PROCIZUMAB – a first-class drug candidate

Procizumab has an innovative mode of action relevant in acute diseases that are associated with massive cell death and uncontrolled release of intracellular DPP3 into the bloodstream. Translocated DPP3 remains active in the circulation where it cleaves bioactive peptides in an uncontrolled manner. Procizumab is able to block circulating DPP3, inhibiting bioactive peptide degradation in the bloodstream. This blockade results in stabilization of cardiovascular and renal function and reduction of short-term mortality.

Preclinical studies of Procizumab in animal models of cardiovascular failure showed impressive and instant efficacy. As an example, injection of PROCIZUMAB in rats with shock-induced cardiovascular failure led to an instant normalization of shortening fraction (see videos below).

Echocardiogram of rat heart with cardiovascular failure before PROCIZUMAB treatment

Echocardiogram of rat heart with cardiovascular failure after PROCIZUMAB treatment

PROCIZUMAB is a humanized monoclonal IgG1 antibody specifically binding circulating DPP3. It will be a first-in-class drug that targets and modulates DPP3 activity, an essential regulator of cardiovascular function.

  • High Preclinical Efficacy: In several preclinical cardiovascular failure models, PROCIZUMAB has shown to improve all clinically relevant endpoints in vivo. It normalizes ejection fraction and kidney function and reduces mortality.
  • GMP material development ongoing: A generic Good Manufacturing Practice (GMP) process is under development.

Acute Heart Failure

Acute Heart Failure

Acute heart failure (AHF) is a relevant public health problem causing the majority of unplanned hospital admissions in patients 65 years of age and above. Despite major achievements in the treatment of chronic heart failure over the last decades, which led to improvement in long-term survival, outcomes of AHF remain poor with 90-day re-hospitalization and 1-year mortality rates reaching up to 30%. Persistence of poor outcomes in AHF might be related to the paucity of improvements in the acute management of those patients. Despite lacking evidence of beneficial effects on outcome, critical treatment of AHF still mainly consists of non-invasive ventilation in case of pulmonary edema, intravenous diuretics and/or vasodilators. In addition, AHF is not a specific disease but the shared clinical presentation of different, heterogeneous cardiac abnormalities. Therefore, there is an unmet need for increased individualization of AHF treatment according to the predominant underlying pathophysiological mechanisms to improve patient outcome [1].

[1] Arrigo et al. (2016) Understanding acute heart failure: pathophysiology and diagnosis. European Heart Journal Supplements