Abstract
This work describes how a small-molecule chemical trigger, reacting through the mediatory of an inverse electron demand Diels-Alder reaction, results in enhanced cellular uptake and selective nanoparticle disintegration and cargo liberation, via gross polymeric morphological alterations. The power of these responsive nanoparticles is demonstrated through encapsulation of the anti-cancer agent doxorubicin and its triggered release, allowing controlled cell death in response to a small-molecule chemical trigger.
Highlights
This work describes how a small-molecule chemical trigger, reacting through the mediatory of an inverse electron demand Diels–Alder reaction, results in enhanced cellular uptake and selective nanoparticle disintegration and cargo liberation, via gross polymeric morphological alterations. The power of these responsive nanoparticles is demonstrated through encapsulation of the anti-cancer agent doxorubicin and its triggered release, allowing controlled cell death in response to a small-molecule chemical trigger
Nanoparticles (NP), have been used to improve drug solubility and enhance therapeutic effectiveness,[4,5] owing to targeting to tumor tissues with improved pharmacokinetics and pharmacodynamics and active intracellular delivery. In this context nanoparticle-based polymersomes, generated from polymeric amphiphiles, are popular allowing the rapid generation of stable vesicles,[6,7,8] and micelles[9,10,11] in water
Remote triggers use an external physical stimulus such as temperature (e.g. polymers exhibiting a lower critical solution temperature, for example, poly(N-isopropylacrylamide)),[19] ultrasound or light
Summary
This work describes how a small-molecule chemical trigger, reacting through the mediatory of an inverse electron demand Diels–Alder reaction, results in enhanced cellular uptake and selective nanoparticle disintegration and cargo liberation, via gross polymeric morphological alterations. The power of these responsive nanoparticles is demonstrated through encapsulation of the anti-cancer agent doxorubicin and its triggered release, allowing controlled cell death in response to a small-molecule chemical trigger.
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