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Dipeptidyl Peptidase 3 (DPP3)
A biomarker for cardiac depression

DPP3, a biomarker for cardiac depression

Recently, a so far unknown disease mechanism leading to short-term organ failure was identified. According to new findings, the release of the cardiac depressant factor Dipeptidyl Peptidase 3 (DPP3*) into the bloodstream plays a major role in a sudden loss of heart function (1,2).  DPP3 is an endogenous enzyme that plays a vital role in the cleavage of cellular peptides. When massive, uncontrolled cell death occurs, for example, in major surgeries (3), cardiogenic shock (1,4), sepsis (5), or burns (6), DPP3 is released into the bloodstream, having a toxic-like effect in the human body. This is because in the bloodstream, DPP3 inactivates peptide hormones such as angiotensin II, which is important for the heart function. This inactivation is leading to cardiac depression and consequently hemodynamic instability, which paves the way for organ dysfunction.

The biomarker DPP3 is convincing in clinical research:

Blood-based biomarker

DPP3 can simply be measured in whole-blood and plasma.

New disease mechanism

Quantifying DPP3 levels in the bloodstream unravels one cause of septic shock (7).

Monitoring tool

Monitoring DPP3 aids in the verification of treatment success (4,5).

Prediction tool

High DPP3 levels predict hemodynamic instability and need of cardiovascular support (4,5).

Risk stratification

DPP3 aids in the stratification of patients at high risk to develop organ dysfunction (3,5,8).

Research findings:

High or rising DPP3 blood levels [1a] indicate worsening of the patient’s status that can lead to short-term organ failure and death. On the other hand, decreasing DPP3 levels [1b] indicate a substantially reduced mortality risk (1).

Healthy state

In healthy state, DPP3 is located intracellularly [1a] and active angiotensin II [1b] contributes to maintaining a normal heart function [1c]. 

Disease state

In a disease state, uncontrolled cell death leads to the release of DPP3 [2a]. Angiotensin II is cleaved by DPP3 [2b], which leads to hemodynamic instability and cardiac depression [2c].


Sphingotest® penKid®, sphingotest® bio-ADM®, sphingotest® DPP3 are offered for in vitro diagnostics. “penKid”, “bio-ADM” and “DPP3” represent the analytes Proenkephalin A 119-159, bioactive Adrenomedullin 1-52, and Dipeptidyl Peptidase 3, respectively.

Reference Literature

(1) Deniau et al. (2019), Circulating dipeptidyl peptidase 3 is a myocardial depressant factor - dipeptidyl peptidase 3 inhibition rapidly and sustainably improves haemodynamics, Eur J Heart Fail.
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(2) Magliocca et al. (2019), Dipeptidyl peptidase 3, a biomarker in cardiogenic shock and hopefully much more, Eur J Heart Fail.
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(3) Gombert et al (2020), In-hospital mortality and organ failure after open and endovascular thoraco-abdominal aortic surgery can be predicted by increased levels of circulating dipeptidyl peptidase 3, Eur J Cardiothorac Surg.
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(4) Takagi et al. (2019), Circulating dipeptidyl-peptidase 3 and alteration in hemodynamics in cardiogenic shock: Results from the OptimaCC Trial, Eur J Heart Fail.
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(5) Blet et al. (2021), Monitoring circulating dipeptidyl peptidase 3 (DPP3) predicts improvement of organ failure and survival in sepsis: a prospective observational multinational study. Crit Care.
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(6) Dépret et al. (2020), Circulating dipeptidyl peptidase-3 at admission is associated with circulatory failure, acute kidney injury and death in severely ill burn patients, Crit. Care.
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(7) van Lier et al. (2021), Promotion of vascular integrity in sepsis through modulation of bioactive adrenomedullin and dipeptidyl peptidase 3. J Intern Med.
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(8) Frigyesi et al. (2021), Circulating dipeptidyl peptidase 3 on intensive care unit admission is a predictor of organ dysfunction and mortality. J Intensive Care.
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