BEVERLY, MA–(Marketwire – Jul 9, 2012) – Cellceutix Corporation (OTCBB: CTIX) (the “Company”), a biopharmaceutical company focused on discovering small molecule drugs to treat unmet medical conditions, reports today that a Site Initiation Visit (“SIV”) has been scheduled in July at the host hospitals, Harvard Cancer Center’s Dana-Farber Cancer Institute and Beth Israel Deaconess Medical Center, for the Company’s clinical trials of Kevetrin™, a novel anti- cancer drug for treating cancers.
A Site Initiation Visit is the last process before the clinical site is activated for enrollment by the sponsor. Amongst other things during the SIV, the research teams receive specific training on the protocol of the human trial to ensure a comprehensive knowledge of responsibilities.
“We are moving forward at a very rapid pace,” commented Leo Ehrlich, Chief Executive Officer at Cellceutix. ”The day of dosing the first patients with Kevetrin™ is quickly approaching and the excitement is building as we have high expectations as a leader in oncology research because of the p53 connection with Kevetrin™. There have been great strides made in understanding how important p53 is in tumor suppression in all stages of cancer lately, but to the best of our knowledge, we are the only company that will be conducting a human trial using a non-genotoxic drug with p53 as the Mechanism of Action. All other research is still in animal model studies or has been shown to damage surrounding DNA; leaving us on the business side in what we consider a very enviable position, and on the medical side offering the possibility of achieving a major breakthrough in the treatment of cancers.”
As a completely new class of chemistry in medicine, Kevetrin™ has significant potential to be a major breakthrough in the treatment of solid tumors. Mechanism of action studies showed Kevetrin’s unique ability to affect both wild and mutant types of p53 (often referred to as the “Guardian Angel Gene” or the “Guardian Angel of the Human Genome”) and that Kevetrin strongly induced apoptosis (cell death), characterized by activation of Caspase 3 and cleavage of PARP. Activation of p53 also induced apoptosis by inducing the expression of p53 target gene PUMA. p53 is an important tumor suppressor that acts to restrict proliferation by inducing cell cycle checkpoints, apoptosis, or cellular senescence.
In more than 50 percent of all human carcinomas, p53 is limited in its anti-tumor activities by mutations in the protein itself. Currently, there are greater than 10 million people with tumors that contain inactivated p53, while a similar number have tumors in which the p53 pathway is partially abrogated by inactivation of other signaling components. This has left cancer researchers with the grand challenge of searching for therapies that could restore the protein’s protective function, which Kevetrin appears to be doing the majority of the time.