LIFE bioCEEd

The project originates from the Medical University of Gdańsk (Poland), building on advanced translational research in neuroimmunology, lipid signaling, and central nervous system (CNS) biology.

The research was initiated to address a fundamental limitation in current multiple sclerosis therapies, namely, the inability to repair damaged myelin and restore neurological function despite effective immunomodulation.

The underlying scientific work leverages deep mechanistic understanding of the oxysterol–EBI2 signaling axis, supported by a combination of in vitro, ex vivo, and in vivo studies, as well as emerging human translational data demonstrating the pathway’s relevance in MS pathology.

This has enabled the identification and development of a novel, drug-like oxysterol analogue capable of modulating immune responses while simultaneously promoting CNS repair processes.

The project focuses on the development of a novel small-molecule therapeutic for the treatment of multiple sclerosis and related demyelinating diseases. The technology is designed to overcome the key limitation of current standard-of-care therapies, which primarily suppress inflammation but do not address myelin regeneration or long-term neurodegeneration.

The core innovation is a chemically optimized oxysterol analogue (CF₃-7α,25-OHC) that enables therapeutic targeting of the EBI2 receptor pathway with improved pharmacokinetic properties and CNS penetration.

Key differentiators include:

• First-in-class dual mechanism of action combining immunomodulation and remyelination
• Selective modulation of immune cell trafficking without broad immunosuppression
• Demonstrated promotion of myelin repair in preclinical models
• Improved pharmacokinetics enabling sustained CNS exposure
• Strong translational rationale supported by human tissue and BBB-model data

The intended purpose is to shift the treatment paradigm in multiple sclerosis from disease control toward functional restoration, enabling not only suppression of disease activity but also repair of existing neurological damage.

This approach has the potential to significantly improve long-term outcomes for patients, particularly in progressive forms of MS where current therapies remain insufficient.

Project originates from the Institute of Molecular Genetics of the Czech Academy of Sciences (Czech Republic), where long-standing research in molecular dermatology and rare genetic skin disorders led to the development of this technology. The project specifically targets Netherton syndrome, a severe orphan genodermatosis caused by mutations in the SPINK5 gene.

The research was initiated to address the fundamental shortcomings of existing therapeutic approaches, which largely provide symptomatic relief without correcting the underlying molecular defect. From its inception, the project has been developed with a strong translational focus, aiming to convert high-quality academic research into a clinically feasible, safe, and scalable therapeutic solution, suitable even for long-term and pediatric use.

The project focuses on a first-in-class topical gene therapy designed to locally restore key biological functions in the skin of patients with Netherton syndrome. In contrast to systemic gene therapies, this approach enables localized gene modulation directly at the site of disease, substantially reducing systemic exposure and associated safety risks.

Key differentiating features include:

• Topical, non-viral gene delivery with localized therapeutic action
• Targeted modulation of disease-driving molecular pathways
• Suitability for repeated and long-term administration
• Strong alignment with orphan-drug development and regulatory pathways

The intended purpose is to deliver a disease-modifying therapy that goes beyond symptomatic management, offering a novel and practical gene-based treatment option for patients with Netherton syndrome and potentially other severe inflammatory or genetic skin diseases.

Project originates from University Hospital Hradec Králové (Czech Republic), building on advanced clinical and translational research in hematology and oncological diagnostics.

The project was initiated in response to a clear clinical need for improved diagnostic tools in multiple myeloma, particularly methods that enable earlier detection and more practical disease monitoring.

The underlying research leverages deep clinical expertise and access to well-characterized patient cohorts, enabling the identification of disease-specific biological signatures detectable in peripheral blood and suitable for diagnostic use.

The project focuses on the development of a novel blood-based diagnostic method for the detection and monitoring of multiple myeloma. The technology is designed to improve sensitivity and practicality compared to current standards, which rely heavily on invasive procedures and often lack sufficient performance in early or low-burden disease.

Key differentiators include:

• Minimally invasive, blood-based diagnostic approach
• Enhanced sensitivity for early-stage and low-tumor-burden disease
• Potential use across diagnosis, treatment monitoring, and relapse detection
• Strong clinical relevance and scalability within hematological oncology

The intended purpose is to support earlier diagnosis, improved patient stratification, and more informed clinical decision-making, with the potential to meaningfully improve outcomes for patients with multiple myeloma.

The project originates from Jagiellonian University (Poland), one of Central Europe's leading research institutions, building on advanced translational research in regenerative medicine, extracellular vesicle (EV) biology, and fibrosis pathophysiology.

The research was initiated to address a fundamental limitation of current fibrosis therapies, namely, their inability to reverse established tissue scarring and restore organ function. Despite significant advances in anti-fibrotic treatment, existing therapies primarily slow disease progression while leaving the underlying fibrotic remodeling process largely unaddressed.

The underlying scientific work focuses on the role of extracellular vesicles as natural biological carriers capable of modulating cellular behaviour and tissue regeneration. Through a series of in vitro and in vivo studies, the research team demonstrated that hypoxia-conditioned extracellular vesicles exhibit enhanced anti-fibrotic and regenerative properties compared to conventionally produced vesicles.

This has enabled the identification and development of a novel extracellular vesicle-based therapeutic platform capable of targeting the molecular mechanisms responsible for fibrosis progression, while simultaneously promoting tissue repair and regeneration.

The project focuses on the development of a novel biological therapy for the treatment of fibrosis and related fibrotic diseases. The technology is designed to overcome the key limitation of current standard-of-care therapies, which primarily slow disease progression but are unable to reverse established tissue damage or restore organ function.

The core innovation is a hypoxia-engineered extracellular vesicle platform derived from human induced pluripotent stem cells (hiPSCs). The technology utilizes a proprietary low-oxygen manufacturing process that enriches vesicle cargo with biologically active microRNAs, including miR-302b-3p, enabling targeted modulation of the TGF-β/SMAD2 signalling pathway, a central driver of fibrosis development across multiple organs.

• First-in-class disease-modifying approach targeting fibrosis at its molecular core
• Direct modulation of the TGF-β/SMAD2 pathway through miRNA-mediated gene regulation
• Demonstrated reversal of fibrotic markers and fibroblast activation in preclinical studies
• Hypoxia-engineered manufacturing process enabling enhanced biological potency and scalable production
• Platform applicability across multiple fibrotic indications, including pulmonary, hepatic, and cardiac fibrosis
• Strong translational rationale supported by both human fibroblast and animal model data

The intended purpose is to shift the treatment paradigm in fibrosis from symptomatic disease management toward regenerative restoration by actively reprogramming pathological tissue remodeling processes and promoting recovery of normal organ function.

This approach has the potential to significantly improve long-term outcomes for patients suffering from progressive fibrotic diseases, where current therapeutic options remain unable to reverse established tissue damage or prevent eventual organ failure.

The project focuses on the development of a novel AI-powered respiratory diagnostic platform for the rapid diagnosis and monitoring of asthma at the point of care. The technology is designed to overcome the key limitations of current standard-of-care diagnostic methods, which are often dependent on effort-intensive spirometry testing, require specialized infrastructure, and provide limited predictive value regarding disease progression or exacerbation risk.

The intended purpose is to enable rapid, objective, and accessible asthma diagnosis across both primary and specialist care settings, while expanding access to reliable respiratory testing for patient populations that are often underserved by existing diagnostic approaches, including children, elderly patients, and individuals with severe respiratory impairment.

The technology has the potential to significantly improve diagnostic accuracy, reduce misdiagnosis rates, and support earlier clinical intervention, ultimately improving patient outcomes while reducing healthcare system burden associated with uncontrolled asthma.

The core innovation is Exhale-Dx™, a handheld diagnostic device that combines advanced breath-analysis sensors with the proprietary ADENA (Adaptive Deep Neural Architecture) artificial intelligence platform. During a single relaxed exhalation, the system captures a multimodal breath signature consisting of thirteen physiological and biochemical parameters, including volatile organic compounds, carbon dioxide waveform characteristics, respiratory flow dynamics, temperature, and humidity.

• AI-powered analysis of multimodal breath signatures rather than reliance on single biomarkers
• Diagnosis performed using normal tidal breathing without forced respiratory manoeuvres
• Point-of-care results delivered in under 60 seconds
• Capability to assess disease control status and predict exacerbation risk
• Fully on-device AI processing without the need for cloud connectivity
• Broad applicability across paediatric, adult, and elderly patient populations

• 93% diagnostic accuracy in distinguishing asthmatic from non-asthmatic patients
• Detection of physiological changes associated with asthma exacerbations up to 72 hours before clinical presentation
• 100% sampling success rate across patients aged 6–85 years
• Successful validation in both adult and paediatric patient populations

The platform represents a potential paradigm shift in respiratory diagnostics by moving from reactive symptom-based assessment toward rapid, objective, and predictive disease management.