Date: 2012-10-17
Type of information:
phase: preclinical data
Announcement: presentation of data at the 3rd Annual Meeting of the Israel Society for Placenta Research
Company: Pluristem Therapeutics (Israel)
Product: PLX cells (Placental eXpanded cells)
Action mechanism: The company\'s patented PLX (PLacental eXpanded) cells drug delivery platform releases a cocktail of therapeutic proteins in response to a variety of local and systemic inflammatory diseases. PLX cells are grown using the company’s proprietary 3D micro-environmental technology and are an off-the-shelf product that requires no tissue matching or immune-suppression treatment prior to administration. The PLX-PAD comprehensive clinical development plan has been recognized by both the EMA and FDA, targeting a sub-population of 20 million patients in the Peripheral Artery Disease (PAD) market.
Disease: fibrosis
Therapeutic area:
Country:
Trial details:
Latest
news: Pluristem Therapeutics, a developer of placenta-based cell therapies, has announced that a reduction of fibrotic processes has been demonstrated in preclinical and in in-vitro studies using Pluristem’s Placental eXpanded (PLX) cells. Lena Pinzur MSc, Pluristem’s Basic and Preclinical Research Manager will present data at the 3rd Annual Meeting of the Israel Society for Placenta Research on October 18, 2012.
Fibrosis, defined as the overgrowth, hardening, and/or scarring of various tissues as the end result of chronic inflammation, can result from a variety of stimuli that includes chronic infections, autoimmune reactions, allergic responses, chemical and radiation insults, radiation, and other causes of tissue injury. Fibrosis can occur in virtually any organ, including the heart, liver, kidney and lung. The fibrotic reaction is attributed to an excessive deposition of extracellular matrix components including collagen and fibronectin.
The basis for Pluristem’s hypothesis that PLX cells act as anti-fibrotic agents comes from animal models given Bleomycin, an anti-cancer agent, known to induce pulmonary fibrosis and widely used to study the mechanisms involved in fibrogenesis. Bleomycin induces chromosomal DNA strands to break, which results in pulmonary inflammation and subsequent fibrosis.
In the experiments, 8-10 week old male mice were randomized to receive Bleomycin alone or Bleomycin plus PLX cells administered into the trachea. Mice that received only Bleomycin served as controls. Pertinent results at 21 days include a statistically significant improvement in oxygen saturation (p<0.05), monitored on a weekly basis during the study and a significant reduction in the collagen (p <0.001) deposition in the lungs when examined histologically. This information may suggest that the PLX cells are reactive to the fibrotic environment.
