期刊
PHARMACEUTICS
卷 14, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/pharmaceutics14010085
关键词
fibrosis; 15-PGDH; SW033291; cyclodextrin; affinity
资金
- NIH [SW033291, 5R00HL135740-04]
- theRadiation Resources Core Facility [R35 CA197442]
- thePreclinical Pharmacology Core of UT Southwestern
- [P30CA043703]
As the prevalence of age-related fibrotic diseases continues to rise, finding new antifibrotic therapies is crucial. This study lays the groundwork for a sustained release platform for a small-molecule inhibitor of the 15-hydroxyprostaglandin dehydrogenase (15-PGDH) enzyme. By using fine-tuned cyclodextrin microparticles, the delivery time of the inhibitor was extended to over one week.
As the prevalence of age-related fibrotic diseases continues to increase, novel antifibrotic therapies are emerging to address clinical needs. However, many novel therapeutics for managing chronic fibrosis are small-molecule drugs that require frequent dosing to attain effective concentrations. Although bolus parenteral administrations have become standard clinical practice, an extended delivery platform would achieve steady-state concentrations over a longer time period with fewer administrations. This study lays the foundation for the development of a sustained release platform for the delivery of (+)SW033291, a potent, small-molecule inhibitor of the 15-hydroxyprostaglandin dehydrogenase (15-PGDH) enzyme, which has previously demonstrated efficacy in a murine model of pulmonary fibrosis. Herein, we leverage fine-tuned cyclodextrin microparticles-specifically, beta-CD microparticles (beta-CD MPs)-to extend the delivery of the 15-PGDH inhibitor, (+)SW033291, to over one week.
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