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Core Technology

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    Mitochondrial Reforming
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    Mutimodal Mechanism
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    Low Toxicity
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    Targeted Therapy
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    Synthetic Lethality
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    Nano Fortmulation

Our research focuses on the development of multimodal therapies that restore mitochondrial function and normalize disrupted metabolic pathways in diseased cells.

These therapies are designed to target specific metabolic processes in various conditions—whether disrupting cancer metabolism to induce energy depletion and cell death, or addressing muscle loss in degenerative diseases like cachexia, muscular dystrophy, and sarcopenia. By tailoring treatments to specific cellular imbalances, we aim to provide new hope across multiple disease areas.

Mitochondria: the hub of metabolic regulation
Targeting dysfunctional mitochondria to restore cellular energy balance.

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  • Apoptosis
  • Muscle & Fat
  • Ferroptosis
  • Obesity
  • BRCAness
  • Sarcopenia

The mitochondria are at the centre of cellular metabolism, coordinating processes that dictate cell survival, energy production, and programmed cell death.

In disease states, including cancer and metabolic disorders, mitochondrial dysfunction leads to abnormal metabolic pathways. We design drugs to normalize these abnormal metabolic pathways, restoring balance and enabling to resume their central regulatory role

Apoptosis

Apoptosis, a controlled form of cell death, is essential for eliminating damaged or abnormal cells and maintaining tissue health. Dysregulation of apoptosis can lead to cancer (low apoptosis) or degenerative diseases (excessive apoptosis).

Mitochondria are central regulators of apoptosis. Key metabolic pathways, including glycolysis and the tricarboxylic acid (TCA) cycle, provide the bioenergetic and signalling molecules necessary for apoptotic processes.

Mitochondrial dysfunction, a hallmark of many cancers, disrupts apoptotic signalling by altering ATP production, membrane potential, and cytochrome c release. Additionally, reactive oxygen species (ROS), generated as byproducts of mitochondrial metabolism, act as critical signalling molecules that activate apoptotic cascades when produced in excess.

Targeting dysfunctional mitochondria can help restore proper apoptotic signalling. By selectively inducing mitochondrial-mediated apoptosis in cancer cells, treatments can effectively combat resistant tumours while preserving healthy cells. This precision-driven mechanism ensures both high efficacy and reduced systemic toxicity in cancer therapy.

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Muscle & Fat

Fat metabolism refers to the breakdown, storage, and utilization of lipids to generate energy or store nutrients, essential for maintaining metabolic homeostasis. Key components of fat metabolism include beta-oxidation, where fatty acids are broken down in the mitochondria to generate ATP, and lipid storage in adipose tissue for future energy needs. Beyond fat metabolism, skeletal muscle plays a crucial role in energy regulation, as it is a primary site for glucose and fatty acid utilization, significantly impacting metabolic health.

Disruptions in beta-oxidation, lipid storage, or muscle metabolism can lead to metabolic imbalance, contributing to obesity, insulin resistance, fatty liver disease, and cardiovascular issues. A decline in muscle mass further exacerbates metabolic dysfunction, as reduced muscle tissue lowers energy expenditure and weakens metabolic resilience, increasing the risk of weight regain and associated metabolic syndromes.

MetaFines’ therapies help restore metabolic balance by targeting both fat and muscle metabolism. Enhancing muscle metabolism not only promotes efficient fat utilization but also preserves lean muscle mass, supporting long-term metabolic stability. This approach strengthens overall metabolic resilience, reducing the risk of obesity-related complications and helping to prevent the yo-yo effect—frequent weight regain after dieting—by improving energy efficiency.

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Ferroptosis

Ferroptosis is an iron-dependent form of cell death caused by excessive lipid peroxidation driven by oxidative stress. It plays a dual role in health, acting as a defence mechanism against cancer while contributing to neurodegenerative diseases when dysregulated.

Ferroptosis is closely linked to disrupted lipid and glutathione metabolism, with mitochondrial dysfunction amplifying oxidative damage. Reactive oxygen species (ROS) are central to this process, as elevated ROS levels drive lipid peroxidation, resulting in membrane damage and cell death.

By restoring the balance in mitochondrial metabolism and antioxidant defences, we can selectively induce ferroptosis in cancer cells, while safeguarding normal tissues from oxidative damage.

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Obesity

Obesity is a metabolic disorder characterized by excessive fat accumulation, increasing the risk of developing type 2 diabetes, cardiovascular diseases, and cancer. Dysregulated fat metabolism, including impaired lipid oxidation and energy storage pathways, promotes chronic inflammation and systemic metabolic imbalance.

MetaFines’ therapies are designed to enhance skeletal muscle mass and optimize muscle metabolism restoring muscle health, improving metabolic stability, and preventing muscle loss during weight reduction. The increase of muscle mass plays a critical role in mitigating the yo-yo effect—frequent weight regain after dieting—by boosting energy expenditure and strengthening metabolic resilience.

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BRCAness

BRCAness refers to a cellular state that mimics the homologous recombination deficiencies typically found in BRCA-mutated cells, making them more vulnerable to DNA damage. Tumours exhibiting BRCAness, such as certain ovarian and breast cancers, rely on these deficiencies for survival, creating an opportunity for targeted therapies like PARP inhibitors.

By inducing a BRCAness state and leveraging synthetic lethality, we can enhance the effectiveness of DNA damage therapeutics, selectively targeting tumour cells with impaired DNA repair mechanisms

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Sarcopenia

Sarcopenia is a condition characterized by the progressive loss of skeletal muscle mass, strength, and function, typically associated with aging or chronic conditions. It leads to reduced mobility and an increased risk of falls and fractures.

Muscle atrophy in sarcopenia is driven by impaired muscle metabolism, including disruptions in the pathways of muscle protein synthesis and degradation, as well as mitochondrial dysfunction. These disturbances result in reduced energy production, increased oxidative stress, and an imbalance between anabolic and catabolic processes in the muscle.

By restoring mitochondrial function and reprogramming muscle metabolism, MetaFines’ therapeutic approach can enhance muscle protein synthesis and reduce protein degradation, effectively balancing metabolism and countering muscle wasting.

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