Psoralen is a naturally occurring furanocoumarin which can interact with DNA chains and is highly light sensitive. Due to it’s interactions with DNA, any medical use of it must be carefully localized to prevent unwanted side effects. Researchers at China Three Gorges University used PCL (AP257, https://akinainc.com/polyscitech/products/polyvivo/index.php?highlight=AP257#h) from PolySciTech : Akina, Inc. (www.PolySciTech.com) to develop pH sensitive nanocarriers which deliver psoralen to the site of arthritis. This research holds promise to develop a treatment for this debilitating disease. Read more: Zhu, Lixian, Zhijie Gao, Tengyue Zhang, Hechao Zhao, Dexian Zeng, and Yanhua Wang. "Psoralen-loaded polycaprolactone microspheres: A pH-responsive drug carrier for the treatment of rheumatoid arthritis." Materials Chemistry and Physics 354 (2026): 132185. https://www.sciencedirect.com/science/article/pii/S0254058426001768
“Developing novel drug carriers for delivery of psoralen (PSO) is crucial to inhibit the pathogenesis of rheumatoid arthritis (RA). This work aims to develop PSO-loaded polycaprolactone (PCL) microspheres through a single emulsion solvent evaporation route, improving the bioavailability and controllable release of PSO. The resulting PCL@PSO microspheres are characterized by multiple physicochemical techniques. Results show the loading of PSO onto PCL, via surface adsorption, increases the size and specific surface area. Accordingly, the encapsulation efficiency and loading capacity of PCL@PSO microspheres are (87.77 ± 0.07)% and (12.28 ± 0.01)%, respectively. Strikingly, such microspheres exhibit pH-responsive drug kinetics, predominantly releasing PSO in alkaline environments in contrast with neutral or acidic conditions. This release pattern, mostly caused by diffusion, is conducive to inhibit inflammatory response whilst promote osteanagenesis in bone microenvironment. Cell experiments confirm PCL@PSO microspheres are cytocompatible with BMSCs cell but strongly toxic to RBL-2H3 cell. Mechanistically, mitochondrial apoptotic pathway, as evidenced by the up-regulation of pro-apoptosis proteins such as Caspase3, Cyto-c and Bax, is activated by PCL@PSO via increased ROS and reduced mitochondria membrane potentials. Further, the up-regulation of APC and LATS1, and the down-regulation of OIP5 are contributed to the apoptosis of RBL-2H3 cell. Moreover, PCL@PSO could down-regulate the expression of histamine receptor HRH1 in RBL-2H3 cell, thereby inhibiting inflammation expansion. However, the study is limited by the absence of in vivo animal validation, and the underlying mechanisms remain to be fully elucidated. In particular, the upstream regulatory pathways governing ROS generation have yet to be comprehensively investigated. Conclusively, it is feasible to use PCL@PSO microspheres as candidate micro-carriers to deliver PSO, terminally inhibiting inflammatory response whilst promoting osteanagenesis, especially for individuals suffered from rheumatoid arthritis.”
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