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The development of Procizumab in shock management represents a significant milestone in treating refractory circulatory failure. Dipeptidyl peptidase 3 (DPP3) is primarily an intracellular protein involved in antioxidant responses. However, acute tissue damage causes the release of this protein into the bloodstream. This circulating form (cDPP3) acts as a cardiac depression factor. Consequently, it degrades angiotensin II, which is essential for maintaining vascular tone. This enzymatic process leads to rapid hemodynamic collapse and multi-organ dysfunction.
Researchers developed Procizumab (invobenitug) to neutralize this pathological driver. Specifically, it is a humanized IgG1 kappa monoclonal antibody that binds human cDPP3 with high affinity. The initial murine variant was generated by immunizing mice with a DPP3-derived peptide. Subsequently, the antibody was humanized through complementarity-determining region (CDR) grafting. Furthermore, the final recombinant antibody is produced in Chinese hamster ovary cells. Importantly, it lacks Fc-mediated effector functions, which minimizes the risk of unwanted immune responses like cell-mediated toxicity.
Non-clinical studies have validated the efficacy of this approach. In cardiac dysfunction models, the antibody successfully inhibited cDPP3 activity and improved hemodynamic parameters. Additionally, pharmacokinetic analyses in rats showed a favorable tissue distribution. Currently, researchers are evaluating the antibody in the PROCARD clinical trial series. This first-in-class therapy aims to move beyond supportive care by addressing the biological root of shock. Therefore, it could significantly reduce the high mortality rates associated with cardiogenic and septic shock.
Procizumab neutralizes circulating DPP3 (cDPP3) to prevent the degradation of angiotensin II. This action helps restore RAAS balance and stabilizes cardiovascular function during acute shock.
When cDPP3 enters the circulation due to cell death, it destroys peptides that regulate heart and kidney function. High levels of this enzyme are strong predictors of short-term mortality and organ failure.
Studies confirmed that Procizumab lacks Fc-mediated immune effector functions, such as phagocytosis or complement-dependent toxicity. This ensures the antibody neutralizes the target without causing broader immune-mediated damage.
Disclaimer: This content is for informational and educational purposes only and does not constitute medical advice. Always seek the advice of a qualified healthcare provider for any medical condition. Refer to the latest local and national guidelines for clinical practice.
References
Genest M et al. Development and non-clinical characterization of Procizumab (invobenitug): a humanized antibody neutralizing circulating DPP3. MAbs. 2026 Dec undefined. doi: 10.1080/19420862.2026.2675077. PMID: 42165222.
Deniau B, Blet A, Santos K, et al. Inhibition of circulating dipeptidyl-peptidase 3 by procizumab in experimental septic shock reduces catecholamine exposure and myocardial injury. PMC. 2024.
4TEEN4 Pharmaceuticals. 4TEEN4 begins trial of antibody therapy for cardiogenic shock. PharmaTimes. 2025.
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Procizumab is a humanized antibody that neutralizes circulating DPP3, a biological driver of shock, by preventing angiotensin II degradation....
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