Research Paper

Pharmaceutical Research

, Volume 30, Issue 2, pp 352-361

First online:

Open Access This content is freely available online to anyone, anywhere at any time.

Targeting of Liposomes via PSGL1 for Enhanced Tumor Accumulation

  • Robert CarlisleAffiliated withUniversity of Oxford Email author 
  • , Leonard W. SeymourAffiliated withUniversity of Oxford
  • , Constantin C. CoussiosAffiliated withUniversity of Oxford



To improve the delivery of liposomes to tumors using P-selectin glycoprotein ligand 1 (PSGL1) mediated binding to selectin molecules, which are upregulated on tumorassociated endothelium.


PSGL1 was orientated and presented on the surface of liposomes to achieve optimal selectin binding using a novel streptavidin-protein G linker molecule. Loading of PSGL1 liposomes with luciferin allowed their binding to e-selectin and activated HUVEC to be quantified in vitro and their stability, pharmacokinetics and tumor accumulation to be tested in vivo using murine models.


PSGL1 liposomes showed 5-fold (p < 0.05) greater selectin binding than identically formulated control liposomes modified with ligand that did not contain the selectin binding domain. When added to HUVEC, PSGL1 liposomes showed >7-fold (p < 0.001) greater attachment than control liposomes. In in vivo studies PSGL1 liposomes showed similar stability and circulation to control liposomes but demonstrated a >3-fold enhancement in the level of delivery to tumors (p < 0.05).


The technologies and strategies described here may contribute to clinical improvements in the selectivity and efficacy of liposomal drug delivery agents.


drug delivery liposome PSGL1 selectin tumor