprocessability prolong lifetimes of photoactuators are important for materials reusage and recycling, and represent a new strategy for the preparation of smart materials.

First, proteins such as serum albumin in blood deactivate cisplatin. [5] Second, cisplatin cannot be efficiently taken up by cisplatin-resistant cancer cells. [6] Third, intracellular biomolecules such as metallothionein (MT) and glutathione (GSH) may strongly bind and sequester cisplatin. [7] Fourth, the DNA of cancer cells that are damaged by cisplatin, can be repaired by proteins. [8] All these deactivation pathways hinder the curative effects of cisplatin. Some strategies have been developed to overcome the abovementioned deactivation pathways. For example, Pt(IV) prodrugs, which release cisplatin in cancer cells, have been developed. [9-12] Pt(IV) prodrugs are more resistant to ligand substitution reactions than cisplatin because Pt(IV) centers are saturated and kinetically more inert. [1] Thus, Pt(IV) can minimize unwanted side reactions with biomolecules prior to DNA binding. Another strategy to overcome deactivation is to combine cisplatin with other anticancer agents such as paclitaxel, 5-fluorouracil, gemcitabine or ruthenium complexes. [13-16] Mixtures of anticancer agents possess multiple targets and actions; this strategy strengthens the therapeutic effects via the different anticancer mechanisms of the different agents. [14] A third strategy to overcome deactivation is to use nanocarriers for the delivery of cisplatin. [17,18] Some Drug resistance is a major problem in cancer treatment. Herein, the design of a dual-responsive Pt(IV)/Ru(II) bimetallic polymer (PolyPt/Ru) to treat cisplatin-resistant tumors in a patient-derived xenograft (PDX) model is reported. PolyPt/Ru is an amphiphilic ABA-type triblock copolymer. The hydrophilic A blocks consist of biocompatible poly(ethylene glycol) (PEG). The hydrophobic B block contains reduction-responsive Pt(IV) and red-light-responsive Ru(II) moieties. PolyPt/Ru self-assembles into nanoparticles that are efficiently taken up by cisplatin-resistant cancer cells. Irradiation of cancer cells containing PolyPt/Ru nanoparticles with red light generates 1 O 2 , induces polymer degradation, and triggers the release of the Ru(II) anticancer agent. Meanwhile, the anticancer drug, cisplatin, is released in the intracellular environment via reduction of the Pt(IV) moieties. The released Ru(II) anticancer agent, cisplatin, and the generated 1 O 2 have different anticancer mechanisms; their synergistic effects inhibit the growth of drugresistant cancer cells. Furthermore, PolyPt/Ru nanoparticles inhibit tumor growth in a PDX mouse model because they circulate in the bloodstream, accumulate at tumor sites, exhibit good biocompatibility, and do not cause side effects. The results demonstrate that the development of stimuli-responsive multi-metallic polymers provides a new strategy to overcome drug resistance.