On April 12, 2017 Kancera reported that PFKFB3-inhibitor KAN0438757 increases the effect of a promising class of drugs for intractable cancer (Press release, Kancera, APR 12, 2017, View Source [SID1234518529]). Kancera has strengthened their development of drugs directed against PFKFB3 and DNA repair through a new recruitment. The European and US patent authorities have announced that a patent will be granted for the PFKFB- inhibitor KAN0438757 and analogues of this substance. Schedule your 30 min Free 1stOncology Demo! Kancera, together with the Thomas Helleday group at the Science for Life laboratory, have previously shown that Kancera’s PFKFB3 inhibitor increases the effect of DNA-damaging treatment such as chemotherapy and radiation by antagonizing cell repair functions. This treatment concept has grown strongly with the demonstration that PARP inhibitors, which act by this type of mechanism, have proven successful in the treatment of ovarian cancer, breast cancer and castration-resistant prostate cancer.
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PARP-inhibitors, such as Veliparib, are effective against cancers that are defective in their ability to repair DNA (recombination-defective), while cancer that retains this ability resists the same treatment.
Studies now show that cancer cells that are resistant to Veliparib become sensitive to treatment when Veliparib is combined with KAN0438757. This means that Kancera’s PFKFB3 inhibitor in combination with PARP inhibitors can combat more treatment-recalcitrant cancers than PARP inhibitors alone. The reason Kancera PFKFB3 inhibitors increase the effect of Veliparib is that they block cancer cells’ ability to repair DNA.
Since normal, healthy cells are neither recombination-defective nor do they depend on PFKFB3 for their DNA repair function, it is possible that such a combination could be well tolerated with few side effects.
Kancera AB (publ) has employed Nina Gustafsson PhD as expert in the biology of DNA repair. Nina will divide her time between Kancera and Thomas Helleday’s Laboratory at the Karolinska Institute, with main responsibility in the latter as project and team leader. Nina holds a PhD from the Karolinska Institute of Medical Sciences and has received numerous research grants for her work on cancer metabolism and its relationship to DNA repair.
"With the recruitment of Nina Gustafsson we strengthen both Kancera’s expertise in DNA repair and our successful collaboration with the Karolinska Institute on the PFKFB3 project," says Thomas Olin, CEO of Kancera.
Kancera has received advance notice from the patent authorities in the EU and the United States that claimed around PFKFB3 inhibitor KAN0438757 will be granted.
About the PFKFB3 project
The project aims to develop inhibitors of the enzyme PFKFB3 so as to strangle cancer cell energy metabolism and thus render them vulnerable to chemotherapy and radiotherapy. Kancera AB has, together with Professor Thomas Helleday and his research group at Karolinska Institutet, made a surprising discovery that shows how the company inhibitor of PFKFB3 enters the cancer cell’s nucleus and enhances the effects of a newly given dose of radiation.