PharmaMar Presents New Data On The Treatment Of Multiple Myeloma And Ovarian Cancer At The AACR Congress

MADRID, April 4, 2017 /PRNewswire/ --

PharmaMar (PHM:MCE) has presented new data on the mechanism of action of plitidepsin and lurbinectedin during the Annual Congress of the American Association of Cancer Research (AACR), which is being held in Washington D.C. (United States) on 1-5 April.

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“To continue working so oncological patients can enjoy access to innovative treatments is a commitment PharmaMar acquired from the outset, one that lies behind every one of our decisions”, says Luis Mora, the Managing Director of PharmaMar’s Oncology Unit. He added that “plitidepsin and lurbinectedin are the nearest future of our company’s portfolio and we hope that they will become a reality in clinical oncological practice so that, together with Yondelis®, they deliver new options to patients and specialists.”

Studies presented by PharmaMar at the AACR2017 Congress

• Plitidepsin targets the moonlighting functions of eEF1A2 in cancer. Losada A, et al. Poster presentation, Section 5, Monday 3 April, 8.00am-12.00pm

• PharmaMar announced last year that the eEF1A2 protein had been identified as a pharmacological target for this molecule. Continuing with this line of research, the company has observed that plitidepsin acts by inhibiting some of the functions of this protein (eEF1A2) and promoting cancer cell death.

• Lurbinectedin reverses platinum dependent IRF1 overexpression and nuclear localization, partially responsible for resistance to platinum drugs in ovarian cancer. Santamaría G, et al. Poster presentation, Section 6, Monday 3 April, 8.00am-12.00pm

Lurbinectedin is a compound under clinical investigation that belongs to the RNA polymerase II enzyme inhibitor family. This enzyme is essential to the transcription process and inhibits tumour growth which causes the death of the tumour. This study demonstrates the capacity of lurbinectedin to reverse cisplatin resistance in ovarian cancer cells caused by the over-expression of the IRF-1 transcription factor. In these cell models, the synergy of the lurbinectedin and cisplatin combination was established.

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