Building human tissue for cardiac health

We’re taking on cardiovascular disease, the world’s biggest killer – one cell at a time. By building human cardiac tissues that mimic the function of the heart, we’re creating new treatment possibilities and fast-forwarding drug development.

Heart disease and cardiotoxicity –
a growing health crisis

Cardiovascular disease (CVD) is a class of diseases that affect the heart or blood vessels and include coronary heart disease, cerebrovascular disease, rheumatic heart disease, and other conditions. Today, CVDs are responsible for close to 20 million deaths annually, representing one-third of the total number of deaths globally.1

More than four out of five deaths from CVDs are due to heart attacks. Many patients suffering from heart attacks face poor health outcomes due to a lack of adequate long-term treatment for the tissue damage caused by the infarction.2-3

In parallel with the increasing prevalence of cardiovascular disease, cardiotoxicity is becoming a growing health concern. Cardiotoxicity is electrical or muscular damage to the heart caused by, for example, adverse reactions to drugs. Moreover, cardiotoxic effects are a common reason for late-stage drug development failures, leading to increased healthcare costs.4

Since cases of cardiotoxicity are particularly common among patients with existing heart conditions, drug safety and the ability to identify harmful components is now more important than ever. Moreover, despite the prevalence of heart disease, cardiovascular drugs constitute only 5 percent of newly approved drugs, largely due to the lack of appropriate translational models.4

33%

of all deaths are due to CVD1

4/5

deaths from CVDs are due to heart attacks1

Paving the way for safer drugs and better treatment

Fluicell’s goal is to prevent death and improve the quality of life for people living with cardiovascular disease. By creating human tissue-based solutions for regenerative medicine and drug development, we are paving the way for safer drugs, new treatment opportunities, and increased pharmaceutical development efficiency. At Fluicell, we are committed to taking on the world’s biggest killer, one cell at a time.

Unlocking the future of cardiac therapy

“To pave the way for new and improved cardiovascular treatments, there is a need to better understand cardiac cell behavior and functionality. Safer and more effective therapies are crucial for improving patient health and well-being.

By utilizing technologies and models designed to capture more physiological human responses to compounds and treatments, and employing tissue-based solutions with single-cell precision, we can unlock the future of cardiac therapy.”

Dr. Michiel Helmes

Dr. Helmes is an expert in cardiac biology, currently serving as an Associate Researcher at Amsterdam University Medical Center, Director at IonOptix, and CSO at Cytocypher. Cytocypher is a partner with Fluicell in the project INTEC, which aims to create new high-precision platforms for cardiac cell analysis.

18.6 million
deaths each year from CVD1
4x
Relative cost of drug development failure compared to direct development costs5
30%
of drug development failures are due to toxicity4

Pushing the boundaries of regenerative medicine and drug development

Fluicell’s unique technology holds the key to developing next-generation tissue-based solutions for heart health. With single-cell precision, our Nexocyte platform makes it possible to create tissues that mimic human histology and have a strong functional resemblance to native heart tissue. Because they account for cell-type diversity, ECM composition, cell-cell interactions, and microenvironment geometry, our tissues provide significant functional benefits for advanced cardiac drug screening applications or for development of tissue-based cardiac therapeutics.

To enable new ways to study cardiac biology and functionality, we combine our tissue-based solutions with our unique single-cell technology to create new research platforms with the goal of improving drug development quality and efficiency.

Together with our partners and collaborators, we continue to make discoveries that change how we treat cardiac disease.

Through in-house development and our different partnerships, we are currently researching the following areas:

  • Cardiac safety pharmacology models
  • Single-cell cardiac screening platform
  • Microelectrode array cardiac assay technology
  • Tissue-based cardiac repair

Tissue-based models for cardiac safety pharmacology

There is a large gap in cardiac safety screening between simplistic cell culture and animal models. Fluicell is building human cardiac tissues that emulate native organ function with the goal of creating screening solutions that increase translational predictability and decrease clinical failure rates. Our models have the ability to replicate complex microenvironment and interplay between cell types found in native cardiac tissue. Thereby we can establish an accurate representation of cardiac biology featuring realistic response to tissue damage or toxic exposure.

tissue-based-models-for-cardiac-safety-pharmacology

High-precision cardiac screening platforms (INTEC)

INTEC is a Eurostars-funded collaboration between Fluicell and Cytocypher, aimed at creating an integrated system that advances the understanding cardiac cell behavior and functionality, allowing for precise evaluations of cardiac therapies early in the discovery process. Our approach involves merging the BioZone microfluidic flow probe from Fluicell with the MultiCell system from CytoCypher/IonOptix, further enhanced with single-cell analysis capabilities, AI algorithms, and proteomics/genomics analysis tools. This integration addresses the urgent demand for improved human models and research tools in CVD drug development.

intec

Microelectrode technology assays

Microelectrode arrays (MEA) are an important technology for measuring activity in heart and nerve cells and are widely used for studying drug efficacy and safety. MEA assays are commonly employed by many pharmaceutical companies in cardiac safety screening to evaluate whether a drug compound causes heart arrhythmia, a common source of cardiac toxicity. At Fluicell, we have designed our Nexocyte platform to be fully compatible with MEA assay technology. The combined power of Fluicell’s cardiac tissue models and the analytic precision offered by MEA assays enables us to gain a deeper understanding of heart tissue function, paving the way for new therapies.

microelectrode-technology-assays

Tissue therapeutics for cardiac repair

Despite the advances in treating myocardial infarction, the mortality rate within five years for heart attack patients is as high as 50 percent. A major factor behind this is the permanent damage to the cardiac tissue caused by the infarction. Finding a way to repair damaged tissue is therefore an important way to significantly improve the health and long-term survivability of heart attack patients. At Fluicell, we have the ability to construct human heart tissues on transplantable material, with potential use as a tissue patch for cardiac repair. Our high-precision tissue engineering technology allows us to tailor the cellular composition to optimize tissue and patch functionality.

tissue-therapeutics-for-cardiac-repair

application examples

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References

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  1. World Health Organisation. Cardiovascular diseases (CVDs). WHO factsheets. Accessed September 25, 2024. https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)
  2. Nadlacki B, et al.Long term survival after acute myocardial infarction in Australiaand New Zealand, 2009-2015: a population cohort study. Med J. Aust. 2021; 214(11):519–25.
  3. Taylor CJ, et al. Trends in survival after a diagnosis of heart failure inthe United Kingdom 2000-2017: population based cohort study. BMJ. 2019;364:l223.
  4. Sun et al. Why 90% of clinical drug development fails and how to improve it? Acta Pharm. Sin. B, 2022.
  5. Sertkaya A, et al. Costs of Drug Development and Research and Development Intensity in the US, 2000-2018. JAMA Netw. Open. 2024; 7(6):e2415445.

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