Research ArticleAtherosclerosis

Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming

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Science Translational Medicine  06 Apr 2016:
Vol. 8, Issue 333, pp. 333ra50
DOI: 10.1126/scitranslmed.aad6100

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  • RE: Cyclodextrin therapy: an unfulfilled promise

    Cyclodextrin therapy: An unfulfilled promise

    The ototoxicity that occurs with currently available 2-hydroxypropyl-β-cyclodextrin precludes its long-term use to treat atherosclerosis [1, 2]. In our report [3] we indicated (Table 1) that the maximum solubility on a molar ratio was 0.05 and 0.09, respectively, far less than an expected ideal ratio of cargo to vehicle of 1:1 [4] . The toxicity makes it important to consider the causes for the low molar ratios and the possibilities for producing more efficient vehicles with little or no toxicity. Many substituted β-cyclodextrins have been synthesized [5] with the two-fold purpose of generating derivatives that increase the water solubility of the vehicle and maintain its property of solubilizing water-insoluble cargo within the torus (cavity).

    The focus on 2-hydroxypropyl-β-cyclodextrin, which may be premature, probably relates mostly to its availability and generally excellent toxicology profile when utilized for drug administration [6]. It is not a single molecule but a mixture of partially substituted isomers [7]; thus the steric relationship of the substituted hydroxypropyl group to the cavity varies. It has been proposed that the substituted group, depending on its position, may project into the cavity and block the entry of cargo [7], a view supported by the knowledge that fully substituted β-cyclodextrin loses the capacity to solubilize cargo.

    Based on this analysis, identifyin...

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    Competing Interests: None declared.

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