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Jul 9, 2012

Genkyotex Raises $26M for Diabetic Nephropathy Drug

  • Swiss firm Genkyotex raised CHF25 million ($26 million) in an extension to its Series C financing round, primarily to support Phase II development of its dual NOX1 and NOX4 inhibitor GKT137831 for the treatment of diabetic nephropathy. Participants in the financing included Eclosion, Edmond de Rothschild Investment Partners, Vesalius Biocapital Partners, and MP Healthcare Venture.

    Genkyotex is focused on developing small molecule therapeutics that selectively inhibit NOX (NADPH oxidase) enzymes involved in controlling the oxidative stress cascade that leads to the generation of reactive oxygen species (ROS) that can cause tissue damage and modify biological pathways implicated in pathologies including metabolic, cardiovascular, pulmonary, and neurological diseases.

    Lead compound GKT137831 is a selective NOX1/4 inhibitor in Phase I clinical development initially for the treatment of diabetic nephropathy. The firm previously received funding from the Juvenile Diabetes Research Foundation to support its work in diabetic nephropathy. A Phase Ib study with GKT137831 is ongoing, and Phase II development could start by the end of 2012 pending positive Phase Ib data, the firm projects.

    NOX enzymes exist in seven isoforms, and a causal role for NOX enzymes in diabetic complications is well recognized, Genkyotex explains. NOX4 plays a key role in glomerular damage and kidney fibrosis, which lead to albuminuria and end-stage renal disease, respectively. NOX1 is also involved in angiogenesis, atherosclerosis, and other diabetic co-morbidities. This indicates that inhibiting both NOX1 and NOX4 could feasibly represent an effective therapeutic option for diabetic nephropathy, the firm states.

    Preclinical studies with GKT137831 in multiple in vivo models suggest that the candidate may in addition have applications in a broad range of indications, including other fibrotic diseases, including atherosclerosis, idiopathic pulmonary fibrosis, liver fibrosis, and angiogeneisis. 


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