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Licensing Opportunity: Novel Scavenger Receptor A1-Targeted Macromolecular Prodrug Platform

Investigators at the NCL have developed a drug delivery platform that targets scavenger receptor A1, a receptor highly expressed in macrophages, monocytes, mast cells, and dendritic cells (myeloid lineages), as well as endothelial cells. The platform is based on the anionic polymer poly(L-lysine succinylated), which contains side chains with pendant carboxylic acids that allow conjugation of drugs through hydrolysable ester bonds and have demonstrated drug release half-lives greater than 10 hours. Through this approach, high levels of prodrug will be preferentially distributed to scavenger receptor A1 expressing cells, such as myeloid/APC, but also to the entire lymphatic system as a result of SR-A1-meditated endothelial transcytosis. Furthermore, active drug is released in a controlled manner – a milestone not yet achieved with current nanomedicine platforms.

The National Cancer Institute (NCI) seeks licensing and/or co-development research collaborations for this novel polymer drug delivery platform. There is the potential for numerous applications and products, including targeted drug delivery of immunomodulatory small molecule drugs, peptide therapeutics, and vaccine antigens for use in cancer, infectious diseases (e.g., HIV), as well as brain delivery for neurodegenerative conditions and glioma. For more information on licensing and co-development opportunities, please visit

Download a one-page brochure describing the macromolecular prodrug technology here which highlights recent applications of this technology using emtricitabine (HIV nucleoside analog reverse transcriptase inhibitor) and PI-103 (pan-class I PI3K/mTOR inhibitor). In support of the platform’s ability to target latent lymphatic HIV reservoirs, the emtricitabine prodrug was demonstrated in rats to increase active drug concentrations in lymphatic tissues 10-fold over the unformulated drug. In a syngeneic mouse B16 melanoma model, the PI-103 prodrug significantly reduced tumor growth at doses as low as 0.1 mg/kg, and increased the targeted-tumor associated macrophage M1 (anti-tumor):M2 (pro-tumor) ratio by ~4 fold. Even 100-fold higher doses (10 mg/kg) were without clinically apparent toxicity.

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