Boehringer Ingelheim and Vanderbilt University have expanded their partnership to develop novel anti-cancer drugs that inhibit the myeloid cell leukaemia 1 (MCL1) protein, which is highly prevalent in many difficult to treat cancers.
Cancer cell
There are currently no therapies available that target MCL1, which when overexpressed, can prevent cancer cells from undergoing programmed cell death (also known as apoptosis).
“Boehringer Ingelheim and Vanderbilt University have the expertise and are jointly focused on discovering breakthrough medicines against the cancer causing proteins KRAS, SOS and now, MCL1,” said Darryl McConnell, PhD, vice president and research site head, Boehringer Ingelheim, Austria. “Together, we are committed to driving scientific research and development forward to help patients win the fight against cancer.”
“MCL1 is one of the top 10 overexpressed genes in human cancer where it plays a role as a survival factor,” added Lawrence J. Marnett, PhD, dean of Basic Sciences in the Vanderbilt University School of Medicine.
“It is a great target for therapy but candidate drugs need to disrupt high affinity protein-protein interactions, which is very challenging,” Marnett continued. “The Fesik laboratory has made impressive strides in developing such compounds and it is exciting to see them advanced toward clinical development through the partnership with Boehringer Ingelheim.”
This will be the third partnership between Boehringer Ingelheim and Vanderbilt University, pursuing the discoveries made in the laboratory of Stephen W. Fesik, PhD, at Vanderbilt University School of Medicine.
“Boehringer Ingelheim has an outstanding oncology drug discovery infrastructure that brings various research and development groups together to tackle challenging cancer targets,” said Fesik, professor of Biochemistry, Pharmacology and Chemistry at Vanderbilt. “In combination with our multidisciplinary team of structural biologists, medicinal chemists and cell biologists, we will work to search for anti-cancer compounds that inhibit MCL1 in order to tackle this complex area of unmet medical need.”