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Nanoparticle Packaging Dramatically Increases Potency of Anti-Cardiovascular Disease Drug

By LabMedica International staff writers
Posted on 06 Jul 2015
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Image: The buildup of fatty substances in blood vessels caused by atherosclerosis stiffens and narrows the blood vessels resulting in the death of heart muscle (Photo courtesy of [US] National Heart, Lung, and Blood Institute).
Image: The buildup of fatty substances in blood vessels caused by atherosclerosis stiffens and narrows the blood vessels resulting in the death of heart muscle (Photo courtesy of [US] National Heart, Lung, and Blood Institute).
The use of biodegradable polymer nanoparticles to encapsulate a promising drug for treating atherosclerosis increased its residence time in the body of a treated mouse from less than one hour to at least four hours (and up to 48 hours or longer).

The drug, D-PDMP (D-Threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol), is a glycosphingolipid synthesis inhibitor. Previous studies had shown that it held considerable promise for the treatment of atherosclerosis and cardiac hypertrophy, but rapid in vivo clearance severely hindered its use in the clinical setting.

To overcome this impediment, investigators at Johns Hopkins University (Baltiomore, MD, USA) sequestered D-PDMP inside a biodegradable polymer composed of polyethylene glycol (PEG) and sebacic acid (SA).

Some PEG-SA nanoparticles were labeled with PEG that contained a radioactive iodine tracer to allow in vivo bio-distribution and release kinetics of D-PDMP to be determined by using gamma-scintigraphy and subsequently, by mass spectrometry. Results published in the June 3, 2015, online edition of the journal Biomaterials revealed that polymer encapsulation increased the residence time of D-PDMP in the body of a treated mouse from less than one hour to at least four hours (and up to 48 hours or longer).

The substantially increased in vivo longevity provided by polymer encapsulation resulted in a 10-fold gain in the drug's efficacy for interfering with atherosclerosis and cardiac hypertrophy in a model based on mice genetically engineered to lack the gene for the apolipoprotein E receptor that were fed a high fat and high cholesterol diet.

"Our experiments illustrate clearly that while content is important, packaging can make or break a drug," said senior author Dr. Subroto Chatterjee, professor of medicine and pediatrics at Johns Hopkins University. "In our study, the right packaging vastly improved the drug's performance and its ability not merely to prevent disease but to mitigate some of its worst manifestations."

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