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The Company’s lead product, Oncoprex™, is a biologic therapy targeting key oncogenic pathways to treat tumors and cancer metastases at the molecular level. The active anti-cancer agent in Oncoprex is TUSC2, also known as FUS1, which is incorporated into nanovesicles and formulated for intravenous administration. TUSC2 was originally discovered as a tumor suppressor and was subsequently confirmed as a powerful pan-kinase inhibitor.

Normal TUSC2 function is inactivated at the early onset of cancer development making it a potential target for all stages of cancer including metastatic disease. TUSC2 protein is reduced or absent in over 80% of lung cancers. Key TUSC2 mechanisms of action include the inactivation of multiple oncogenic kinases, the induction of apoptosis and the control of cell signaling and inflammation.

Data shows that the majority of cancer drugs could be positively impacted with the addition of TUSC2-mediated therapy. Oncoprex is a biologic anti-cancer therapy comprising a cassette containing the TUSC2 pan-kinase inhibitor incorporated into nanovesicles and administered to patients intravenously. Oncoprex nanovesicles are non-immunogenic, allowing the particles to travel through the patient’s body to selectively and preferentially target cancer cells.

Oncoprex has been evaluated as a single agent in a phase I clinical trial in Stage IV lung cancer patients at the University of Texas MD Anderson Cancer Center (UTMDACC). This study established the phase II dosage and demonstrated that Oncoprex was well tolerated. Tumor regressions were observed in primary lung tumors and metastatic cancers in liver, pancreas, and lymph nodes. Analyses of pre- and post-treatment patient biopsies demonstrated that intravenous Oncoprex monotherapy selectively and preferentially targeted patients’ cancer cells resulting in TUSC2-mediated clinical anti-cancer activity.

Our research has shown significant cancer killing synergy when Oncoprex is combined with a variety of Tyrosine Kinase Inhibitors (TKIs) including EGFR, AKT, PDGFR and src targeted TKIs. Data from in vivo studies in multiple cancers shows that Oncoprex works synergistically with EGFR TKIs in both EGFR mutation negative (EGFR wild type) cancers and EGFR mutation positive cancers resistant to EGFR TKIs. The studies included combination use with Oncoprex and either Iressa® (gefitinib), Tarceva® (erlotinib) as well as other TKIs. The studies demonstrated that combining Oncoprex with EGFR TKIs in EGFR wild type cancers resulted in significantly enhanced anti-cancer activity.

Pre-clinical data showed that when Oncoprex is combined with EGFR TKI therapy in EGFR mutated and TKI resistant cancers, the Oncoprex combination overcomes drug-induced and intrinsic therapeutic resistance by simultaneously inactivating the EGFR and the AKT signaling pathways in the cancers that have become resistant to EGFR TKI therapy, thus inducing apoptosis. Importantly, synergistic anticancer results were also obtained from studies combining Oncoprex with EGFR TKIs in K-ras associated cancers, which are significant in that patients with K-ras mutation cancers are, in general, unresponsive to EGFR TKIs.

An FDA approved phase I/II clinical trial protocol will be used to evaluate Oncoprex + erlotinib in Stage IIIb/IV NSCLC patients without an activating EGFR mutation(prior chemo)and patients with an activating EGFR mutation, progressing on erlotinib. Pre- and post-treatment biopsies from each patient will be analyzed for prognostic biomarkers.