New Study to Highlight MitoPharm's Schisandrin B Ability to Protect Against Heart Damage

SEATTLE--(BUSINESS WIRE)--MitoPharm Corporation, Inc. (Pinksheets:MTPM), announced today the results of Dr Robert Ko's, MitoPharm CTO, most recent study, which together with the previous findings on long-term schisandrin B treatment, suggests that schisandrin B can precondition heart cells, and most likely brain cells too, making them more resistant to stress conditions such as heart attack and stroke.

“Cell death isn't an event; it's a process. And in principle, a process can be interrupted. The process appears to begin in the mitochondria, which control the cell's self-destruct mechanism, known as apoptosis, and a related process, necrosis.”

Coronary heart disease remains a major health problem and the exploration of possible preventive measures aimed at ameliorating the bad consequences, including debilitation and death, arising from heart attack or cardiac arrest has been an area of intensive research. Even Newsweek recently reported in the story Doctors are reinventing how they treat sudden cardiac arrest, which is fatal 95 percent of the time. A report from the border between life and death that, “Cell death isn't an event; it's a process. And in principle, a process can be interrupted. The process appears to begin in the mitochondria, which control the cell's self-destruct mechanism, known as apoptosis, and a related process, necrosis.”

Co-incidental with the Newsweek report, Dr. Robert Ko, MitoPharm’s CSO, has just announced the latest of a series of studies on the preventive effects of Schisandrin B against heart diseases including heart attacks. In a research paper entitled “Schisandrin B decreases the sensitivity of mitochondria to calcium ion-induced permeability transition and protects against ischemia-reperfusion injury in rat hearts”;

Chiu PY, Leung HY, Siu AHL, Poon MKT, Ko KM.;Acta Pharmacologica Sinica 2007 (in press); Dr. Ko explained the pharmacology of Schisandrin B in heart protection in animal studies.

“Mitochondrial function is garnering mainstream coverage. It's becoming even clearer that mitochondria are crucially involved in determining whether cells under stress can survive or die. This recent study from the laboratory at HKUST has further corroborated its previous studies [1,2,3,4,5] that schisandrin B can target at mitochondria and render them more resistant to permeability transition – a process that eventually leads to necrotic and apoptotic cell death. This can effectively salvage the heart from ischemia/reperfusion injury, an experimental condition mimicking the heart attack,” Dr. Robert Ko, Mitopharm’s CSO.

MitoPharm will provide further updates at research report publishing time.

About MitoPharm

MitoPharm, Inc., www.mitopharm.com, is a biotechnology company that will operate in research & development, marketing, and sale of drugs, dietary supplements, and functional beverages. The initial products are based on a newly formulated compound, (-) Schisandrin B, that is the result of over 15 years of research and development by one of its founding shareholders, the Hong Kong University of Science and Technology.

Published scientific studies have confirmed that (-) Schisandrin B enhances the mitochondrial glutathione antioxidant status, a crucial factor in maintaining mitochondrial function and cell survival, plus it also induces the expression of heat shock proteins, another group of important molecules for cell protection. These biochemical actions differentiate (-) Schisandrin B from other existing, known compounds, either synthetic or naturally occurring, in its ability to protect organs including the heart, the liver, and the brain.

About HKUST

Hong Kong University of Science and Technology (HKUST) is a dynamic, international research university that is recognized as a leading science and technology institution. With an all PhD faculty, HKUST has established itself as an intellectual powerhouse and is securing a place at the top of the academic world. It's an innovator in teaching and research, plus HKUST's top-class facilities have lead to groundbreaking work in science, engineering, business, humanities and social science. For more information, visit www.ust.hk.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended (the "Exchange Act"), and as such, may involve risks and uncertainties. Forward-looking statements, which are based on certain assumptions and describe future plans, strategies, and expectations, are generally identifiable by the use of words such as "believe," "expect," "intend," "anticipate," "estimate," "project," or similar expressions. These forward-looking statements relate to, among other things, expectations of the business environment in which the Company operates, projections of future performance, potential future performance, perceived opportunities in the market, and statements regarding the Company's mission and vision. The Company's actual results, performance, and achievements may differ materially from the results, performance, and achievements expressed or implied in such forward-looking statements.

[1] Chiu PY, Ko KM: Time dependent enhancement in mitochondrial glutathione status and ATP generation capacity by schisandrin B treatment decreases the susceptibility of rat hearts to ischemia-reperfusion injury. Biofactors 2003; 19: 43-51.

[2] Chiu PY, Ko KM: Schisandrin B protects myocardial ischemia-reperfusion injury partly by inducing Hsp25 and Hsp70 expression in rats. Mol. Cell. Biochem. 2004; 266: 139-144.

[3] Ko KM, Chiu PY: Structural determinants of schisandrin B for enhancing mitochondrial functional and glutathione status as well as heat shock protein expression in rat hearts and H9c2 cells. Mol. Cell. Biochem. 2005; 276: 227-234.

[4] Chiu PY, Leung HY, Poon MKT, Ko KM: Chronic schisandrin B treatment improves mitochondrial antioxidant status and tissue heat shock protein production in various tissues of young adult and middle-aged rats. Biogerontology 2006; 7: 199-210.

[5] Chiu PY, Leung HY, Siu AHL, Poon MKT, Ko KM: Schisandrin B decreases the sensitivity of mitochondria to calcium ion-induced permeability transition and protects against ischemia-reperfusion injury in rat hearts. Acta Pharmacol. Sin. (in press) (please find the article in the attached)