Brain cancer remains difficult to treat due to problems with drug delivery. Researchers at Clemson University used PLA-NHS (cat# AI174 https://akinainc.com/polyscitech/products/polyvivo/index.php?highlight=AI174#h) to conjugate this polymer to amine-modified hyaluronic acid. This co-polymer was used for delivery of doxorubicin to glioblastoma cells. This research holds promise to provide for treatment of brain cancer in the future. Read more: Chaudhri, Apoorvi, Molli Garifo, Pranavi Thatavarthi, Torrick Fletcher Jr, and Jessica Larsen. "Hyaluronic acid-b-polylactic acid polymersomes facilitate CD44-mediated delivery of doxorubicin to glioblastoma in vitro." bioRxiv (2026): 2026-05. https://www.biorxiv.org/content/10.64898/2026.05.26.727934.abstract
“Glioblastoma represents a highly aggressive brain tumor with low survival and no response to chemotherapy and radiation therapy. Temozolomide, the current standard of care chemotherapy, improves patient survival by only about 6 months because of several resistance mechanisms, including unmethylated MGMT, which enables repair of chemotherapy-induced DNA damage. Thus, additional treatments strategies are necessary to investigate efficient responses towards glioblastoma. Doxorubicin (DOX) is a chemotherapeutic agent that is independent of MGMT methylation and instead works through inhibition of topoisomerase (TOPO) II, an enzyme necessary for DNA replication of the tumor. The inability of doxorubicin to cross the blood-brain barrier (BBB) precludes its use in glioblastoma. Polymersome nanoparticles have the potential to transport agents across the BBB. Here, we develop hyaluronic acid-b-polylactic acid (HA-PLA) polymeric nanoparticles called polymersomes, encapsulate them with DOX and investigate the ability of our system to induce apoptosis in a human glioblastoma cell line. The HA-PLA polymersomes show specificity and receptor-mediated endocytosis towards CD44-positive U87 glioblastoma cells due to the natural affinity of HA (hyaluronic acid) to CD44. Our HLA-PLA-DOX system promotes apoptosis of glioblastoma through inhibition of topoisomerase (TOPO) II. Thus, our system could allow tumor specificity through HA-CD44 affinity and slow drug release through pH sensitivity of PLA in the acidic tumor microenvironment.”
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