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Kancera acquires Fractalkine project

thomas olin kancera

Swedish Kancera is to acquire Fractalkine project from Acturum Life Science and the payment for is to be carried in three steps with total of 6 million shares.

Due to positive efficacy data in disease models of cancer and pain, Kancera’s Board of Directors has decided to exercise the exclusive option to acquire the Fractalkine project. Kancera has previously announced that the company owns an option to acquire exclusive rights to the Fractalkine project (excluding the therapeutic area respiratiory diseases) during an evaluation period of 24 months (from September 2015).

The project has now generated positive results in multiple disease models of cancer and pain. The results show desired treatment effects that are important for Kancera´s further product development and commercialization of the project. The results will be published at a later date, in collaboration with the academic partners involved. In light of the positive results Kancera Board have decided to acquire the Fractalkine project. The acquisition will be carried out in connection with the completion of the ongoing transfer of results and know-how from Acturum and AstraZeneca to Kancera.


Payment for the project to Acturum Life Science AB will be made into three steps by a total of 6,000,000 shares, of which the first payment is due at the submission of the application for authorization of a clinical trial after an approval by Kancera´s shareholders. In parallel, the company intends to validate a broader use of the drug candidate (KAN0440567) in order to demonstrate its full commercial potential.


The Fractalkine project

Fractalkine is an immune regulatory factor that sends signals via the CX3CR1 receptor, also called G-protein coupled receptor 13 (GPCR13). In the healthy individual, Fractalkine and its receptor regulate migration of immune cells from the blood capillary wall into areas where the immune system is needed. Animal studies show that Fractalkine and its receptor are not essential for survival and that important immune functions remain intact indicating that inhibition of the Fractalkine signaling by a drug probably will be tolerated without significant adverse effects. Fractalkine and its receptor have been linked to the growth and proliferation of pancreatic, breast and prostate cancer. Also, cancer cells that have the Fractalkine receptor on their surface migrate towards nerve ends that have Fractalkine on their surface. Thus, cancer cells are led to surround and apply pressure on nerves and thereby cancer pain may arise.

Another proposed mechanism for how Fractalkine and its receptor affect the development of tumors is that they contribute to the transformation of the body’s macrophages from being a threat against the cancer (the M1 form) to supporting the cancer (the M2 form). This mechanism is also suggested as a predictive factor for responsiveness to the new immuno-oncology drugs that act through PD-1 and PD-L1 such as nivolumab, pembrolizumab and pidilizumab. During 2014 and 2015 studies have been published demonstrating that the absence of Fractalkine in tumor cells is a significant marker for how successful the immuno-oncology treatment is expected to be (see e.g. the publication in Nature on November 27, 2014, Vol. 515, pp 563). In the light of these observations, there are good reasons to further study if inhibition of the Fractalkine signaling with KAN0440567 (AZD8797) has the potential to increase the proportion of patients responding to the new immuno-oncology drugs that act through PD-1 and PD-L1.