On January 24, 2012 Priaxon, utilizing its proprietory PriaXplore platform for small molecule drug discovery, and Boehringer Ingelheim reported they will prolongate their research and development collaboration on mdm2/p53 inhibitors for the treatment of cancer (Press release, Boehringer Ingelheim, JAN 24, 2012, View Source;detail=28 [SID1234535648]).
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The companies will continue working jointly to identify and advance drug candidates into pre-clinical development. Thereafter, Boehringer Ingelheim will drive the development and commercialisation of the potential cancer treatments arising from the collaboration.
"Priaxon has been able to develop promising mdm2/p53 inhibitors with its PriaXplore technology", said Dr Juergen Kolb, CEO of Priaxon. "We are proud that Boehringer Ingelheim appreciates Priaxon as a competent partner by prolongating the collaboration to advance the high potency lead compounds. We enjoy the fair and creative atmosphere of this cooperation very much."
Priaxon is entitled to up to EUR 86 million in milestone payments upon achievement of certain development, regulatory and commercial milestones as well as royalties on potential future net sales of products.
About mdm2/p53 Inhibition
The human p53 tumor suppressor protein has been one of the most investigated proteins in cancer research due to the fact that loss of p53 function through mutation and/or deregulation is involved in about 50% of all human cancers. The role of p53 in controlling the cell cycle and monitoring the integrity of the genome has made it known as the "guardian of the genome". Besides the functional loss of p53 through mutation, it can also be inactivated by the overexpression or amplification of MDM2 (murine double minute 2), which is the case in many p53 wild-type tumors. Thus, disruption of the MDM2-p53 interaction is considered a novel therapeutic strategy for cancer cells that still are endowed with wild-type p53, and a variety of small molecule drug like compounds have been reported that bind to the p53 binding site of MDM2.