Magnetoelectric Nanoparticles Accurately Target Diseased Cells With Systemically Toxic Drugs

Tech ID: 18-047/19-014

Inventors: Prakash Daniel Nallathamby, Paul Helquist

Overview

Magnetoelectric nanoparticles precisely deliver toxic drugs to diseased cells and avoid damaging healthy ones.

Technology Summary

Vacuolar ATPase (V-ATPase) is a highly conserved evolutionarily ancient enzyme with remarkably
diverse functions in eukaryotic organisms. In several cancers (incl. breast, ovarian, cervical,
prostate, glioblastoma, & leukemia), V-ATPase plays a key role in cancer progression, migration,
and cancer cell survival. V-ATPase inhibitors are an underutilized class of chemotherapeutics that
are particularly effective inhibitors of metastasis and drug resistance. But ubiquity of V-ATPase
dramatically increases off-target effects of V-ATPase inhibitors. Researchers at the University of
Notre Dame have developed magneto-silica nanoparticles (MagSiNs) capable of delivering
combinations of V-ATPase inhibitors with standard chemotherapeutics to increase antitumoral
activity and prevent the progression of metastatic cancers. Further, these MagSiN nanocarriers
can be localized into cancer cells with high specificity and then release the chemotherapeutics
only when triggered by an external electromagnetic field of specific magnetic field strength and
frequency.

Market Advantages:
• Targeted delivery of chemotherapeutic agents reduces off-target effects.
• Increased stability of drugs while bound to the MagSiNs increases efficacy when
released at the tumor site
• Dual-loaded MagSiNs permit the targeted delivery of both inhibitors and
chemotherapies concurrently.
• Significantly increased efficiencies for stand-alone chemotherapies (18 fold) and
dual-chemotherapies (20 fold) permits lower dosing of hyper-toxic therapeutics to
diseased cells while reducing off-target toxicity to healthy cells.
• MagSiNs permit the co-formulation and co-delivery of both hydrophobic and
hydrophilic therapeutics.

Technology Readiness Status
TRL 3.5 - Critical function established via in-vitro studies, in-vivo studies underway

Seeking: Licensing and Research Collaboration

Contact

Richard Cox

rcox4@nd.edu

574.631.5158