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AnaBios - Heart Tissue Assays
EX VIVO Human Platforms for Cardiovascular Drug Discovery. Broadly defined, cardiovascular disease is the leading cause of death for men and women across most racial and ethnic groups in the United States with one person dying approximately every 34 seconds1. To drive successful clinical translation of new cardiovascular medicine, AnaBios develops relevant human ex vivo platforms for many cardiovascular diseases, including—but not limited to—heart failure with preserved ejection fraction (HFpEF), heart failure with reduced ejection fraction (HFrEF), atrial fibrillation and arrhythmogenic disorders. These platforms are designed to identify relevant targets, verify therapeutic approaches and ultimately enable successful clinical translation for new compounds and therapies.
AnaBios ex vivo models can be used across many stages of the drug discovery pipeline to build a strong program and enable clinical success.
- AnaBios’ human cardiac tissues provide tissue samples help to establish foundational information regarding a target’s omic footprint under healthy and diseased conditions.
- CardioPRIME® can be used to ensure target engagement and functional modulation at the cardiomyocyte level.
- Trabeculae and cardiomyocytes can be used to ensure anatomical specificity and safety.
- Disease tissue can be used to ensure therapeutic potential and efficacy.
Table 1 (see below) lists representative models and uses across cardiovascular diseases while Figure 1 provides examples of implementation
In Figure 1 above, cardiomyocytes from two different healthy donors demonstrate decreased sarcomeric shortening (negative inotropy) in response to application of the myosin activator Mavacamten.
In Figure 2 (above), investigational Drug X action and specificity were determined by comparing functional effects on healthy human ventricular and atrial trabeculae tissue. Both tissues showed dose dependent response to Drug X application. However, response in atria were larger and addition of isoproterenol, on top of Drug X, caused severe disruption of contractile force demonstrating a potential atrial safety signal under concomitant beta-adrenergic signaling.
In Figure 3 (above), trabeculae from heart failure (HFpEF) patients were used in a case study verifying how diseased human tissue can be used to verify potential therapeutic endpoints. In this example Omecamtiv, a myosin activator, was able to increase contraction amplitude while N106, a SERCA2a activator did not have an effect on contraction amplitude. The results suggest that myosin modulation may be a more clinically translatable pathway than sarcomeric Ca2+ modulation in treating HFpEF.