Merck and Luminex Corporation Enter Agreement
News Jul 04, 2013
Merck and Luminex Corporation have signed a collaboration and license agreement to develop a companion diagnostic device that will be evaluated to help screen patients for recruitment into Merck's clinical development program for MK-8931, a novel oral beta amyloid precursor protein site cleaving enzyme (BACE) inhibitor and Merck's lead investigational candidate for Alzheimer's disease (AD). Financial terms were not disclosed.
“Evaluation of biomarkers that may provide an indicator of disease onset and enable earlier diagnosis is an important goal toward facilitating early intervention and potentially improving the treatment of Alzheimer’s disease,” said Darryle D. Schoepp, Ph.D., senior vice president, head of Neuroscience and Ophthalmology at Merck Research Laboratories.
Schoepp continued, “We look forward to working with Luminex to advance our ongoing clinical development program for MK-8931.”
Luminex will be responsible for development, regulatory submission and commercialization of the candidate companion diagnostic device, which will employ Luminex’s xMAP® Technology to measure concentrations of two candidate biomarkers (Aβ42 and t-tau) in cerebrospinal fluid (CSF) samples from patients with mild cognitive impairment (MCI).
The candidate device will be evaluated as a means to identify subjects with MCI who have a higher risk of developing AD to support patient selection for Merck’s therapeutic BACE inhibitor clinical program.
“This collaboration has the potential to deliver a novel companion diagnostic to identify patients at increased risk of developing Alzheimer’s disease,” added Patrick J. Balthrop, president and CEO of Luminex.
Balthrop continued, “We are pleased to leverage our technologies and development capabilities and look forward to expanding our activity into the companion diagnostic segment of personalized medicine.”
The accumulation of beta amyloid in the brain is a key pathological characteristic related to AD. Recent clinical evidence supports the hypothesis that the measurement of the investigational biomarkers Aβ42 and t-tau in CSF may be useful in identifying patients at greater risk of developing AD.
Currently, AD is diagnosed by clinical examination (i.e., medical history; physical, neurological, psychiatric and neuropsychological exams; and Magnetic Resonance Imaging [MRI] or Computed Tomography [CT] scan).
An AD diagnosis can only be confirmed by histopathological identification of core features, including beta amyloid deposits and plaques, in post-mortem brain samples.
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