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. Author manuscript; available in PMC: 2019 Jul 1.
Published in final edited form as: J Colloid Interface Sci. 2018 Feb 20;521:261–279. doi: 10.1016/j.jcis.2018.02.053

Figure 12.

Figure 12

Schematic representation of the redox responsive FRET-MSNs. (A) The coumarin-labeled cysteine on the surface of the FRET-MSNs acts as a donor and the FITC-β-CD acts as an acceptor thereby forming a FRET system when the disulfide bond is intact (left). The disulfide bond is cleaved in the presence of redox stimuli and then the molecular valve FITC-β-CD is removed from the surface of the MSNs. Thereby the FRET between coumarin and FITC is abolished. (B) The drug delivery is triggered by glutathione, rich in the cytoplasm of cancer cells. Simultaneously, change of FRET signal report the uncaging event and estimate the dosing amount of drug. Figure 1A is a magnified representation of Figure 1B, indicating the FRET system. Reproduced with permission from Ref110. Copyright (2013) American Chemical Society.