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Pathological mechanisms contributing to CIPN The pathological mechanisms underlying the development of CIPN have been studied extensively, and likely involve direct effects on the viability of sensory neurons, as well as cell-type specific consequences that occur downstream of on-target pharmacological activity of these cytotoxic drugs

It can be administered via infusion, intramuscular (IM), or intravenous (IV) injection

found that ASCT2 ligands chloroalanine, aminooxetane-3-carboxylate (AOC), and -FBP also inhibit ASCT2-mediated glutamine uptake in human melanoma cells [104]

Once we established that PD exhibited SCAN hyperconnectivity, we hypothesized that PD treatments would be associated with reduced hyperconnectivity