Leveraging the deep expertise of our lung specialists, our lung‑on‑Chip models accurately replicate key regions of the lung—including the alveolar barrier and bronchial airways. They are available in different levels of complexity (from mono‑ to triple‑culture systems, including air–liquid interface models and breathing like motion) and can be generated using primary cells or cell lines. These models are well suited for both safety assessment and efficacy testing.

Our gut-on-chip model, based on human primary cells or cell lines, exhibits robust barrier integrity and incorporates key epithelial subtypes to create a physiologically relevant system under peristalsis. This platform offers a reliable solution for evaluating compound and nutrient efficacy, as well as gastrointestinal toxicity in response to oral drugs and biologics.

Renal proximal tubular epithelial cells (RPTECs) are cultured on‑chip to reproduce the structure and functionality of the proximal tubule, creating a simple yet sufficiently complex model capable of evaluating compound‑induced nephrotoxicity and studying excretion processes and dynamics related to ADME.

Our interstitial lung disease model, composed of donor-derived epithelial cells and lung fibroblasts, demonstrates key fibrotic markers, with efficacy testing validated using the FDA-approved drug nintedanib. In addition, our proprietary epithelial cell line, when combined with lung fibroblasts and fibrotic inducer, exhibits characteristic fibrotic hallmarks. Both models provide robust platforms for evaluating anti-fibrotic compound efficacy and assessing safety related to fibrotic risk.

Our Gut-on-Chip models recreate key inflammatory processes underlying Crohn’s disease and ulcerative colitis by integrating human intestinal epithelial co‑cultures with physiologically relevant biomechanical cues. Exposing epithelial cells to controlled pro‑inflammatory cytokine cocktails, the Gut‑on‑Chip platform enables the induction of a ‘leaky‑gut’ phenotype characterized by barrier disruption, altered epithelial differentiation, increased cytokine release, and immune‑modulated responses. The incorporation of rhythmic, peristalsis‑like mechanical stretch enhances model sensitivity to inflammatory triggers and more accurately reflects in vivo intestinal dynamics.

Our COPD models recreate key physiological features of the diseased lung, enabling controlled and reproducible investigation of chronic obstructive pulmonary disease mechanisms. Using human alveolar and airway cell types cultured under air–liquid interface and breathing‑like mechanical stretch, these Lung‑on‑Chip systems allow the study of inflammatory responses, barrier dysfunction, oxidative stress, and tissue remodeling characteristic of COPD.

Our infection models allow the study of both viral (e.g. SARS-CoV-s, influenza) and bacterial pathogens (e.g. S. pneumoniae, E. coli) under physiologically relevant conditions. These models support a wide range of functional readouts reflecting native tissue responses—such as barrier integrity, cytokine release, pathogen replication dynamics, and host–pathogen interactions. Moreover, the models can be operated within BSL‑3 facilities, enabling the safe handling of high‑risk infectious agents while preserving experimental fidelity.

Our pulmonary hypertension model, developed using alveolar endothelial and/or epithelial cells, replicates key pathological features such as increased vascular permeability (indicated by reduced TEER) and elevated inflammatory markers. This physiologically relevant platform is suitable for efficacy testing of therapeutic candidates.