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About Us

Who is Hamit-Darwin-Freesh?

We are, and always have been a small company.  We began 23 years ago.  Our early efforts lead the way to a novel approach in epilepsy drug design; largely through the application of computational chemistry and molecular modeling tools.  New ways to engage in rational antiepileptic drug discovery have been uncovered.  Our work is nearing completion is this field, as we complete the synthesis of a library of compounds which should extend the options available for the treatment of epilepsy syndromes with safer and more efficacious drugs.


Now, we bring to bear many years of experience on one of the greatest challenges of our time; i.e., the prevention of Alzheimer’s disease (AD).  OUR MISSION TODAY IS TO DISCOVER A SAFE AND EFFECTIVE TREATMENT THAT WILL PREVENT AND AND HALT IT’S PROGRESSION.  We are results driven, and enjoy a record of success in our laboratory studies.  With expertise in pharmacology, clinical neurology, computational chemistry, molecular modeling, synthetic organic chemistry, and cellular and molecular biology we began our assault on this disease over twelve years ago.  We have been working relentlessly, with the singular goal being the prevention of AD, and halting its progression.


We approach our goals with humility.  We recognize how daunting this challenge is.  Failure in over 400 clinical trials is fodder for fear and apprehension.  However, we believe that a solution to this matter will unexpectedly, rapidly evolve over the next 6-12 years.  We do not believe that any single compound will be effective in the prevention of AD.  The neuropathology of AD is simply too complex, and includes many so called ‘independent variables’ (i.e., contributing mechanisms) that likely contribute to the disease. Significant covariance likely exists  among these variables, but we suspect a fixed-dose combination of two drugs will be required to prevent, and halt the progression of AD. Synergy will likely play a role in the success of such combinations simply because there do exist multiple mechanisms of pathology.  


Unfortunately, virtually all clinical trials to date were designed to discover the ‘magic bullet;’ i.e., a single molecule that will cure AD.  Failures were due to unacceptable toxicity or lack of efficacy.  We are all in a hurry to cure AD, and oftentimes the duration of the trial is insufficient to prove efficacy; or it was started too late in the course of the disease.  Regarding fixed dose combination trials there is a dearth of such studies.


Most scientists working in this field no longer believe that the so-called “hard plaque” in the extracellular space plays a primary causal role in AD pathology.  For well over a decade now scientists have increasingly focused their efforts on the so-called “soluble β-amyloid(1-42) oligomers,” as evidence has mounted that the pathology seen in AD stems largely from one, or a spectrum of such oligomers.   Yet there are many other putative mechanisms for the neurotoxicity associated with AD pathology, and these will be discussed in the section “About Alzheimer’s Disease.”


Our work is presently focused in two areas.  We have developed a small library of synthetic compounds that both prevent the aggregation of the β-amyloid(1-42)  peptides, and facilitate the disaggregation of the above referenced soluble oligomers.  These are novel small organic compounds, not known to any molecular data base.  We believe we understand their mechanism, which indeed is also novel, and unexpected. 

Finally, we are also engaged and an effort to discover small molecules that will safely modulate microglial phagocytosis and mitigate the microglia mediated inflammation thought to play a role in AD pathogenesis. (Also see the section "About Alzheimer's") Our early studies have been encouraging, but progress remains to be made.

Principal Scientists
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