With over a hundred thousand transplants needed every year and limited availability leading to the death of 20 patients each day, long term viability of solid organ transplants is imperative. Early allograft transplant rejection is well controlled by immunosuppression of T cells, but late organ loss due to allograft vascular (AV) disease and chronic immune damage are unmet medical needs. Chronic AV disease and ongoing immune damage are leading causes of late transplant organ loss. In prior work, we demonstrated that implant of an allograft kidney with a conditional deficiency of the N-deacetylase N-sulfotransferase 1 (Ndst1-/-) enzyme in the endothelium and myeloid precursors (C57Bl/6 background) led to a significant decrease in early rejection after implant into wild type BALB/c mice with normal Ndst1 expression [1-3]. This finding suggested that pre-transplant modification of the endothelial polysaccharide surface layer (EPSL) and glycosaminoglycans (GAGs) in donor organs may be beneficial in reducing early and late AV disease and subsequent rejection. The glycocalyx has a central role in the immune response as it serves as a scaffold for new cell growth and chemokine-directed immune cell recruitment [4]. Prior literature has also demonstrated marked improvement in both early and late rejection after treatment with a chemokine modulating protein, M-T7 [5,6]. M-T7 is a 37KDa glycosylated protein that significantly reduces intimal hyperplasia following vascular injury. M-T7 blocks binding of C, CC, and CXC chemokine classes to glycosaminoglycans, interfering with development of chemokine gradients that direct immune cell migration. M-T7 given immediately after renal allograft transplants and for 10 days after transplant effectively reduces acute rejection and longer-term rejection when given with cyclosporine treatment