Progenics Awarded NIH Grant to Advance Novel C. Difficile Antibody Therapy

Progenics Pharmaceuticals, Inc. announces the award of a grant totaling $4,143,652 from the National Institutes of Health (NIH) for Progenics program to develop novel monoclonal antibodies to treat Clostridium difficile (C. difficile) infection. C. difficile is a bacterium that represents the leading cause of hospital-acquired diarrhea in the United States and a serious global public health challenge. Progenics monoclonal antibodies constitute a non-antibiotic treatment strategy that is designed to block the harmful effects of the disease-causing toxins produced by C. difficile.

"The award acknowledges the growing burden of C. difficile infection and the need for innovative therapies that go beyond standard antibiotic approaches."

."We are honored to receive this competitive NIH award and are gratified that NIH elected to support our program based on its scientific merit, innovation and therapeutic potential," said Paul J. Maddon, MD, PhD, founder, CEO and chief science officer of Progenics Pharmaceuticals, Inc. "The award acknowledges the growing burden of C. difficile infection and the need for innovative therapies that go beyond standard antibiotic approaches."

The three-year award supports research and preclinical development of Progenics humanized monoclonal antibodies against C. difficile toxins. The award was made under the American Recovery & Reinvestment Act of 2009 through the "NIH Directors Opportunity for Research in Five Thematic Areas" program. NIH established this program to support projects that address research endeavors that have high short-term impact, and a high likelihood of enabling growth and investment in biomedical research and development, public health, and health care delivery.

C. difficile is an anaerobic, spore-forming bacterium that represents the leading cause of hospital-acquired diarrhea and life-threatening pseudomembranous colitis. C. difficile-associated disease (CDAD) affects an estimated 750,000 individuals each year in the U.S. and is responsible for more deaths than all other intestinal infections combined. Recent outbreaks of hypervirulent strains have been reported globally, significantly increasing the economic burden of CDAD and requiring new treatment strategies to combat this worldwide public health challenge. Upon infection, C. difficile produces two protein toxins (toxins A and B) that can damage the cells that line the colon, leading to CDAD. CDAD encompasses a spectrum of diseases ranging from mild-to-severe diarrhea to potentially life-threatening complications such as toxic megacolon and sepsis. CDAD often occurs when an individual is exposed to C. difficile while taking antibiotics, since a course of antibiotic treatment can disrupt the normal (beneficial) intestinal bacteria, providing opportunities for C. difficile to become established. Current treatments for CDAD consist of narrow-spectrum antibiotics, such as vancomycin or metronidazole that may impede regrowth of the normal colonic bacteria. Although current therapies are generally effective in treating CDAD, the disease frequently relapses after antibiotic treatment ceases.

Progenics' humanized monoclonal antibodies are designed to block the cytotoxic effects of C. difficile toxins and enable the normal bacteria in the colon to become reestablished. In laboratory studies, the humanized monoclonal antibodies potently neutralized the cell-killing activities of the toxins produced by both conventional and hypervirulent strains of C. difficile. In a preclinical efficacy study conducted in a stringent hamster model of CDAD, treatment with a combination of humanized monoclonal antibodies (one against toxin A and the other against toxin B) provided a highly statistically significant (P<0.0001) survival advantage relative both to no treatment and to treatment with vancomycin, a current standard antibiotic therapy.

Hide comments

Comments

  • Allowed HTML tags: <em> <strong> <blockquote> <br> <p>

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Publish