Boehringer and MD Anderson extend KRAS cancer collaboration

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Boehringer Ingelheim, Biberach, Germany, February 2007

Boehringer Ingelheim and The University of Texas MD Anderson Cancer Center have extended and expanded a collaboration exploring medicines targeting lung cancer with KRAS mutations. 

The collaboration was launched in 2019 and in its next phase will explore new molecules from Boehringer’s KRAS (Kirsten rat sarcoma) and TRAILR2 (TNF-related apoptosis-inducing ligand receptor 2) portfolios, with a particular focus on non-small cell lung cancer.

Under the new agreement, joint research will continue for five additional years.

The two organisations began their collaboration shortly after Amgen created a stir at the American Society of Clinical Oncology (ASCO) conference with the first clinical evidence of an effect on solid tumours from a KRAS-targeting drug.

Amgen has now filed sotorasib with the FDA, based on data from a phase 2 trial in patients with advanced or metastatic KRAS G12C mutated non-small cell lung cancer.

Mirati, a biotech from California, specialises in drugs targeting the mutation and is a step behind Amgen with its rival adagrasib.

Novartis signed a deal to evaluate Mirati’s drug soon after ASCO 2019.

Boehringer and MD Anderson said the new agreement allows them to research a first in first-in-class SOS1 pan-KRAS inhibitor known as BI 1701963.

They will also work on an inhibitor of KRAS G12C that could compete with sotorasib (BI 1823911) and an MEK inhibitor (BI 3011441), as well as a novel undisclosed bi-specific TRAILR2 agonist.

Boehringer Ingelheim expects several drugs to be entered into a “Virtual Research and Development Center” with MD Anderson.

KRAS is the most frequently mutated gene that causes cancer and is expressed in one in seven of all human metastatic cancers.

Mutation rates are more than 30% in lung adenocarcinomas, more than 40% in colorectal cancers and more than 90% in pancreatic cancers.

Tumour cell-selective activation of TRAILR2 can trigger cancer cell death in indications of high medical need, including lung and gastrointestinal malignancies.

Scientists from MD Anderson earlier this week published evidence from mouse models showing that blocking a protein called CREB1 could block mutant KRAS, plus another cancer gene called g53, potentially slowing or halting the spread of pancreatic cancer.