Drug Activation on Demand for Reducing Side Effects in Cancer Treatment

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Michael Rosholm Mortensen

Beløb

DKK 350,000

År

2019

Bevillingstype

Internationalisation Fellowships

Hvad?

The project aims at improving the treatments of cancer by reducing the side effects of the medication. Since the side effects of treatments generally are results of poor localization of the drug molecules to the site of treatment and the drugs being active during circulation, the focus will be on developing a strategy that addresses both of these issues. Therefore, the project deals with developing a novel targeted drug that will first be activated at the tumour site.

Hvorfor?

There are two main reasons for reducing the side effects in disease treatment. First, the patient will suffer less from the treatment. Second, since side effects often restrict the dosage of the drug due to toxicity, it might be possible to escalate the dosage, which could result in treatments that are more efficient. Furthermore, cancer treatment generally requires the injection of a highly potent drugs that will kill the cancer cells. However, even if masked as prodrugs, the high concentration of the potent molecules can result in activity at the injection site right after injection. For these reasons, an efficient treatment showing drug activation on demand at the site of disease is desirable.

Hvordan?

The proposed project is a targeted drug delivery approach that is aimed at activating the immune defence at the tumour site. It is different from common targeted drug delivery methods, since it addresses the issue of drugs being active during circulation. The project aims at delivering an inactivated cytokine - a protein that is inherent to our immune defence and capable of activating the immune cells - at the tumour site and activating it exclusively at the tumour site. The inactivated cytokine will be fused to a targeting protein such as an antibody for targeting of the tumour. The use of a second constituent will activate the cytokine allowing for pre-targeting of the tumour with the inactivated cytokine construct followed by activation when the construct has accumulated at the tumour.

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