Posted by Ischemic stroke is a leading cause of mortality and long-term disability worldwide, with limited pharmacological interventions available. Researchers in Arizona US have shown that HPβCD can access acute and subacute ischemic infarcts in a mouse model of stroke. Because the blood–brain barrier is disrupted after ischemia, HPβCD selectively accumulates in the injured hemisphere (even days after the event!) while being rapidly cleared systemically via the kidneys. This study demonstrates that CDs can reach lipid- and immune-rich lesion sites in the injured brain.
FITC-HPβCD was 8used to (1) assess the penetration and distribution of FITC-HPβCD within acute and subacute infarcts, which are sites of persisting blood-brain barrier (BBB) impairment, and (2) validate the accumulation of FITC-HPβCD in previously identified target organs, including the kidneys, liver, and spleen, using an aged (15-month-old) male mouse model of ischemic stroke induced by distal middle cerebral artery occlusion.
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Becktel, D.A., Le, E.H., Frye, J.B. et al. 2-Hydroxypropyl-β-cyclodextrin accesses acute and subacute infarcts in a mouse model of ischemic stroke. Fluids Barriers CNS 23, 32 (2026). https://doi.org/10.1186/s12987-026-00767-9