Cellmid MK antibodies effective in brain cancer trials

By Trevor Hoey. Published at Oct 6, 2016, in ASX Biotechs

Shares in Cellmid (ASX:CDY) were up approximately 30% at one stage on Wednesday after the company released promising results regarding the preclinical collaborative trials being undertaken in relation to its anti-midkine antibodies (MK antibodies).

The results demonstrated that MK antibodies produced by its wholly-owned subsidiary LYRAMID, are effective in improving tetrahydrocannabinol (THC) treatment response in animal models of cannabinoid resistant glioblastoma multiforme, one of the most common and aggressive forms of brain cancer.

CDY’s chief executive, Maria Halasz, highlighted the fact that there is currently no effective treatment for glioblastoma with tumours recurring even after the most intensive combination of surgery, radio and chemotherapy. Existing treatments only extend survival from three months to just over a year with very few glioblastoma patients surviving beyond three years.

CDY’s collaborators at Complutense University in Madrid have previously shown that high levels of MK were found to be associated with aggressive tumours and poor survival in glioblastoma patients.

While it is now widely accepted that medicinal cannabis has a number of benefits in cancer treatment including relieving pain and nausea and improving appetite, there is now sound scientific proof that distinct chemical components of cannabis called cannabinoids are potent anti-cancer agents with direct anti-tumour actions including induction of cancer cell death.

CDY noted that, as is the case with many cancer drugs, tumours can develop resistance to cannabinoids.

The promising aspect of this study is that MK antibodies used in combination with the cannabinoid THC inhibited tumour growth in gliomas that are resistant to THC.

The testing is still in its early stages, so investors should approach the company with caution, factor in all information and seek professional financial advice before making an investment decision.

Consequently, overcoming THC resistance highlights a potential treatment strategy using MK antibodies to enhance glioblastoma sensitivity to treatment, and provides a strong rationale for the continued clinical development of MK antibodies to treat brain cancer in combination with cannabinoids.

As highlighted by Halasz, the results of this study add to the already significant intellectual property assets ready for clinical development by LYRAMID, as well as providing additional collaboration opportunities with companies focused on improving their existing therapeutic approaches using cannabinoids in the treatment of glioblastoma multiforme.

Delving a little deeper into the intricate details of the testing procedure it becomes evident just how significant this development is.

To test whether the results using Glioma Initiating Cells (GICs) in cell culture conditions would translate into reduced in vivo tumour growth, Prof Velasco implanted the GICs into mice, and in an effort to mirror the disease in humans allowed the tumours to grow to a detectable size before starting treatment.

Mice with tumours were treated with MK antibody and THC treatments and tumour growth was tracked for a further 12 weeks. The tumours in mice that were administered THC alone continued to grow steadily while those treated with both THC and a form of midkine antibody grew much slower for the 12 week treatment period and were significantly smaller by the end of the experiment.

From this research and other data collated from in vitro testing it has now become evident that MK neutralisation with MK antibodies sensitises tumours to the anti-tumour action of THC.

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