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M3 Executive Summary Final

M3 Executive Summary Final



Executive summary for M3 Biotechnology, a pre-clinical biotechnology company with breakthrough technology in protein multimerization.

Executive summary for M3 Biotechnology, a pre-clinical biotechnology company with breakthrough technology in protein multimerization.



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    M3 Executive Summary Final M3 Executive Summary Final Document Transcript

    • M3 Biotechnology, Inc Founders: Joe Harding , Jay Wright, Lewis Rumpler Contact Info: Lewis Rumpler Cell: 509-850-2802Regulating Protein- lewis.rumpler@gmail.com email:Protein Interactionwith NovelPeptidomimeticCompoundsBackgroundProtein-Protein interaction represents asizable contribution to systems biology anddisease pathology and concomitantly atarget rich environment for new drugs. Yet,modulating these important interactions hasremained elusive. M3 Biotechnology (M3) hasdiscovered a number of peptidomimeticcompounds that demonstrate, perhaps forthe first time, the ability to control a M3 Biotechnology Highlights •Significant IP estate optioned from Washington State University with foundational IP •Lead compounds with in vitro and in vivo data supporting commercialization in CNS, oncology and M3 BIOTECHNOLOGY, INC. www.m3bio.com
    • M3 Biotechnology, Inc. foremost with their ability to support M3 HGF Agonist Program new connectivity among neurons and potential recovery of lost function There are approximately 10 million have long biological half-lives. An regardless of the underlying cause. diagnosed dementia patients in the overview of M3 Antagonist U.S. and that number continues to M3 HGF Antagonist Program advantages: grow every year as our population Very potent with effective doses three ages. The costs of treatment and care First, the HGF/ c-Met system is over- orders of magnitude lower that other of these patients are in excess of $70 activated in more than 50% of all anti-cancer therapeutics billion annually and are increasing human cancer cells. This activation Highly specific for the HGF rapidly. Unfortunately, the current leads to changes in the behavior of dimerization site, thus they appear to treatment options for the these cells, which contribute to a exhibit little toxicity management of dementia are neoplastic phenotype. Included in Very inexpensive to manufacture at severely limited and largely these changes in behavior are the pennies per dose ineffective. Recently these obstacles following: increased proliferation Likely to be formulated for oral have been overcome by scientists at rate, decreased cell-to-cell adhesion, delivery, making them far easier to M3 and Washington State University increased migratory behavior, administer than biologics. who have elucidated the mechanism increased ability to transit into and of action of these molecules and out of the vasculature, and a decrease developed stable, orally active Markets and IP in anoikis (a form of programmed cell analogs, which can reverse cognitive death) in response to suspension. The M3 has negotiated an option on a dysfunction in models of both acute last four changes encourage these significant IP estate from Washington and chronic dementia. Thus, these cells to metastasize from the primary State University that includes: issued, molecules, typified by the lead (initial) tumors to distant locations published and provisional patents compound MM201, represent a new where secondary tumors can be covering key composition of matter class of drugs for the practical established. M3 has synthesized a and use claims critical to M3 treatment of dementia. MM201 large family of small molecules that commercialization. overview: block the interaction of HGF and c- Potent hepatocyte growth factor Met. They have been shown to: 1) All markets addressed by M3 mimetic that activates the c-Met directly block the binding of HGF to c- technology are significant in size and receptor Met; 2) block c-Met dependent demonstrate unmet medical need. Reverses spatial learning and proliferation and migration; 3) inhibit M3 will look for smaller niche memory deficits in a scopolamine, the cellular pathways activated by c- applications such as retinopathy, acute cholinergic deficit model when Met; 4) block angiogenesis; 5) pancreatic cancer, ALS and diabetic delivered orally directly kill HGF/c-Met over- ulcers where clinical endpoints are Produces a dramatic expansion of expressing cancers, and, 6) and most well defined, achievable and patient functional synaptic connections importantly block the growth of enrollment attainable. among hippocampal neurons primary tumors and the Has a circulating half-life > 48 hours establishment of metastatic tumors. The potential of HGF mimetics lies Some of these molecules have been shown to exhibit no overt toxicity and M3B SUMMARY: The Company is intending to commercial its lead programs that include HGF agonists (CNS) and antagonists (oncology and angiogenesis). It has a option on a significant IP estate from Washington State University, a novel discovery platform that is extensible into a broad array of proteinM3 BIOTECHNOLOGY, INC www.m3bio.com