Kevetrin "Trumps" the "Competition" Kevetrin™

Kevetrin "Trumps" the "Competition"

Kevetrin™ Stands Out in Its Mechanism of Action by Activating Both Transcription-Dependent and Transcription-Independent Pathways to Promote Apoptosis in a Non-Genotoxic Manner and Targets Both Mutated and Wild Type p53

BEVERLY, MA–(Marketwire – Apr 25, 2011) – Cellceutix Corporation (OTCQB:  CTIX ) (OTCBB:  CTIX ), a biopharmaceutical company focused on discovering and developing small molecule drugs to treat unmet medical conditions including drug-resistant cancers, announced that at the 102nd annual American Association for Cancer Research (AACR) meeting held in Orlando, FL, April 2nd to 6th, four posters described new compounds that directly affected p53 function. p53, also known as the “Guardian Angel of the human genome” due to its crucial role in controlling cell mutations, is a tumor suppressor protein that is encoded by the TP53 gene in humans and has been widely regarded as possibly holding a key to the future of cancer therapies. Aside from Cellceutix’s compound, Kevetrin™, none of the other three compounds demonstrated success against a broad spectrum of cancers.

Compound A and Compound B, reported by Wang, et al, (Ascenta Therapeutics, Abstract #LB-204) and MI-63 reported by Scott et al, (Abstract #4507) showed efficacy in tumors limited to wild type p53. Pernaza et al, (Abstract #3242) reported that compound E12/DP13-117 was also “expected to work” on tumors containing only wild type p53. These novel compounds only affect tumors with wild type p53. Kevetrin™ affects both wild type and mutant p53 by modulating E3 ligase processivity, a unique mechanism of action which distinguishes it from the other three drugs.

CEO of Cellceutix, Leo Ehrlich, commented, “It is often times difficult to explain the magnitude of the potential of Kevetrin™. Compounds that affect only wild type p53 address only a fraction of the tumors that Kevetrin™ has the potential to treat. This past June, an emerging biopharmaceutical company announced they had signed an agreement with a major pharmaceutical company covering early-stage agents being investigated for their potential to restore tumor cell apoptosis related to p53. Per the announcement, milestone payments could reach approximately $400 million in addition to royalties from sales. It seems that that compound is also at an earlier stage of development than ours. Considering that Kevetrin could potentially address double the number of cancer patients with either mutated or wild type p53, I would expect Kevetrin™ to have a value significantly greater than that.”