The research results show that the company’s Fractalkine blockers have the potential to disrupt cancer cells’ resistance to chemotherapy and thereby significantly improve the treatment of advanced cancer such as ovarian cancer.
Kancera is now planning for clinical preparatory studies with the aim of defining an optimal dosing strategy for the Fractalkine blocker KAND567, the company states in a press release. Positive results would enable the start of a clinical study in cancer patients in 2022.
“The greatest obstacle to the effective treatment of many cancers is the increasing resistance of the cancer to chemotherapy as the disease progresses. Pioneering preclinical results are published today that show that Kancera’s Fractalkine blockers can render resistant cancer cells sensitive to chemotherapy again. This opens up attractive opportunities for the company in another therapy area, in addition to myocardial infarction and COVID-19. Since KAND567 is already in clinical development, the prerequisites are good to be able to start a first study in cancer patients already in 2022 ,” says Thomas Olin, CEO of Kancera.
The new preclinical research results show that KAND567 reverts previously treatment-resistant cancer cells to a state sensitive to today’s standard treatment as soon as after 72 hours of treatment, describes the company. Specific blockade of the Fractalkine receptor with KAND567 leads to inhibition of the cell’s DNA repair system, which increases the damage to the cancer cell and more cancer cells die. KAND567 has been shown to be effective even if the cancer cell carries gene variants that normally impede effective treatment (wild-type BRCA and mutated p53), the company reports.
Collaboration with Karolinska Institutet and SciLifeLab
These findings have been generated in a research collaboration with Nina Gustafsson’s research group at Karolinska Institutet and SciLifeLab, where Kancera’s doctoral students participated within the framework of the EU project SYNTRAIN.
The treatment concept
KAND567 affects the same type of DNA repair mechanism that is blocked in the genetically determined blood disease Fanconi Anemia. In Fanconi patients, DNA-damaging cancer drugs such as cisplatin, carboplatin and mitomycin C are particularly effective. This is because the damage is not repaired effectively, which results in the cancer cells being killed more easily. An over-activation of this specific DNA repair mechanism, on the other hand, is linked to a worse prognosis in ovarian cancer, breast cancer and lung cancer.
Kancera’s treatment concept is based on the same type of synergistic effect between specific drugs that formed the basis for the establishment of PARP inhibitors (e.g. AstraZeneca’s Lynparza) in the treatment of, above all, ovarian and breast cancer. PARP inhibitors have significantly prolonged survival without disease progression in patients with certain mutations and then mainly in earlier stages of the disease, i.e. before resistance to chemotherapy arises. PARP inhibitors are still one of the most important advances in the treatment of women’s cancer and sales amounted to approximately USD 900 million in 2018, with an expected annual growth of 32 percent until 2027.
Plans to apply for orphan drug status
In the field of cancer, Kancera’s drug candidates are initially intended to be combined with or replace PARP inhibitors after first- and second-line treatment in combination with DNA-targeted chemotherapy. The company plans to apply for orphan drug status for KAND567 and KAND145 within the indication ovarian cancer, in order to further increase product protection in addition to existing patent applications.
Photo of Thomas Olin: Kancera