DispersinB for the diabetic foot

NewsBot · Jan 15, 2008

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Press release from Kane Biotech:
Kane Biotech receives $405,000 contribution from the National Research Council Canada Industrial Research Assistance Program (NRC- IRAP) to Develop DispersinB™ Antibiofilm Wound Gel Product

WINNIPEG, Manitoba (January 15, 2008) - Kane Biotech Inc. (TSX-V:KNE), a biotechnology company engaged in the development of products that prevent and disperse microbial biofilms, is pleased to announce that it has received a $405,000 contribution from the National Research Council Industrial Research Assistance Program (NRC-IRAP). The contribution will be applied to the development of the Company’s novel antibiofilm topical wound gel containing its patented DispersinB™ technology. DispersinB™ wound gel is being developed to treat chronic wound infections.

“We are very pleased that the NRC-IRAP has chosen to support the development of this important technology for treating chronic wounds such as diabetic foot ulcers and venous leg ulcers,” stated Gord Froehlich, President and CEO of Kane Biotech. “DispersinB™ is a first of its kind technology that both prevents and removes the biofilm in chronic wounds allowing antiseptics and antibiotics to offer highly effective microbial control.”

Chronic wounds are a serious debilitating complication of vascular disease, diabetes and prolonged immobility and are a huge unmet clinical need that costs the U.S. healthcare system $20 billion per year. “We are currently preparing our pre-IDE regulatory package for the United States Food and Drug Administration to test DispersinB™ in a chronic wound human clinical trial. NRC-IRAP support will greatly assist in our product development,” added Mr. Froehlich.

NRC-IRAP provides a range of both technical and business oriented advisory services along with potential financial support to growth-oriented Canadian small and medium-sized enterprises. Working directly with these clients, NRC-IRAP supports innovative research and development and commercialization of new products and services.

Biofilms are a major cause of a number of serious medical problems in humans and animals including chronic and medical device related infections. They develop on surfaces such as catheters and prosthetic implants, inner ears, teeth, gums, lungs and the urogenital tract. Biofilms are pervasive and costly to the healthcare industry; approximately 80% of all human bacterial infections involve biofilms.
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NewsBot · Jul 2, 2008

Press Release:
A New Study Shows DispersinBTM Helps Our Body's Immune Cells to Kill Bacteria

Kane Biotech Inc. (TSX VENTURE:KNE), a biotechnology company engaged in the development of products that prevent and remove microbial biofilms, is pleased to announce a research publication on its DispersinBTM technology. The manuscript appeared in the recent online edition of Microbial Pathogenesis (2008), doi: 10/1016/j.micpath.2008.05.007.

The publication, entitled "Both leukotoxin and poly-N-acetylglucosamine surface polysaccharide protect Aggregatibacter actinomycetemcomitans cells from macrophage killing" authored by Dr. Jeffrey B. Kaplan and his colleagues, demonstrates that when biofilm-embedded Aggregatibacter actinomycetemcomitans (A.a) is treated with DispersinBTM it makes the bacteria susceptible to macrophage killing. Previously, it has been shown that bacteria in a biofilm are 100 to 1000 times more resistant to antimicrobials and host's immune responses than their planktonic counterparts.

"Our studies showed that the pre-treatment of biofilm-embedded "A.a" cells with DispersinBTM removes the biofilm and renders the cells sensitive to killing by the body's macrophages", stated Dr. Jeffery Kaplan, University of Medicine and Dentistry of New Jersey.

"The findings of Dr. Kaplan's group suggest that when DispersinBTM is used in products such as wound gels and device coatings, either in combination with an antimicrobial or alone, it makes biofilm-embedded bacterial pathogens susceptible to killing by both antimicrobials and macrophages or by our body's macrophages alone", added Dr. Sri Madhyastha, Chief Scientific Officer of Kane Biotech.

DispersinBTM is a novel antibiofilm enzyme capable of both inhibiting and dispersing bacterial biofilms. Kane Biotech has received a patent from the U.S. Patent and Trademark Office for DispersinBTM and has been awarded a $405,000 contribution from the National Research Council-Industrial Research Assistance Program (NRC-IRAP) to further develop this technology. Kane Biotech is presently using DispersinBTM alone, and in combination with other antimicrobial agents, to develop a wound care therapy and a proprietary medical device coating.
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NewsBot · Jul 2, 2008

Here is the research referred to above:

Both leukotoxin and poly-N-acetylglucosamine surface polysaccharide protect Aggregatibacter actinomycetemcomitans cells from macrophage killing.
Venketaraman V, Lin AK, Le A, Kachlany SC, Connell ND, Kaplan JB.
Microb Pathog. 2008 Jun 5. [Epub ahead of print]

Two virulence factors produced by the periodontopathogen Aggregatibacter actinomycetemcomitans are leukotoxin, a secreted lipoprotein that kills human polymorphonuclear leukocytes and macrophages, and poly-N-acetylglucosamine (PGA), a surface polysaccharide that mediates intercellular adhesion, biofilm formation and detergent resistance. In this study we examined the roles of leukotoxin and PGA in protecting A. actinomycetemcomitans cells from killing by the human macrophage cell line THP-1. Monolayers of THP-1 cells were infected with single-cell suspensions of a wild-type A. actinomycetemcomitans strain, or of isogenic leukotoxin or PGA mutant strains. After 48h, viable bacteria were enumerated by dilution plating, macrophage morphology was evaluated microscopically, and macrophage viability was measured by a Trypan blue dye exclusion assay. The number of A. actinomycetemcomitans CFUs increased approximately twofold in wells infected with the wild-type strain, but decreased by approximately 70-90% in wells infected with the leukotoxin and PGA mutant strains. Infection with the wild-type or leukotoxin mutant strain caused a significant decrease in THP-1 cell viability, whereas infection with the PGA mutant strain did not result in any detectable changes in THP-1 viability. Pre-treatment of wild-type A. actinomycetemcomitans cells with the PGA-hydrolyzing enzyme dispersin B rendered them sensitive to killing by THP-1 cells. We concluded that both leukotoxin and PGA are necessary for evasion of macrophage killing by A. actinomycetemcomitans
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