Summary

CoDa is developing wound healing and other therapies, including dermatologic appearance medicines, based on a new platform technology known as "gap junction modulation." CoDa has demonstrated that modulating cellular gap junction communication not only reduces inflammation, swelling and scarring, but also improves the rate and quality of healing. Despite some advances in past decades, the wound healing market continues to be largely unsatisfied with extensive unmet medical needs. The same is true for the anti-scarring market. CoDa's technology is posed to revolutionize tissue repair for therapy and appearance by use of a new class of therapeutics that can modulate multiple cellular wound responses in any tissue, and in any wound.

Background

Wound healing is a multi-billion dollar business that continues to grow in parallel with worldwide demographic trends. While mechanical devices have made some progress in improving wound healing, therapeutics have fallen short after an abundance of clinical failures and poor sales for the few approved treatments. Historically, wound healing treatments targeted use of agonists – such as growth factors and cytokines – whereas CoDa is taking a reverse approach to improving healing with a new drug, new target and new mechanism of action by temporarily interrupting cell-cell communication in injured tissue. This antagonist approach is fundamentally different than previous failed methods, and is based on blocking mechanisms that impair wound healing and increase scarring rather than adding single factors selected from the many that populate the multiplex wound-healing cascade.

CoDa

For several years CoDa's founders sought to answer the question: Can early intervention or blockade of a single component of a biological cascade that causes cell death improve the wound healing process? CoDa has demonstrated improved wound healing in a wide range of preclinical models using its antagonist molecule to modulate intercellular communication via "gap junctions." This promising avenue of research took a dramatic turn in late 2005 when a seriously injured human patient, who failed to respond to all available wound therapies, received treatment with CoDa's molecule under a compassionate use approval. The result was compelling: in spite of a hopeless prognosis (blindness following a severe eye burn), one application of CoDa's drug triggered wound healing through re-epithelialization, which progressed to complete recovery. Based on this result, additional compassionate uses have been approved, again with healing results that have startled attending physicians. Such striking anecdotal results, in addition to preclinical successes in numerous animal and tissue models, are strongly suggestive that this antagonist mechanism can positively influence tissue repair. CoDa has initiated a comprehensive clinical development program aimed at demonstrating via placebo-controlled trials that its preclinical and anecdotal human results are evidence of a drug molecule with relevant therapeutic efficacy. To this end, and based on a commitment of $23 million of venture capital, the company has assembled an experienced development team and initiated a clinical program to demonstrate safety and efficacy in acute and chronic eye and skin wounds.