Synergy of SCIB1 with checkpoint inhibitors

RNS Number : 8318O

Scancell Holdings Plc

12 August 2014

 



12 August 2014

Scancell Holdings Plc

Synergy of SCIB1 with checkpoint inhibitors

Combining SCIB1 with PD-1 blockade enhances tumour destruction and extends survival times

Scancell Holdings plc ('Scancell' or the 'Company'), the developer of novel immunotherapies for the treatment of cancer, is pleased to announce new data demonstrating that animals treated with a combination of SCIB1, Scancell's ImmunoBody® vaccine in development for the treatment of melanoma, and checkpoint inhibition (blockade of the PD-1 immune checkpoint pathway), showed enhanced tumour destruction and significantly longer survival times than when either treatment was used alone.

We have previously shown that administration of SCIB1 alone induced potent tumour-specific T cell responses associated with increased T cell infiltration into the tumour and enhanced proliferation of T cells within the tumour resulting in tumour rejection and long-term survival in 50% of animals.  In our new study, PD-1 blockade, when used alone, resulted in tumour rejection and long-term survival in 55% of animals.  However, the combination of PD-1 blockade with SCIB1 vaccination further enhanced T cell infiltration, resulting in tumour rejection and long-term survival in 85% of animals.  These results highlight the potential benefits of combining SCIB1 with PD-1 blockade in the treatment of cancer.

Checkpoint inhibitors can enable the host immune system to recognise, attack and destroy cancer cells. However, checkpoint inhibitors cannot work on their own if the patient fails to mount an adequate immune response to the tumour.  Taking the brake off immunosuppressive T cells with PD-1 blockade, whilst simultaneously pressing the accelerator with active immunotherapies such as SCIB1 is increasingly regarded as the logical next step towards overwhelming the disease and increasing efficacy.  These data confirm for the first time that the combination of SCIB1 with PD-1 blockade enhances tumour destruction and prolongs survival in animal models.

Prof Lindy Durrant, Joint CEO of Scancell and Professor of Cancer Immunotherapy at Nottingham University, commented:  "The rationale for combining SCIB1 and PD-1 blockade in the clinical setting is increasingly compelling.  The high immune response rates demonstrated with our SCIB1 vaccine, teamed with the enhanced T cell infiltration using PD-1 blockade, prolongs survival and strongly supports the hypothesis that combining SCIB1 with checkpoint inhibitors will be even more effective in the treatment of cancer than when either treatment is used alone."

For Further Information:

Dr Richard Goodfellow, Joint CEO Professor Lindy Durrant, Joint CEO	Scancell Holdings Plc Scancell Holdings Plc	+ 44 (0) 20 3727 1000
Christopher Golden/Stephen Keys	Cenkos Securities	+ 44 (0) 20 7397 8900
Mo Noonan/Simon Conway	FTI Consulting	+ 44 (0) 20 3727 1000

About Scancell

Scancell is developing novel immunotherapies for the treatment of cancer based on its ImmunoBody® and Moditope® technology platforms. Scancell's first ImmunoBody®, SCIB1 is being developed for the treatment of melanoma and is being evaluated in a Phase 1/2 clinical trial. Data from the trial demonstrate that SCIB1 has a marked effect on tumour load, produces a melanoma-specific immune response and highly encouraging survival trend without serious side effects.

Scancell's ImmunoBody® vaccines target dendritic cells and stimulate both parts of the cellular immune system; the helper cell system where inflammation is stimulated at the tumour site; and the cytotoxic T-lymphocyte or CTL response where immune system cells are primed to recognise and kill specific cells.

Scancell has also identified and patented a series of modified epitopes that stimulate the production of killer CD4 T cells that destroy tumours without toxicity. The Directors believe that the Moditope® platform could play a major role in the development of safe and effective cancer immunotherapies in the future.

 

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