Probiodrug said today it launched a collaboration with VU University Medical Center (VUmc) Alzheimer Center to assess several new molecular biomarker assays for their diagnostic, pharmacodynamic, and therapeutic potential in Alzheimer’s disease (AD). The value of the collaboration was not disclosed.
The partners plan to analyze cerebrospinal fluid (CSF) samples from well-characterized AD patients at different stages of disease, compared with CSF from age-matched control samples. The assays are designed to detect the presence and concentration of pyroglutamated amyloid beta (pGlu Abeta), a highly toxic peptide produced by the enzyme glutamaminyl cyclase (QC) that has been linked with cognitive decline in individuals with AD.
The collaboration seeks to correlate CSF concentrations of pGlu Abeta with the stage of AD in which they occur.
“A correlation between pGlu Abeta concentration and AD disease stage would validate the therapeutic approach of inhibiting QC, in support of the Phase II study for our innovative QC inhibitor PQ912,” Inge Lues, Ph.D., Probiodrug’s chief development officer, said in a statement. “The results of this comprehensive analysis should give us further insights into the relevance of pGlu Abeta and pGlu Abeta-containing oligomers in the pathology of AD.”
There are currently no validated therapeutic biomarkers for the treatment of AD, aside from several costly and cumbersome diagnostic markers, said Philip Scheltens, professor of cognitive neurology and director of VUmc Alzheimer Center.
“The work we are undertaking with Probiodrug could lead to earlier identification of disease, which could allow treatment to commence before irreversible damage has been done,” he added.
The collaboration is consistent with what Probiodrug has said is its current strategy of focusing resources exclusively on AD, reflected earlier this month when it sold its experimental cyclin-dependent kinase 9 (CDK9) inhibitor program to AstraZeneca for an undisclosed price.
But as GEN observed last year, the road to development of new drugs for AD has been paved with failure: The only five drugs now approved for treating the disease only manage to slow progression of symptoms six to 12 months.
