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Senhwa Biosciences Announces CX-5461 Research Findings to be Presented at AACR

Studies Identify PI3K Pathway Combinations and MYC Driven Cancers

SAN DIEGO and NEW TAIPEI CITY, Taiwan, March 27, 2014 /PRNewswire-iReach/ -- Senhwa Biosciences, Inc. announced today that results from research with its first-in-class Pol I inhibitor, CX-5461, will be presented at the 2014 American Association for Cancer Research (AACR) annual meeting held on April 5-9 in San Diego, CA. Prof. Ross Hannan and Prof. Rick Pearson of the Peter MacCallum Cancer Centre (PMCC) will present data highlighting synergistic combinations of CX-5461 with PI3K pathway inhibitors and its potential for the treatment of MYC driven lymphoma, melanoma and ovarian cancers. CX-5461, which activates p53 through a unique mechanism, is currently in Phase I clinical trials for the treatment of patients with blood cancers.

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The data driving CX-5461's development for combination therapies and expansion into solid tumors will be presented on Monday, April 7, 2014, from 1-5 pm in the San Diego Convention Center. The poster "Co-ordinated inhibition of ribosome synthesis and function provides a novel and potent therapeutic approach to treat MYC driven malignancy", abstract 2735, will be in Hall A-E, Section 34 at Board 6, and "Targeting Ribosome Biogenesis with CX-5461 as a Potential Treatment for Melanoma and Ovarian Cancer", abstract 2718, will be in Hall A-E, Section 33 at Board 19.

"We are excited to build upon the preclinical work that launched CX-5461 into a Phase I trial in hematological malignancies", commented Prof. Grant McArthur, Head of the Cancer Therapeutics Program at PMCC. "In addition to the use of CX-5461 in cancers with wild-type p53, we continue to explore the broader combination potential for a molecule with a unique mechanism of action. The research clearly identifies impressive activity in MYC driven cancers, which gives rises to particularly aggressive and difficult to treat disease."

"The potential of this first-in-class molecule as both a single agent and in combination is reflected in the impressive data from PMCC. These studies inform and support our development strategy for CX-5461," said Dr. Tai-Sen Soong, President of Senhwa Biosciences. "Single agent trials in hematological malignancies are being pursued in both Australia and the US, with combination strategies in both solid and blood cancers being formulated."

About CX-5461

Senhwa's lead anticancer compound for treating hematological malignancies is CX-5461, a p53 activating Pol I inhibitor, currently in a Phase I clinical trial at the Peter MacCallum Cancer Centre in Melbourne, Australia. CX-5461 has a unique mechanism of action that enables selective activation of p53 in tumor cells but not in normal healthy ones, destroying malignant tissue while sparing the patient from the serious side effects associated with cancer therapies.

About Senhwa Biosciences

Senhwa Biosciences identifies and develops innovative therapies that have the potential to fundamentally change the way patients are treated. Our central philosophy is to unearth validated targets or therapies that could significantly improve treatment, but have not yet been properly exploited. As a value-added development company, Senhwa aims to take innovative therapies that could impact the current standard of care and drive them through clinical Proof-of-Concept.

Senhwa has a strong Management Team with proven track records in developing new drugs and targeted agents. Headquartered in Taiwan, but with a vital operational base in San Diego, California, the Senhwa Team is well positioned to oversee the development of their compounds by collaborating with a diverse range of global Investigators and service providers. Clinical trials are ongoing or planned for Australia and the US, and service providers work from their bases in North America, Asia, Australia and Europe.For more information on Senhwa and its programs, please visit www.senhwabiosciences.com.

Media Contact: Sean O'Brien, Senhwa Biosciences, 8585526808, [email protected]

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