Mithridion, Inc, a biopharmaceutical company focusing on developing drugs for serious Central Nervous System (CNS) disorders, announced progress with its pipeline of potential oral small-molecule drugs for Alzheimer's disease (AD) and schizophrenia. New product options have been developed for MCD-386, a clinical-stage drug candidate with 'first-in-class' potential for improving memory and cognition in AD, improving cognition in schizophrenia, and for disease-modifying effects (or stopping disease progression) in AD. The new product options, all in preclinical research, include MCD-386 Forte (a high dose version), MCD-386 Transderm (potentially deliverable via a skin patch), and MCD-396 Forte/Transderm, combining the benefits of both technologies.
Mithridion also announced progress in laboratory studies demonstrating the potential disease modifying activity of its drug leads, or their ability to stop or slow down the disease processes in AD. No currently available drug treats the underlying causes of AD, and this is a major unmet clinical need.
Mithridion is currently developing a controlled release formulation of MCD-386 (MCD-386CR) for Alzheimer's disease. The first part of phase I clinical trials was completed in late 2008, as previously announced. The company plans to evaluate the safety, tolerability and pharmacokinetics of MCD-386CR in a randomized, double-blind, placebo-controlled, ascending multiple-dose phase-Ib study to commence in the fourth quarter of 2009. MCD-386 Forte is a new high-dose product option, designed to maximize the disease modifying potential of MCD-386.
The Transderm technology is designed to deliver MCD-386 or MCD-386 Forte via a skin patch, offering convenience to patients and caregivers, as well as further performance benefits. Mithridion has proven the feasibility of these new product options in preclinical testing in laboratory models, not only for MCD-386, but also for one of the company's new drug leads described below.
Mithridion now has strong evidence in a laboratory animal model that its drug leads activate a key targeted signalling pathway that they were designed to activate. This builds upon previous research in vitro, in cell lines, demonstrating multiple modes of potential disease-modifying actions. Furthermore, in a transgenic mouse model of AD, one of Mithridion's drug leads reduced the amount of A-beta peptide, a major contributor to the dysfunction and death of neurons, in the hippocampus, a memory centre of the brain.
In its next-generation drug leads, currently in preclinical research, Mithridion has been successful in enhancing further the disease-modifying attributes for AD, and has been successful in adding new attributes potentially enhancing the profile of activity for treating not only cognitive impairment, but also psychotic symptoms in schizophrenia.
Trevor M. Twose, chief executive officer of Mithridion commented on the results, "We are very encouraged with progress. The demonstration of multiple modes of potential diseasemodifying actions means that our drug leads should be able to treat the underlying causes of neuron death in AD, even if several processes contribute to it, which seems likely. Not only do we now have an important proof of this concept in vivo, but also we have been able to use this knowledge to create exciting next generation drug leads for treating AD and schizophrenia. We are actively seeking major pharmaceutical company partners for our greatly expanded portfolio of product options."