Novel class therapies developer Vedanta Biosciences has entered into a translational collaboration with the NYU Langone Medical Centre in New York, US, to develop effective microbiome-derived immunotherapies for cancer patients being treated with checkpoint inhibitors.

As part of the deal, Vedanta will work closely with Dr Jeffrey S. Weber-led team of oncologists from Langone Laura and Isaac Perlmutter Cancer Centre.

The collaboration will focus on clinical studies that would be directed towards the identification of new microbiome immunotherapies for cancer.

Vedanta chief scientific officer Dr Bruce Roberts said: “Dr Weber is a pioneer in translational research, particularly in immunotherapy and the development of checkpoint inhibitors.

"Dr Weber is a pioneer in translational research, particularly in immunotherapy and the development of checkpoint inhibitors."

“We look forward to working with Dr Weber to expand Vedanta’s portfolio of immune activating microbial cocktails for use in standalone immunotherapy and in combination with checkpoint inhibitors.”

The researchers will also try to discover different mechanisms, by which the gut microbiome can influence the efficacy of checkpoint inhibitors in cancer patients.

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Dr Weber said: “Checkpoint inhibitors are a major advance in cancer therapy, but many patients do not respond to therapy, and some patients who do respond will eventually relapse.

“Recent data suggests an important role for the microbiome in the anti-tumour activity of immunotherapy, and our other studies of the microbiome will offer interesting new clinical insights into how and why these treatments work.

“Further understanding of the role of the microbiome in immunotherapeutic responses against cancer may also lead to new and improved therapies.”

A recent study conducted by Vedanta co-founder Dr Kenya Honda at Keio University has revealed human-dwelling bacterial strains can activate immune cells in the gut that can be used for immunotherapies.

Other researches demonstrate that gut bacteria can potentially modulate the therapeutic responses to checkpoint blockades, along with other classes of cancer therapeutics.