Genetic & Stress Induced Disease Modeling

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Genome Biologics offers predictive cardiotoxicity disease modeling and screening services using TrueCardium® human cardiac organoids to evaluate drug-induced cardiac injury and functional impairment. Our platform supports modeling of NCE-related toxicity, including anthracycline cardiotoxicity and kinase inhibitor liabilities, enabling early identification of adverse cardiac risk beyond conventional 2D assays or animal studies. These human-relevant models provide scalable endpoints for cardiac safety pharmacology, regulatory-aligned NAM workflows, and translational de-risking in drug development.

TrueCardium® enables advanced modeling of diabetic cardiomyopathy and HFpEF (heart failure with preserved ejection fraction) through metabolic and stress-induced perturbations that replicate human cardiometabolic dysfunction. These disease models capture lipid accumulation, oxidative stress, fibrosis, and impaired relaxation dynamics in a multicellular 3D cardiac organoid system. Genome Biologics provides these HFpEF platforms for therapeutic target validation, efficacy testing, and mechanistic studies in one of the highest unmet-need areas in cardiovascular medicine.

Genome Biologics develops human cardiac organoid models of inflammation-driven remodeling, enabling mechanistic investigation of immune-triggered cardiac dysfunction and fibrosis. TrueCardium® supports modeling of cytokine exposure, endotoxin stress (e.g., LPS), and clonal hematopoiesis–associated inflammation (CHIP), capturing structural and functional remodeling processes that contribute to heart failure progression. These platforms are ideal for evaluating anti-inflammatory cardiovascular therapies and identifying human-specific pathways missed in animal systems.

TrueCardium® ischemic injury models reproduce hypoxia-induced myocardial damage and post-infarction remodeling in a physiologically relevant human cardiac organoid environment. By mimicking oxygen deprivation, reperfusion stress, and tissue injury responses, these models enable evaluation of cardioprotective compounds, regenerative strategies, and mechanisms of infarct-associated heart failure. Genome Biologics provides ischemia-relevant screening and mechanistic packages for partners developing therapies targeting myocardial infarction and cardiac repair.

Genome Biologics offers specialized TrueCardium® disease models for mitochondrial cardiomyopathies and metabolic energy-deficiency disorders, capturing impaired oxidative phosphorylation, altered substrate utilization, and contractile dysfunction. These models are highly relevant for rare mitochondrial syndromes as well as broader cardiometabolic drug safety evaluation, including mitochondrial toxicity screening. Our platform supports mechanistic discovery and therapeutic validation in human cardiac systems where mitochondrial dysfunction is a primary driver of disease.

TrueCardium® enables modeling of rare and orphan cardiovascular diseases using patient-specific or genetically engineered iPSC-derived cardiac organoids. Genome Biologics supports custom development of rare cardiomyopathy and congenital disease models for precision drug discovery, target validation, and translational efficacy testing. These human-relevant platforms provide an essential foundation for therapeutic development in diseases where clinical cohorts are limited and animal models often fail to capture human pathophysiology.

Assess compound-induced cytotoxicity and cardiac cell injury in TrueCardium® human organoids to identify early cardiotoxicity liabilities. These assays provide robust viability and biomarker-based safety endpoints for preclinical drug screening.

Endpoints

Cell viability: CellTiter-Glo®, Alamar Blue

Cell death & membrane integrity: LDH release

Cardiac injury biomarkers: hs-Troponin T (hsTnT)

Secreted stress reporters (custom panels)

Measure beating strength, calcium handling, and functional impairment in human cardiac organoids to evaluate drug-induced contractile dysfunction, arrhythmia risk, and therapeutic efficacy.

Endpoints

Beating rate & force quantification

Calcium transient dynamics

Electromechanical coupling assays
Drug-response contractility profiling

Profile metabolic flux and mitochondrial health in TrueCardium® organoids to detect energetic liabilities, oxidative stress, and cardiometabolic drug effects - critical for predicting human-relevant mitochondrial cardiotoxicity.

Endpoints

Seahorse metabolic flux (OCR/ECAR)
Oxygen consumption & hypoxia response
Lactate production assays
Mitochondrial membrane potential (JC-1/JC-10)

Quantify cardiomyocyte and stromal proliferation in human cardiac organoids to support regeneration studies, hypertrophy programs, and evaluation of growth-modulating therapeutics.

Endpoints

DNA synthesis assays: EdU incorporation
Proliferation markers: Ki-67
Mitotic activity: Phospho-Histone H3
Cell-cycle progression reporters

Detect cellular senescence and aging-associated stress pathways in TrueCardium® disease models, supporting drug development for heart failure, fibrosis, and age-driven cardiometabolic disease.

Endpoints

Senescence-associated β-galactosidase (SA-β-gal)
p16INK4a activation reporters
Inflammatory SASP profiling (optional add-on)
 

Generate deep mechanistic insight from TrueCardium® screening studies through transcriptomics, proteomics, metabolomics, and spatial profiling - enabling biomarker discovery and regulatory-grade mechanism-of-action packages.

Endpoints

Bulk RNA-seq & single-cell RNA-seq
Spatial transcriptomics
Proteomics & phosphoproteomics
Metabolomics pathway mapping