The BioMAP® Diversity PLUS® Panel was built out of a need for biologically relevant in vitro models of human disease, and is used by leaders in the pharmaceutical, nutraceutical, and cosmetics industries to better understand their candidate—molecules, from discovery to preclinical safety. BioMAP Diversity PLUS systems are comprised of human primary cell-based assays stimulated to recapitulate disease states and to model complex tissue and disease biology of organs (vasculature, immune system, skin, lung) and general tissue biology. Phenotypic profiling with BioMAP Diversity PLUS evaluates the biological impact of test agents in conditions that preserve crosstalk and feedback mechanisms relevant to in vivo outcomes. Use BioMAP Diversity PLUS to inform on potency, selectivity, safety, mechanism of action, and disease indication of a test agent for actionable insights that help progress the right molecules to the clinic.
What is BioMAP Diversity PLUS?
- 12 individual BioMAP human primary cell-based co-culture systems which predictively model drug effects on multiple tissues and disease states
- 148 clinically relevant biomarker readouts determined by careful curation of clinical data
- Data from 4,500+ reference compounds which underpin powerful and predictive analytics
- Results as data files and as visualized profiles
What can BioMAP Diversity PLUS do for you?
- Prioritize candidates based upon on- and off-target effects, cell potency, and mechanism-of-action
- Predict safety and toxicity prior to initiating in vivo testing or clinical trials
- Perform competitive benchmarking to thousands of clinical compounds
- Identify new indications for drug repurposing and repositioning
Impact of Aspirin on Disease Models of BioMAP Diversity PLUS
Aspirin modulates key immune, inflammatory, matrix-remodeling and hemostasis-related biomarkers in human primary cell-based models of various stimulated tissue conditions including vascular inflammation and immune response models.
Aspirin was profiled at four concentrations (1000 µM, red; 330 µM, orange; 100 µM, yellow; and 37 µM, green) in the BioMAP® Diversity PLUS® Panel and concentrations were selected based on clinical Cmax values. The range of historical vehicle control data is represented by the gray region closest to the axis. Annotated peaks represent biomarker activities demonstrating statistically significant changes during compound treatment relative to historical vehicle controls.
Aspirin, also known as acetylsalicylic acid (ASA), is a nonsteroidal anti-inflammatory drug (NSAID) that is used to reduce pain, fever, and inflammation, and as an antithrombotic drug at reduced doses. Aspirin is active with 14 annotated biomarker readouts and is not cytotoxic at the concentrations tested in this study. Aspirin is antiproliferative (gray arrows) to activated human primary T cells (SAg), coronary artery smooth muscle cells and endothelial cells in models of chronic inflammation (CASM3C, 3C), and dermal fibroblasts in a model of inflamed wound healing (HDF3CGF).
Aspirin impacts inflammation-related activities (decreased Eotaxin 3, VCAM-1, MCP-1, IP-10, sPGE2), immunomodulatory activities (decreased CD40, secreted IgG, HLA-DR), tissue remodeling activities (decreased collagen III, uPAR; increased MMP-1), and hemostasis-related activities (increased thrombomodulin (TM)).
The decrease in PGE2 (prostaglandin E2) levels seen in a model of TH1 type chronic inflammation and monocyte activation is a sentinel biomarker of COX inhibitors such as aspirin, ibuprofen, diclofenac and others. The opposite effect, increased levels of PGE2 in the same context, is a key biomarker present in a BioMAP toxicity signature that correlates with skin irritation due to sustained production of prostaglandins leading to vascular permeability.
