Insight Into Cellceutix Corporation's Breakthrough Cancer Compound

BEVERLY, MA--(Marketwire - May 3, 2011) - Cellceutix Corporation (OTCQB: CTIX), a biopharmaceutical company focused on discovering and developing small molecule drugs to treat unmet medical conditions including drug-resistant cancers, today provided additional insight into the uniqueness of Kevetrin™, its flagship cancer compound in development. Kevetrin™ is a proprietary novel molecule which has a distinct advantage over other compounds in development, or drugs in current use. The advantage lies in its mode of action. Kevetrin not only activates p53 in a non-genotoxic manner, it also acts as a double-edged sword in killing tumor cells. Kevetrin activates both transcription-dependent and transcription-independent pathways to promote apoptosis (programmed cell death). Kevetrin also alters E3 processivity of MDM2. Monoubiquitination of p53 by Kevetrin not only stabilizes both wild type and mutant p53, but also induces apoptosis in mutant p53. Kevetrin showed potent efficacy in many mutant and wild type tumor xenograft models, thus Kevetrin demonstrated effectiveness in a wide range of tumor types. To the best of our knowledge, no other compound has shown such potent efficacy in tumors of varied p53 status.

The development of cancer is a multistage process driven by a progressive accumulation of mutations and epigenetic abnormalities in multiple genes that have highly diverse functions. Today's commonly used drugs (e.g. trastuzumab, gefitinib and imatinib) target either specific molecules (such as HER2 for trastuzumab and EGFR for gefitinib) or functions as a multikinase inhibitor (imatinib). This approach is based on the observation that a tumor cell, despite its plethora of genetic alterations, can seemingly exhibit dependence on a single oncogenic pathway or protein for its sustained proliferation and/or survival, termed oncogene addiction. These agents target specific oncogenes in human cancer and causes cell death. However, the clinical responses in most of the cases are relatively short-lived. This is most clearly illustrated in the case of erlotinib where clinical response typically averages only 6-9 months in duration and is almost invariably followed by disease progression. Thus clinical experience with molecular targeted agents shows that cancers can escape a given state of oncogene addiction through mutations in other genes and pathways.

The activation (or reactivation) of p53 is a promising strategy for cancer treatment. Restoration of p53 tumor suppressor pathways triggers massive apoptosis through the intrinsic mitochondrial mediated pathway of apoptosis. This approach has the capacity to treat a wide range of tumors, but demonstrating success has been elusive to researchers. MDM2, an ubiquitin ligase for p53, plays a central role in the stability of p53. Nutlins and RITA compounds inhibit the interaction between p53 and MDM2. Both compounds induce apoptosis in the tumor, but are limited to normal or wild type p53. Additionally, Nutlin has been shown to be genotoxic. Other compounds, e.g., CP-31398, PRIMA-1, ellipticine, target mutant p53 only. Mutant p53 is a complex target since it is not one protein, but rather an extensive array of proteins with different properties that limit the range of tumors treated by these compounds. In addition, the clinical use of ellipticine has been limited by toxic side effects.

Based on these scientific parameters, Kevetrin has the unique ability to target tumors independent of p53 status and induce apoptosis thereby controlling tumor growth in a wide range tumor types, setting it apart from today's therapies and other compounds in development.

About Cellceutix

Cellceutix Corporation is a preclinical cancer, anti-inflammatory and autism drug developer. Cellceutix owns the rights to eight drug compounds, including Kevetrin, which it is developing as a treatment for certain cancers, KM-133, for the treatment of psoriasis, and KM-391, for the treatment of autism. More information is available on the Cellceutix web site at