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Jennerex Publishes Promising Results from Cancer Clinical Trial of JX-594 in Lancet Oncology
Date:5/21/2008

ated with long-term survival in many patients, including four who survived for 11 to over 18 months. Mechanism-of-action of JX-594 was validated in patients by demonstration of tumor-specific replication and tissue destruction with JX- 594, in addition to high-level active expression of the GM-CSF protein in the blood of patients. These results led to the initiation of a Phase II liver cancer trial that is now open in the U.S., and will shortly begin enrolling patients at sites in South Korea and Canada, as well.

About JX-594

JX-594 is a cancer biotherapeutic, currently in Phase II trials, from a proprietary class of targeted and armed oncolytic poxviruses. Tumor destruction and safety was shown in patients with diverse cancer types in three Phase I trials; treated patients were end-stage and had no effective therapies available. JX-594 multiplies selectively within cancer cells, leading to their destruction. These newly created copies of JX-594 are then released and are able to infect and eradicate other tumor cells both locally and in distant sites in the body. This cycle of JX-594 replication, cancer cell destruction, release and spread is then repeated. Normal cells are not affected by JX-594 resulting in safety and tolerability. The poxvirus strain backbone of JX-594 has been used safely in millions of people as part of a worldwide vaccination program against smallpox. This strain naturally targets cancer cells due to common genetic defects in cancer cells. JX-594 was engineered to enhance this natural safety and cancer-selectivity by deleting its thymidine kinase (TK) gene, thus making it dependent on the cellular TK expressed at persistently high levels in cancer cells. To enhance product efficacy, JX-594 is also engineered to express the GM-CSF protein. GM-CSF complements the cancer cell lysis work of the product candidate, leading to a cascade of events resulting in tumor necrosis, tumor vasculature shutdown and an anti-tumoral immune attack.
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