Actionable Human-Safety Data
Without the Guesswork

Liver:
Cell viability in liver models is measured using ATP quantification assays, which reflect metabolic activity and overall cell health. Additional markers include LDH release (membrane integrity) and live/dead staining. These assays are essential for screening for drug candidates, as reduced viability correlates with hepatotoxic potential. Viability endpoints are integrated with functional assays (albumin) to provide a holistic view of liver health and response to injury. The platform’s flexible dosing schedule enables assessment of viability over treatment durations exceeding 20 days.

Intestine:
In intestinal models, cell viability is assessed using ATP assays and metabolic indicators such as Alamar Blue reduction. These readouts quantify the proportion of living, metabolically active cells and are sensitive to cytotoxic insults from drugs or inflammatory stimuli. Viability assays are performed alongside barrier integrity and inflammatory markers to distinguish between reversible and irreversible damage. Maintaining high cell viability is crucial for modeling helathy states and evaluating toxic potential of therapeutic interventions.

Liver Barrier Integrity:
While the liver is not a classical barrier organ, hepatocyte tight junctions and sinusoidal endothelial integrity are important for maintaining selective permeability and preventing leakage of toxic substances. In vitro, barrier integrity can be inferred from LDH release, albumin secretion, and the maintenance of polarized cell layers. Disruption of these features is indicative of liver injury and compromised function.

Intestinal Barrier Integrity:
Barrier integrity is a defining feature of intestinal models, measured by transepithelial electrical resistance (TEER) and permeability assays. High TEER values indicate intact tight junctions and functional epithelial layers, while drops in TEER signal barrier disruption—a hallmark of IBD, infection, or drug-induced toxicity. Permeability to fluorescent tracers or macromolecules further quantifies barrier function.

Liver:
Oxidative stress in liver models is assessed by measuring glutathione (GSH) levels. GSH depletion is an early indicator of hepatocyte injury.

Intestine:
In intestinal models, oxidative stress is measured using ATP and Alamar Blue quantification and assessment of redox-sensitive gene expression. Oxidative stress contributes to barrier dysfunction, inflammation, and epithelial cell death in drug-induced injury.

Liver:
Gene expression profiling in liver models utilizes RNA sequencing and qPCR to quantify transcripts associated with hepatocyte function, injury, fibrosis, and inflammation. Key genes include CYP450 enzymes, transporters (BSEP, MRP), albumin, and markers of apoptosis or necrosis. Differential expression analysis reveals drug-induced changes, disease signatures, and therapeutic responses. Integration with histological and functional data enables comprehensive characterization of model fidelity and mechanistic pathways.

Intestine:
For intestinal models, gene expression analysis targets epithelial differentiation markers, tight junction proteins, cytokines, and fibrosis-related genes. RNAseq distinguishes healthy from diseased tissue by identifying upregulation of inflammatory mediators, downregulation of barrier proteins, and altered extracellular matrix components. These data provide molecular validation of model architecture and disease relevance, supporting drug-induced toxicity assessments.

Hepatocyte (Liver-Specific)
Hepatocytes are the principal functional cells of the liver, responsible for metabolism, detoxification, and protein synthesis. Our models assess hepatocyte health via albumin production, CYP activity, and transporter function. Maintenance of polarized morphology and bile canaliculi formation are indicators of mature hepatocyte phenotype. Drug-induced changes in hepatocyte function are central to DILI prediction and mechanistic toxicology.

Enterocyte (Intestine-Specific)
While hepatocytes are liver-specific, intestinal models focus on enterocytes, goblet cells, and other epithelial subtypes. Enterocyte function is assessed via transporter activitu and barrier maintenance. The interplay between epithelial cells and immune/stromal compartments is critical for modeling disease and drug response.

Liver:
Liver injury is evaluated using a combination of cell viability, functional assays (ALT/AST, albumin), and histological markers (necrosis, fibrosis). LDH release and ATP depletion are early indicators, while chronic injury manifests as collagen deposition and altered gene expression. Advanced models replicate clinical patterns of injury, enabling mechanistic studies and therapeutic screening. Sensitivity and specificity of injury detection are benchmarked against FDA-classified compounds.

Intestine:
Intestinal injury is characterized by loss of barrier integrity, increased cell death, and upregulation of inflammatory and fibrotic markers. TEER drops, permeability increases, and histological evidence of ulceration or crypt loss are key endpoints. These features are central to modeling chemotherapy-induced mucositis, and drug-induced GI toxicity.

Liver:
Inflammatory markers in liver models include cytokines (IL-6, TNF-α), chemokines, and immune cell infiltration. Multiplexed assays and immunostaining quantify the inflammatory response to drugs or disease stimuli.

Intestine:
In intestinal models, inflammatory markers encompass cytokines and chemokines (IL6, IL-8, IL-1β, MCP1) and immune cell recruitment. Elevated levels correlate with barrier dysfunction, epithelial cell death, and disease severity in drug-induced injury. Advanced platforms enable dynamic measurement of inflammatory responses, supporting the development of precision medicine approaches.