Zensun focuses on studying the mechanism of disease and seeking treatments for patients who have energy metabolism diseases. We are delving deeply and widely into the relationship between energy metabolism pathways and the occurrence and development of disease in order to discover key sites for drug targeting. We are making every effort to apply our advances in scientific research to clinical treatment in order to improve the quality of patients’ lives.

During nutrient metabolism, the chemical energy of nutrient components is transferred into ATP, which transports and provides the required energy to maintain the activities of life.

Physiologically, energy metabolism abnormalities and reduction of mitochondrial activity are two important characteristics of aging. As people age, there is a significant reduction in the level of CoQ10 [1], an essential coenzyme of mitochondrial ATP synthesis. The level of ATP is decreased by 50%, when comparing people age 70 with people age 20[2]. Obviously, a decline in the level of energy metabolism is a common phenomenon in the elderly. Aging is also associated with other declines in physical abilities that may affect nutrient intake. The ability to taste and smell food declines with age, physical activity may decline due to a variety of ailments such as arthritis, and the sensation of hunger may also decline [3]. A reduction of nutrient intake in the elderly may ultimately lead to a decrease in the level of energy metabolism (ATP production). Because the level of energy metabolism has a close relationship with normal organ functions, degenerative diseases, such as gastrointestinal dysfunction and nervous system diseases, may be the result in the elderly patient.

In gastrointestinal diseases, studies have shown that mitochondrial molecular or energy metabolism disorders may be involved in the pathogenesis of constipation. Improving mitochondrial energy metabolism may therefore be a fundamental solution for improving and restoring the function of organs of the gastrointestinal tract [4]. Research into methods of enhancing the level of energy metabolism in the gastrointestinal tract has indicated that this approach may lead to increasing intestinal motility and curing constipation.

Zensun has recognized the important relationship between energy metabolism and the mechanism of constipation. Based on this understanding of the disease mechanism, Zensun is creating new metabolic drugs, targeting many key sites of energy metabolism, to solve gastrointestinal dysfunctions and to bring abnormal gastrointestinal movement back to a normal rhythm. We will provide a safe and effective product without dependence for patients with functional constipation.

In neurological diseases, studies have shown that the level of energy metabolism is reduced significantly in the brain of Alzheimer's patients. Glucose metabolism via glycolysis and the Krebs cycle are important components of energy metabolism, and neurological activity in brain tissue depends entirely on energy provided by glucose metabolism. Some studies have found that abnormal glucose metabolism is associated with the development and progression of neurodegenerative diseases, such as Alzheimer's disease (AD). With exacerbation of the disease, the level of glucose metabolism in the brain decreases, and functional activities of the entire brain area gradually diminish [4,5].

proprietary combination drug ZS-07, Zensun has found that brain energy metabolism can be enhanced by increasing glucose metabolism, and this drug showed a significant therapeutic effect in an AD animal model. We are now studying correlated molecular mechanisms in order to achieve breakthrough success in the field of AD therapy and hope to provide an effective product for patients with AD.


[1] Mancuso M, Orsucci D, Volpi L, et al. Coenzyme Q10 in neuromuscular and neurodegenerative disorders[J]. Current drug targets, 2010, 11(1): 111-121.

[2] Short K R, Bigelow M L, Kahl J, et al. Decline in skeletal muscle mitochondrial function with aging in humans[J]. Proceedings of the National Academy of Sciences of the United States of America, 2005, 102(15): 5618-5623.

[3] Montejo González J C, Culebras-Fernández J M, García de Lorenzo y Mateos A. Recomendaciones para la valoración nutricional del paciente crítico[J]. Revista médica de Chile, 2006, 134(8): 1049-1056.

[4] Abolhassani N, Leon J, Sheng Z, et al. Molecular pathophysiology of impaired glucose metabolism, mitochondrial dysfunction, and oxidative DNA damage in Alzheimer's disease brain[J]. Mechanisms of ageing and development, 2016.

[5] Jagust W, Gitcho A, Sun F, et al. Brain imaging evidence of preclinical Alzheimer's disease in normal aging[J]. Annals of neurology, 2006, 59(4): 673-681