We are developing other recombinant therapeutic proteins to be expressed by our ProCellEx™ protein expression system, with an emphasis on treatments for which there are large, established pharmaceutical markets and where our proprietary protein expression system enables us to develop and commercialize recombinant proteins that are patent-protected and therapeutically equivalent or superior to the existing treatments. We select additional therapeutic candidates for development by testing candidates in-house and through collaborations with academic partners. We have identified several product candidates oriented towards specialty disease and therapeutic market segments, including treatments for Fabry disease. In addition, we are conducting initial research to evaluate potential programs in the fields of monoclonal antibodies, cytokines and vaccines. We plan to file an investigational new drug application (IND) with the FDA with respect to an additional product during second half of 2010. In addition, we are developing a new method for delivering active recombinant proteins systemically through oral administration of transgenic plant cells expressing such biotherapeutic proteins.
We are developing a proprietary alpha Galactosidase enzyme, currently titled PRX-102, which is a therapeutic enzyme for the treatment of Fabry disease, a rare genetic lysosomal storage disorder in humans, the symptoms of which involve the accumulation of lipids in the cells of the kidneys, heart and other organs. Fabry disease affects more than 8,000 people globally. We believe that the treatment of Fabry disease is a specialty clinical niche with the potential for high growth. Currently there are two drugs available on the market to treat Fabry disease. Fabrazyme, made by Genzyme, was approved for the treatment of Fabry disease in the European Union in 2001 and the United States in 2003.. Genzyme reported $431 million in worldwide sales of Fabrazyme in 2009, compared to $494 million in 2008. According to Genzyme, it suffered a temporary interruption in production of Fabrazyme in 2009 associated with the remediation of a contamination in one of its manufacturing facilities, and, as a result, shipments of Fabrazyme were limited during the second half of 2009. The other approved drug for the treatment of Fabry disease in the European Union is Replagal, which is sold by Shire plc. Shire reported $194 million in sales of Replagal in 2009. According to public reports by Shire, it filed a BLA with the FDA for Replagal in the United States in December 2009. We are currently in the animal evaluation testing phase of the development of PRX-102, which tests are based on a well established mouse model for Fabry disease and expect to profile an IND with FDA following such trials. As was the case in our development of prGCD, our development of PRX-102 involves the expression by our proprietary protein expression system of a naturally occurring enzyme to be used in enzyme replacement therapy for the treatment of Fabry disease. Based on our experience with prGCD and the experience of other companies developing enzyme replacement therapies for Fabry disease, we have reason to believe that, if favorable data is accumulated in preclinical and phase I clinical trials, the FDA may allow us to proceed directly with a pivotal phase III clinical trial without the need to complete a phase II clinical trial. However, there can be no assurance that we will initiate preclinical or Phase I clinical trials and if we do, that such trials will result in favorable data. In addition, there can be no assurance that the FDA will allow us to proceed directly with a phase III clinical trial after completion of a phase I clinical trial.
PRX-105 is a plant cell expressed PEGylated recombinant human Acetylcholinestrase (AChE) for the use in the biodefense arena for therapeutic and prophylactic indications for nerve agents attack. The development program is conducted under FDA and Israeli Ministry of health and is under license agreement with Yissum Research and Development, the technology transfer arm of the Hebrew University of Jerusalem, Israel, and with the Boyce Thompson Institute, Inc., affiliated with Cornell University. Protalix has extended its agreement with Yissum to include a collaborative research program to be conducted in the laboratory of Professor Hermona Soreq, a world leader in this field. In addition, Professor Aharon Ciechanover, a Laureate of the Nobel Prize in Chemistry, member of Protalix Scientific Advisory Board, and former head of the Israeli Defense Forces (IDF) chemical warfare defense program, closely advises the AChE program. Protalix completed its phase I clinical trial of PRX-105 in June 2010, The trial established the pharmacokinetics of the protein and demonstrated that single dose, intravenous administration of PRX-105 is safe and well tolerated. The Company plans to perform additional safety studies in healthy volunteers and animals in collaboration with civil and military agencies in the United States and Israel, for which discussions have been initiated. Given the nature of the biodefense indications for which the Company is developing PRX-105, efficacy trials of PRX-105 in humans (phase II and phase III) are not required. The phase I clinical trial of PRX-105 is a first in human, open label, non-randomized, single-dose study. PRX-105 was administered intravenously by slow bolus injection to 10 healthy volunteers in the trial. The trial was conducted in collaboration with Professor Hermona Soreq. Pre-clinical studies have indicated that PRX-105 successfully protects animals exposed to organophosphate nerve gas agent analogs, in both the prophylactic and post-exposure settings.
We are developing pr-antiTNF, a biosimilar version of etanercept (Enbrel™) using the Company's proprietary ProCellEx™ technology. pr-antiTNF is a plant cell expressed recombinant fusion protein made from the soluble form of the human TNF receptor (TNFR), fused to the Fc component of a human antibody IgG1 domain. Pr-antiTNF has an identical amino acid sequence to Enbrel™. In vitro and preclinical animal studies have demonstrated that pr-antiTNF exhibits similar activity to Enbrel™. Specifically, pr-antiTNF binds TNF alpha thereby inhibiting it from binding to cellular surface TNF receptors and protects L929 cells from TNF-induced apoptosis in a dose-dependent manner. In a proof-of-concept in vivo study using an established arthritis animal model, pr-antiTNF administered intraperitoneally significantly improved the clinical arthritis parameters associated with this accepted arthritis mouse model including joint inflammation, swelling and tissue degradation. Data from the collagen induced arthritis animal model studies are expected to be presented at an upcoming scientific conference.