Owing to its primary amine group, Dox has also been conjugated to polymer prodrugs obtained by RDRP via the formation of imine linkage. A PLlys-b-PMPC copolymer was prepared by ATRP of MPC from a protected PLlys-based ATRP macroinitiator. The PLlys block was then deprotected to release its primary amine groups which were sequentially conjugated to 4-carboxylbenzaldehyde (CBA) to confer a pH-dependent charge conversion property, and to Dox via formation of imine linkages (Figure ). Due to the amphiphilic nature of the resulting polymer prodrug, it formed micelles of 90 nm diameter with PMPC as the hydrophilic shell and PLlys-imine-Dox as the hydrophobic core. They exhibited accelerated drug release kinetics due to: (i) a surface pH-triggered charge conversion and (ii) a pHdependent structural disassembly due to imine bond hydrolysis and Dox release. Interestingly, due to the inherent imine linkage stability, the micelles remained stable at physiological pH over 30 days. Cell internalization studies showed greater endocytosis of the micelles at pH 6.8 than at pH 7.4, in addition to a more efficient drug release under acidic environment, leading to a similar cytotoxicity and cell apoptosis level on 4T1 and HeLa cells compared to those of the free drug. Another strategy to achieve similar amphiphilic polymer prodrugs is to polymerize glycidyl methacrylate (GMA) from a linear PEG-functionalized ATRP macroinitiator, which epoxy rings were post-functionalized by CBA to install pendant aldehyde groups for subsequent Dox conjugation via imine bond formation. This polymer prodrug was able to self-assemble into micelles, whose average diameters ranged from ~100 nm for a PGMA average chain length of 21 repeat units to 260 nm for 89 repeat units. A pH-triggered Dox release up to 80 % within 12 h was observed, which was explained by a conformational modification of the hydrophobic core into a semi-hydrophobic one under acidic conditions leading to an improved diffusion of the protons H + . A fast internalization of the micelles in HepG2 cells followed by a pH-driven release of Dox into the cytosol and its accumulation in the nucleus were demonstrated by confocal microscopy.