Merck and Luminex Corporation enter agreement
Posted: 13 March 2013 | | No comments yet
Collaboration to support patient selection for the clinical development of MK-8931, Merck’s lead investigational medicine for AD…
Merck (NYSE: MRK), known as MSD outside the United States and Canada, and Luminex Corporation (NASDAQ:LMNX) 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. “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. “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.
About Alzheimer’s Disease and Amyloid Hypothesis
Alzheimer’s disease (AD) is a devastating, irreversible and ultimately fatal disease that progressively destroys neurons in the brain, leading to a deterioration of cognitive function. The symptoms include loss of memory that progresses into behavioral changes, alterations in thinking and reasoning skills that interfere with daily activities, and dementia. AD is the most common cause of dementia, accounting for approximately 50-75 percent of the estimated 35 million dementia cases globally.1,2 About 5.4 million people in the United States are currently living with AD.3 There are currently no disease-modifying treatments available for AD, and treatment options are limited to providing symptomatic improvements with only modest and short-term effects.
While the exact cause of AD remains unknown, the current prevailing hypothesis asserts that AD occurs due to the accumulation of beta amyloid proteins in the brain. Beta amyloid precursor protein site cleaving enzyme (BACE) is believed to be a key enzyme in the production of beta amyloid peptide, which contributes to the formation of plaques in the brain. Evidence suggests that inhibiting BACE decreases the production of beta amyloid and may therefore reduce amyloid plaque formation and modify disease progression.
About Merck’s BACE Inhibitor Development Program and MK-8931
Merck is advancing several innovative programs in Alzheimer’s disease, including candidates designed to modify disease progression as well as improve symptom control. Merck’s lead candidate in disease modification is MK-8931, an investigational oral BACE inhibitor.
Results of Phase I clinical studies demonstrated that MK-8931 can reduce levels of beta amyloid in cerebral spinal fluid (CSF) by greater than 90 percent in healthy volunteers and people with AD without dose-limiting side effects. Based on these results, Merck is conducting a global, multi-center Phase II/III clinical trial, EPOCH, to evaluate the safety and efficacy of MK-8931 versus placebo in patients with mild-to-moderate AD and has plans to initiate a trial in prodromal subjects. Information is also available at www.clinicaltrials.gov.
In December 2012, Merck and GE Healthcare announced a clinical study collaboration, license and supply agreement for use of [18F]Flutemetamol, an investigational positron emission tomography (PET) imaging agent, to support development of MK-8931.
- Alzheimer’s Disease International. Types of Dementia: Alzheimer’s Disease. Available at: http://www.alz.co.uk/info/alzheimers-disease.
- Alzheimer’s Disease International. Dementia Statistics. Available at: http://www.alz.co.uk/research/statistics.
- Alzheimer’s Association. Alzheimer’s Fact and Figures. Available at: http://www.alz.org/alzheimers_disease_facts_and_figures.asp.