Science

Acute kidney injury

The big challenge

If acute renal failure supervenes in a critically ill patient, it immediately means a considerable worsening of the prognosis and can be fatal in itself if the consequences are not treated. This is why a specific treatment that can stop kidney-damage early in the process has been in such demand for many decades now.

Unfortunately it has so far proved impossible to find a specific treatment for AKI. One of the reasons is that the treatment must be given as soon as possible after the harmful process has started and before the cell damage has become permanent. This has not been possible while the diagnosis was dependent on slowly responding functional markers of kidney failure.

It has not been possible to develop effective specific treatments because early diagnosis has not been possible without using markers. This vicious circle will be broken as soon as there is a reasonably effective specific treatment for kidney damage, which will support the market for diagnostics of this condition by means of the fast-responding markers. AKI Therapeutic’s drug development aim is to create such a treatment.

Rationale for treatment of AKI

The rationale for a treatment is obviously that one wants to stop or counteract the kidney-damaging process as early as possible. This will be shown by the AKI markers stopping to rise and starting to fall, while adequate kidney function is maintained throughout the process so that dialysis is unnecessary and any long-term side effects are avoided or diminished. If the developed drug has a favorable toxicity profile, it will also be used prophylactically in patients who are considered to be at particular risk of kidney damage.

AKI Therapeutics

Our treatment

AKI Therapeutics has combined known technologies for innovative use in the development of a drug (AKI-051) that will constitute an effective specific treatment of the cell-damaging processes underlying the early stage of acute renal failure, thereby slowing the pathology of its onset. The essential part of the technology is that the active substances are given in the form of conjugates with a carrier molecule that targets them specifically to the kidney’s tubular epithelial cells, which are damaged in acute kidney injury, and at the same time away from the immunocompetent cells of the body’s defense system against infections, the function of which must not be impaired by these substances.

In preparatory studies, a number of active substances have been identified that protect against ischemic cell and organ damage, which must be bound to the targeting carrier molecule in order to increase their effect on the tubular cells. For this purpose, the optimal targeting molecule has been identified and will be used in our treatment (AKI-051), a protein which is secreted and taken up by the kidney even in the early stages of acute renal failure.

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