CRP is a molecule that is formed as an acute phase protein as a result of inflammatory events and infections and is involved in the disposal of dead but also vital cells as well as infection prevention. This causes, among other things, that wounds are kept open, so that immune cells have the time to reach the wound to fight invading pathogens. This makes sense as long as the wound is on the skin, as pathogens can penetrate here. In the case of organ damage, such as a heart attack or stroke, CRP leads to an increase in primary damage.

Over the last two decades, the survival rate after acute heart attack has improved significantly. However, the prognosis of the patient after the infarction has only moderately improved, i.e. the occurrence of follow-up infarctions and, above all, the development of unstable angina pectoris or heart insufficiency still poses a considerable risk and causes high follow-up costs.

This is where the therapy starts with CRP reduction. PentraSorb® CRP binds CRP from the patient’s plasma with the help of a fully synthetic ligand, thus reducing the damage after infarction and thus also the pathological reconstruction processes at the heart.

CRP also seems to have a pathological influence in stroke and rheumatism, so the PentraSorb® CRP is also designed for the treatment of stroke and rheumatism.

The mode of action of the PentraSorb® CRP is shown schematically in the following diagram:

Schematic representation of the mode of action of the PentraSorb® CRP


Specific adsorbers for CRP reduction are a novelty. CRP-reduction drugs are not currently available on the market.