An in vitro “avatar” for precision medicine — from 3D culture to individualized treatment decisions
Patient-derived organoids (PDOs) are cells isolated from a patient’s tumor tissue and cultured in a three-dimensional matrix gel to form miniature in vitro organ models. These “spheroids”, only a few hundred micrometers in diameter, faithfully recapitulate the histological features, gene mutation profile and drug response behavior of the original tumor at both the structural and functional level. Compared with conventional two-dimensional cell culture, organoids preserve the three-dimensional architecture, cell–cell interactions and microenvironmental features of the tumor, so that in vitro drug sensitivity results show a remarkable correlation with actual clinical response.
In recent years, organoid technology has moved from the laboratory to the forefront of clinical translation. Studies have shown that organoid-based drug sensitivity testing (DST) can achieve a prediction accuracy of over 83%, with a sensitivity of about 80% and a specificity of about 86%, providing a reliable in vitro evaluation platform for individualized precision medication.
In organoid drug sensitivity screening experiments, researchers typically expose mature organoids to candidate compounds at a range of concentrations, then assess changes in cell viability by live/dead cell staining, ATP luminescence assays or Caspase activity detection, plot dose–response curves and calculate IC50 values. High-quality inhibitors are the core element that ensures the reliability of screening results — the high-purity, high-activity inhibitors provided by AbMole cover targeted small molecules, monoclonal antibodies and more, offering a solid reagent foundation for organoid drug sensitivity research.
Organoids self-organize into three-dimensional structures in Matrigel or BME matrix gel, mimicking the extracellular matrix components of the in vivo tumor microenvironment and maintaining cell polarity and differentiation status.
Whole-exome sequencing (WES) or targeted sequencing confirms that the gene mutation profile overlap between organoids and the primary tumor usually exceeds 90%, ensuring the genetic fidelity of the model.
Set 5–10 concentration gradients based on the real plasma drug concentration range, with 3–5 replicate wells per concentration, together with negative controls, blank groups and positive controls.
Including the CCK-8 colorimetric assay, CTG luminescence assay, Calcein-AM/PI live/dead staining, SYTOX Green nucleic acid staining and Caspase 3/7 apoptosis detection, among others.
The growth rate (GR) inhibition metric replaces the traditional IC50, eliminating systematic errors caused by differences in cell seeding density and division rate, and improving the reliability of results.
Microfluidic chip technology (such as InSMAR-chip) can complete drug sensitivity testing in about one week, requiring only 1,000–5,000 cells per unit, enabling rapid, low-input, high-throughput screening.
The products below are organized by cancer type, covering targeted small-molecule inhibitors, monoclonal antibodies and immune checkpoint inhibitors, among others.
Tumor organoids are exposed to a standardized inhibitor panel, and sensitive compounds are identified using metrics such as IC50, AUC and GR values, providing in vitro functional evidence for treatment decisions. Studies have confirmed that organoid DST predicts response to chemotherapy and targeted therapy with over 80% accuracy.
By comparing drug response differences between sensitive and resistant organoid models, combined with transcriptomic sequencing and proteomic analysis, researchers can uncover resistance-related signaling pathway activation, metabolic reprogramming or epigenetic modifications, providing target clues for overcoming resistance.
Test the synergistic effects of different inhibitor combinations on the organoid platform (e.g. an EGFR inhibitor combined with a MEK inhibitor, or a PARP inhibitor combined with an immune checkpoint inhibitor), calculate synergy scores with the Bliss independence model or the Loewe additivity model, and screen for optimal combination regimens.
Use organoid biobanks for high-throughput compound screening to evaluate the activity profile of drug candidates across tumors of different molecular subtypes. Compared with traditional cell lines, organoids better reflect the heterogeneity of clinical tumors, improving the success rate of candidates advancing to later-stage trials.
Establish association models between specific gene mutations (such as EGFR T790M, KRAS G12C and BRCA1/2 loss) and drug sensitivity, integrate organoid drug sensitivity data with genomic information, and develop predictive biomarkers to guide precise stratified treatment.
In parallel with tumor organoid drug sensitivity screening, culture normal tissue organoids (such as intestinal or liver organoids) for toxicity testing, calculate the therapeutic index, and select highly selective, low-toxicity candidate compounds to reduce development risk.
The product information and functional descriptions listed here are for research reference only. Organoid drug sensitivity screening experimental design should be optimized according to the specific research objectives and sample characteristics.
Products are for research use only. Not for human use. We do not sell to patients.
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