Lambda Biologics lung organoids replicate the architecture and function of human alveoli, giving you a reliable system to study pulmonary fibrosis, test antiviral therapies, and model respiratory infections. Built with optimized differentiation methods, our organoids deliver consistent cell composition and maturity - so you can generate data you trust from discovery through translational research.
Price | 4929€+ |
Organism | Human |
Product Type | Adult lung tissue-derived organoid, iPSC-derived organoid |
Tissue | Lung |
Disease | Fibrosis(IPF), Infection Respiratory and ENT Disease |
Applications
Toxicity
Organoid Based
Anti-Virus
Influenza Virus
Adenovirus
Disease Modeling
Respiratory and ENT Disease
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These organoids are generated directly from patient lung tissue or biopsy samples. The cells are cultured under optimized conditions that preserve their native genetic profile and cell-to-cell interactions. As a result, tissue-derived organoids faithfully reproduce the cellular composition and microenvironment of the original lung tissue. Their patient-specific nature makes them particularly valuable for personalized medicine, disease modeling, and translational research.
Using induced pluripotent stem cells (iPSCs), we recreate the early developmental processes of the lung. iPSCs are guided through stepwise differentiation into mature lung cell types and structures, producing scalable and customizable organoids. These models reflect a wide range of genetic backgrounds and environmental conditions, making them powerful tools for long-term studies, high-throughput drug screening, and regenerative medicine applications.
Lambda Biologics lung organoids faithfully reproduce the architecture of human lung tissue, including key structures such as alveoli. They contain diverse cell types – type I and II alveolar epithelial cells, ciliated cells, and secretory cells – capturing the complexity and function of real lung tissue in a reproducible model.
After infecting PSC-derived lung organoids with H1N1 and H3N2 influenza viruses and treating them with candidate drugs at different concentrations (25, 50, 100, 200 µM), RT-PCR analysis revealed a dose-dependent reduction in viral RNA copy numbers. Notably, a significant decrease in viral RNA copy numbers was observed in the candidate drug-treated groups for both H1N1 and H3N2 influenza, suggesting that these candidate drugs may effectively inhibit influenza virus replication.
In the tissue-derived lung organoids with fibrosis induced by TGF-β, immunohistochemical analysis revealed that Nintedanib treatment led to a reduction in the expression of fibrosis markers, A-SMA and Vimentin, confirming its antifibrotic effect. Similar trends were observed in some candidate drug groups, with certain candidates showing a significant decrease in fibrosis marker expression, suggesting potential antifibrotic effects. These findings indicate that Nintedanib and specific candidate drugs may have potential as therapeutic agents for pulmonary fibrosis.