Age-related macular degeneration (AMD) is a common degenerative disease affecting the central retina (macula). A key feature is the formation of new choroidal blood vessels growing into and damaging the central retina. Implementation of anti-angiogenic drugs like aflibercept or brolucizumab has improved the prognosis of neovascular AMD. However, around 15% of patients do not respond to these treatments. And even if the treatments are effective against neovascularization, they cannot halt retinal degeneration. In addition, the treatments have to be repeated every one to two months, which is a considerable burden for patients. A potential curative solution might be gene therapy with adeno-associated virus (AAV) vectors targeting choroidal endothelial cells (EC) to counteract neovascularization. However, successful gene transfer to choroidal ECs remains challenging. Here, we aimed to identify novel AAV variants with improved tropism and enhanced efficiency in transducing choroidal ECs. We found that modified AAV1 capsids can robustly transduce primary mouse choroidal ECs (transduction efficiency in the range of 60% and higher), in contrast to parental AAV1 or other naturally occurring serotypes. The engineered AAV1 variants carry the peptide insertions first described in AAV2.GL and AAV2.NN, previously identified AAV2 variants with enhanced transduction efficiency for retinal cells. The promising in vitro transduction properties were further evaluated in vivo in mice and ex vivo in human retinal explants. Future more, we started to test our variants in vivo. Overall, our study identified new AAV1-based capsid variants that could be used for the gene therapy of AMD in the future.