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    AMPK activator O304- a novel type 2 diabetes and obesity drug


    Séminaire de l'Institut Cochin

    Jeudi 16 mai 2019 - 12h00 - Salle de conférence Rosalind Franklin, 2ème étage


    Helena Edlund

    Umeå Centre for Molecular Medicine,
    Umeå University, Sweden


     invitée par Raphaël Scharfmann

    Institut Cochin, 22 rue Méchain, 75014 Paris



    Type 2 diabetes, associated cardiovascular disease, and obesity increase at an alarming rate globally. AMP-activated protein kinase (AMPK) activation represents an attractive pharmacological approach to treat these metabolic and cardiovascular disorders, but no direct AMPK activator is presently in clinical use. I will present data on the novel PANAMPK activator O304 that in vitro suppresses the dephosphorylation of p-T172 AMPKα, a key mechanism to increase AMPK activation. In mice fed high fat diet, O304 reduced insulin resistance, dysglycemia, β-cell amyloid formation and diabetes, as well as fatty liver development and obesity. O304 also improved left ventricular diastolic function and increased stroke volume without causing cardiac hypertrophy or glycogen accumulation, and in lean aged mice O304 enhanced peripheral blood flow and endurance capacity. In a proof-of-concept phase IIa clinical trial in type 2 diabetes patients on Metformin O304 reduced fasting plasma glucose levels and insulin resistance and also improved peripheral microvascular perfusion and reduced blood pressure. 


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