Creating new, successful central nervous system drugs is tough, and Lundbeck knows this better than most after canning an internal CNS effort.
The drug in question, Lu AF11167, was meant to represent a new approach to treat the negative symptoms of schizophrenia, and worked by inhibiting the activity of the PDE10-enzyme in the brain.
This affects the signaling of the neurotransmitter dopamine in a manner that Lundbeck had hoped would specifically improve negative symptoms while positive symptoms remain controlled.
This, however, was not to be. After looking over data from a key, phase 2 proof-of-concept trial, a futility interim analysis found that the trial “is unlikely to achieve statistical significance on its primary endpoint,” according to an update from Lundbeck.
This endpoint was the mean change from baseline to week 12 on the Brief Negative Symptom Scale (BNSS).
Lundbeck said the trial would now be stopped, but noted this was not due to safety concerns, only efficacy. A breakdown of the data will published “at a later date.”
The pharma has form in tripping up on tough CNS trials, and two years back, a phase 3 trial of Lundbeck’s Lu AF35700 in treatment-resistant schizophrenia also missed its primary endpoint.
“Negative symptoms are a symptomatology of schizophrenia, for which there is no approved medical treatment today. It is disappointing that Lu AF11167 did not show the efficacy needed to treat this area which impacts many patients and represents a huge unmet medical need,” said Dr. Johan Luthman, EVP of R&D at Lundbeck.
This also comes two months after the company said it was planning to axe up to 160 jobs from across its organization in a major R&D shake-up in order to focus on where “the science is the most promising.”