About Us
Kleis Therapeutics is developing first-in-class oral therapies that prevent fibrosis; a fundamental biological process driving many chronic, life-limiting diseases.
Fibrotic diseases affect millions worldwide and account for around 40% of deaths in the world. Fibrosis occurs when Transglutaminase 2 (TG2) proteins accumulate in tissues. TG2 is unusually resistant to natural degradation, meaning it builds up over time. This build-up disrupts normal tissue repair, triggers excessive scarring, and ultimately compromises organ function.
This mechanism underpins a wide range of high-burden conditions, including:
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Fibrostenosing Crohn’s Disease
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Cardiac fibrosis
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Chronic Kidney Disease
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Idiopathic Pulmonary Fibrosis
These diseases share a common problem; current treatments do not stop fibrosis. They manage inflammation or symptoms, but they cannot prevent the progressive scarring that leads to surgery, organ failure, and escalating healthcare costs.
Kleis’ approach directly targets the root cause - TG2-driven fibrosis, offering the potential for the first disease-modifying oral therapy across multiple major markets.
Fibrosis
Fibrosis is driven by a complex cascade of biological signals
But one key enzyme, Transglutaminase 2, plays a central role in generating fibrosis that leads to damaged organs.
By inhibiting TG2, our approach aims to:
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Interrupt the scarring/fibrotic process
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Prevent progression to irreversible fibrosis
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Allow remodelling of the fibrosis leading to restoration tissue function
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Offer a safe, oral, scalable treatment option
Technology
Kleis Therapeutics is developing highly selective small-molecule inhibitors that block the pathological activity of TG2; a key driver of fibrosis across multiple organs.
TG2 is a multi-functional protein involved in essential cellular processes such as adhesion, proliferation and signalling.
Under disease conditions, TG2 increases and and begins crosslinking proteins in the extracellular matrix, creating the rigid, irreversible scar tissue that underpins fibrosis.
Our inhibitors are engineered to:
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Bind precisely to the active site of TG2
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Switch off pathological crosslinking, while
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Preserve TG2’s normal physiological functions
This selective mechanism positions Kleis to deliver first-in-class, disease-modifying therapies that target fibrosis at its source not just the inflammation around it.