Aneurysmal Subarachnoid Hemorrhage is caused by an artery rupture in the brain leading to bleeding in the subarachnoid space in the brain. Affects patients in their 40–60s, with amongst the highest morbidity and mortality rates associated with cerebrovascular disease. Nimodipine a calcium channel blocker, approved in 1986 with questionable clinical effectiveness.
ALOX15 is a second generation inhibitor of ALOX15, stops the progression of the disease with improved outcomes and significantly reduced infarct size in rodent models. We are also progressing a biomarker driven Phase I/II clinical trial powered by a 50% increase in the MTD of LX15002 and improvements of outcomes in SAH patients.
Ischemic stroke occurs when a blood vessel in the brain is blocked, and the brain does not get the amount of blood needed to function. It is the second leading cause of death globally and the leading cause of morbidity.
ALOX15 plays a driving role in key mechanisms of ischemic stroke: brain edema, oxidative stress, blood–brain barrier disruption, and neuronal cell death. ALOX15 inhibitors have shown robust efficacy in multiple rodent ischemic stroke models and represent a promising target. We have advanced most of the IND enabling studies and planning for a biomarker driven, all powered Phase I trial.
Chemotherapy with FOLFIRINOX (5FU, Leucovorin, 5-fluorouracil, irinotecan, and oxaliplatin) is the standard of care (SoC) for PDAC. Despite this aggressive approach FFRX metastases rates remain high, the median survival of PDAC patients is less than 11 months. Over-expression of ALOX12 correlates with metastatic potential of ALOX12 cancers and the incidence of recurrence and metastasis in PDAC patients. We have shown that stromal ALOX12 inhibition is a promising target effect, preventing PDAC progression and therapy resistance.
Our ALOX12 inhibitor is in late stage IND enabling studies, with a progressing of the clinical trial in metastatic models.
Diabetes mellitus is a prevalent illness and its trajectory continues to rise worldwide, with Type 1 diabetes (T1D) accounting for 5–10% of all diabetes cases. T1D develops on the basis of autoimmune and inflammatory destruction of pancreatic beta islet cells, with the progressive reduction of insulin.
ALOX12 is a major contributor to beta cell inflammation and damage associated with T1D. We have developed a selective ALOX12 inhibitor that suppresses inflammatory cell activation, limits beta cell destruction, and preserves beta islet function. In murine models of T1D, treatment with our ALOX12 inhibitor reduces hyperglycemia, preserves beta cell mass, and prevents progression of disease.
