DelMar Pharmaceuticals Presents Overview of VAL-083's Unique Anticancer Mechanism

- October 17th, 2016

VANCOUVER, British Columbia, and MENLO PARK, Calif., Oct. 17, 2016 /PRNewswire/ — DelMar Pharmaceuticals (NASDAQ:DMPI) , a biopharmaceutical company focused on the development and commercialization of new cancer therapies, is pleased to announce that the Company presented additional data regarding VAL-083’s unique anti-cancer mechanism on Saturday October 15, 2016 at the 12th Meeting of the European Association of Neuro-Oncology (EANO) in Mannheim, Germany.

VANCOUVER, British Columbia, and MENLO PARK, Calif., Oct. 17, 2016 /PRNewswire/ — DelMar Pharmaceuticals (NASDAQ:DMPI) , a biopharmaceutical company focused on the development and commercialization of new cancer therapies, is pleased to announce that the Company presented additional data regarding VAL-083’s unique anti-cancer mechanism on Saturday October 15, 2016 at the 12th Meeting of the European Association of Neuro-Oncology (EANO) in Mannheim, Germany.
DelMar’s poster presentation can be viewed at http://www.delmarpharma.com/scientific-publications.html.
“These data further differentiate VAL-083’s mechanism of action against cancer from the current standard of care in the treatment of glioblastoma multiforme (GBM), the most common and aggressive form of brain cancer,” said Dr.Dennis Brown, DelMar’s Chief Scientific Officer.
Temozolomide, the current front-line therapy generates its anti-tumor activity by methylation of the O6-position of guanine, resulting in a base-pair mismatch which can be lethal to the tumor cell if not repaired.  The majority of patients exhibit a high expression of the DNA repair enzyme “MGMT”, which readily repairs temozolomide-derived DNA damage leading to tumor resistance and treatment failure.  GBM patients failing temozolomide have a very poor prognosis with median survival of 6 – 9 months.
VAL-083 attacks the tumor’s DNA at a different location and in a different way, rapidly forming durable cross links at the N7-position of guanine.  These cross-links are not repaired by MGMT.
“These cross-links result in double-strand breaks during DNA replication which are more potent and more difficult for the cell to repair in comparison to the DNA damage conferred by temozolomide.  In particular, MGMT does not act against the type of DNA damage resulting from VAL-083 treatment,” added Dr. Brown.
“The EANO meeting provided an opportunity to introduce our VAL-083 to European neuro-oncology thought-leaders,” said Jeffrey Bacha chairman & CEO of DelMar.  Expanding our relationships with key opinion leaders on a global basis will provide opportunities for collaboration as we expand the development of VAL-083 beyond our current focus in the refractory, Avastin-failed population.
“Importantly, poor patient outcomes due to MGMT-mediated chemo-resistance were a consistent theme throughout the conference. Based on our research, we believe VAL-083’s unique mechanism and ability to circumvent the tumor’s MGMT resistance mechanism may provide a foundational opportunity as a new treatment paradigm,” stated Mr. Bacha.
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