Respiratory diseases like chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, and acute infections are leading causes of death worldwide, yet effective treatments remain limited due to inadequate disease models. The alveolus, composed of alveolar type 1 (AT1) and type 2 (AT2) epithelial cells, relies on a dynamic stretch–recoil cycle for normal function - an essential process disrupted in respiratory disease. Current flexible alveolar models often rely on primary or immortalised cells and are limited by low throughput. The aim of this project is to address these limitations by developing a scalable, stem cell-derived alveolar model to enable high-throughput, physiologically relevant alveolar modelling. Induced pluripotent stem cells (iPSCs) underwent directed differentiation to generate iPSC-derived alveolar type 2 cells (iAT2s). A high-throughput flexible platform was constructed using a custom membrane in 96-well format then cyclic stretch . The membrane could be stretched 5% to 35% to model foetal or adult breathing mechanics, respectively. Without stretch, iAT2s could be successfully cultured on the flexible membrane for more than two weeks, without evidence of cytotoxicity. Next, we exposed iAT2s to cyclic stretch for 5 or 10 consecutive days. iAT2s showed an initial burst of cell death at day 3, which stabilised by day 5. Although AT1 cells arise from AT2 cells in vivo during the foetal-breathing induced-stretch, we did not observe evidence of iAT2-to-iAT1 transition. In conclusion, we have established a high-throughput platform to investigate how stretch influences alveolar epithelial biology. Future studies will explore how altering the stiffness and elasticity of the membrane, or viral infections alters iAT2 fate and behaviour in response to stretch.