Beyond innovative technology, our drug discovery process is structured to streamline and expedite the drug development process through leveraging the extensive experience of the team and the multi-indication applications of our compounds. From concept-to-development, approval and beyond - our systematic approach is geared toward moving potential drugs for traumatic brain injury (TBI), Alzheimer's disease (AD) and other neurodegenerative diseases from the laboratory to market as quickly and efficiently as possible.
Our Company is striving to develop ground-breaking therapeutics that are directed toward newly-identified causative targets, such as cysteine proteases. By employing a virtual business model, we will recruit the best business, scientific and clinical resources available and motivate them to tackle this challenge with an urgent and unified effort and an eye toward minimizing costs, sharing risk, and vigorously protecting and defending our intellectual property. By maintaining a commitment to honesty, openness, and a dedication to the highest standards obtainable, we can be confident in our expectation that we will be successful in bringing value to the patient, their care givers, and ultimately to the nation and the world.
ALSP’s strategy to combat the ravages of neurodegenerative disease is to deploy its proprietary class of compounds to inhibit papain-like cysteine proteases. The Company’s initial focus on traumatic brain injury (TBI) is increasingly supported by mounting evidence that one of these cysteine proteases in particular, cathepsin B, when inappropriately expressed, as is the case in (TBI) and Alzheimer's disease (AD), and many other neurodegenerative diseases creates a dangerous intersection at which inflammatory, apoptotic, and necrotic pathways are activated. ALSP believes these pathways constitute the underlying pathology of neurodegeneration.
Consequently, the efficient reversal of the over expression of this key enzymes can completely mitigate all of these pathways at once and prevent the neuronal destruction that they mediate. Doing so significantly improves measures of memory deficit and neuro-motor dysfunction in TBI and AD animal models, respectively. The inhibition of these protease not only reduces neuro-inflammation, but also provides potent neuronal protection by multiple mechanisms. Data from TBI and AD models using cathepsin B knock-out animals indicate that this protease plays a dominant role at this toxic intersection and suggests that its inhibition should not have undesired consequences.
Cathepsin B activity is significantly elevated in TBI and AD. This enzyme has been well studied with respect to its contribution to pathways leading to caspase activation and programmed cell death (apoptosis) of the neuron, to inflammatory pathways that include TNF-a, Il-1β and metallo-proteinase activation, and to tissue necrosis. ALSP’s lead compound, ALP-495, is a potent inhibitor of cathepsin B. Elimination of the drug is primarily through the kidney and the gut without multi-dosing accumulation. Extensive work with ALP-495-related tool compounds suggests that this class of compounds has a wide therapeutic window.