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Evaluate drug candidate toxicity at clinically relevant concentrations in a co-culture human kidney model
The Kidney-Chip is a BioKit Model that Emulate has internally developed and validated. It is available as a BioKit, which includes pre-qualified cells, Organ-Chip consumables, and validated protocols, with guarantees on characterization and functionality.
Evaluate drug candidate toxicity at clinically relevant concentrations in a co-culture human kidney model
The Kidney-Chip is a BioKit Model that Emulate has internally developed and validated. It is available as a BioKit, which includes pre-qualified cells, Organ-Chip consumables, and validated protocols, with guarantees on characterization and functionality.
Inside the Kidney-Chip, cells achieve an in vivo-like phenotype, with high differentiation, normal epithelial cell polarity and morphology, and demonstrated functional transporter activity. This allows for a more physiological analysis of healthy kidney function and the nephrotoxicity of drug candidates. Long-term culture enables users to take multiple measurements for mechanistic studies, biomarker discovery, and nutrient metabolism.
The Kidney-Chip includes primary human proximal tubule epithelial cells and renal microvascular endothelial cells, enabling cell-cell interactions unlike monoculture cell models.
The Kidney-Chip maintains functionality—including albumin reabsorption and characteristic cell morphology—for up to 14 days in culture, unlike conventional cell lines which lose differentiation over time.
Shear stress from media flow significantly improves epithelial cytoarchitecture, with greater polarization, cell height, and cilia formation than kidney epithelial cells in static culture.
Sodium/phosphate (Na/Pi) co-transporter expression is increased on the Kidney-Chip in the presence of kidney-specific endothelial cells—effects not seen in mono-culture models or co-cultures with non-kidney-specific endothelial cells.
Established preclinicalin vitromodels have limited utility in predicting early indicators of nephrotoxicity due to the inability to recreate the dynamicin vivomicroenvironment. Cell lines have diminished transporter expression and functionality over time and are often not sensitive enough to respond to clinically relevant drug concentrations. Meanwhile, animal models have species differences in renal transporters, drug pharmacokinetics and pharmacodynamics, and metabolic responses. Taken together, improved preclinical kidney models are needed to improve patient safety.
Unlike conventional in vitro models, the Kidney-Chip can model mechanisms of drug-induced nephrotoxicity at clinically relevant drug concentrations. Side-by-side studies demonstrate the Kidney-Chip has better concentration-dependent responses than static epithelial monoculture models. A diverse array of endpoints can be measured, including morphological damage, cell death (LDH, ALP), oxidative stress, and a kidney injury panel (KIM-1, clusterin, TFF3, VEGF).
