Our Approach

We are a clinical stage company developing first-in-class small molecule therapeutics that treat the underlying pathologies of immuno-inflammatory diseases HIT and T1D as well as several programs in the discovery phase.

The Target


12-lipoxygenase (12-LOX) oxidizes fatty acid substrates, including arachidonic acid, leading to the production of the proinflammatory metabolite 12-HETE. 12-LOX overexpression and 12-HETE production have been linked to numerous syndromes and diseases, including Heparin-Induced Thrombocytopenia (HIT) and Type 1 Diabetes (T1D), creating the ideal target for small molecule inhibition. These diseases have inadequate treatments and high levels of unmet need. We aim to improve clinical outcomes for these patients with our first-in-class drug products.

Learn More

Heparin-Induced Thrombocytopenia (HIT)

HIT is a rare and life-threatening syndrome that occurs in up to 3% of patients receiving heparin. HIT arises from an aberrant immune response to heparin and leads to platelet activation and a vicious feed forward cycle of continued platelet activation, aggregation and blood clotting. These blood clots cause deadly heart attacks, pulmonary embolism, stroke and amputation. Current treatment options do not address the underlying cause of the disease and carry a significant risk of deadly side effects.

VLX-1005 will address the underlying platelet driven pathophysiology of HIT and shut down the pathologic activation of platelets without increasing bleeding. Inhibiting platelet 12-LOX reduces 12-HETE, a proinflammatory metabolite shown to play an important role in platelet activation. By addressing the underlying mechanistic basis of HIT, VLX-1005 addresses a serious unmet clinical need and should vastly improve clinical outcomes.

Type 1 Diabetes (T1D)

Type 1 Diabetes is caused by an abnormal immune response which results in damage and destruction to insulin-producing pancreatic β cells. Inflammatory signals increase the production of 12-LOX in β cells, leading to an overabundance of 12-HETE that ultimately stresses β cells, leading to a reduction in insulin production and cells more susceptible to immune attack.

We are developing a disease-modifying therapy for Type 1 Diabetes. Elevated 12-LOX levels have been observed in insulin producing β cells of auto-antibody positive, new-onset and T1D patients. By blocking 12-LOX activity in the pancreas and shutting down production of 12-HETE, β cells are protected from immune attack. Our approach holds promise to sustain β cells in these patients.