CAG-Cre-GFP AAV (Serotype AAV-BI30)

AAV-BI30 is ideally suited to accelerate neurovascular research, providing a rapid and easily adaptable method to access CNS endothelial cells and offering distinct advantages over existing vectors. Unlike AAV-PHP.V1, at a 1x1011 vg dose, AAV-BI30 tropism within the CNS is almost exclusively restricted to endothelial cells, eliminating the need for complex workarounds (e.g., cross-Cre-dependent approaches) to restrict cell type specificity. AAV-BI30 is more efficient and versatile than AAV-BR1, particularly for applications targeting retinal, spinal cord, or cerebral vascular arteries and veins. While AAV-BI30 tropism appears to be primarily biased toward CNS vasculature, transduction of hepatocytes and endothelial cells has been observed in pulmonary microvessels, aorta, and renal interlobular vessels. Importantly, peripheral endothelial cell transduction is strictly restricted to these cell populations—most organs show little or no endothelial cell transduction. For most research applications, the advantageous properties of AAV-BI30 may more than compensate for this drawback. However, in cases where CNS specificity is critical, a Cre-dependent viral genome could be combined with a CNS-specific transgene driver (e.g., MFSD2A:CreERT2 or SLCO1C1:CreERT2) to minimize peripheral transduction with AAV-BI30.