New Studies Support Use Of Agent To Reduce, Stabilize Vulnerable Plaques

 

April 19, 2012
Representative cross-section of an atherosclerotic plaque in the coronary artery of a human that died of a myocardial infarction. The atherosclerotic plaque fills the entire left portion of the artery, is separated from the central cavity by the fibrous cap, and restricts blood flow in the artery.

April 19, 2012 — Spherix Inc. announced results from its recently completed studies using near-infrared spectroscopy on autopsy samples from humans who had confirmed cardiovascular disease. Results showed that these atherosclerotic plaques had abnormally high amounts of macrophages and reduced levels of collagen and elastin. Reducing collagen and elastin weakens the plaques and contributes to plaque rupture, myocardial infarction and/or stroke (see photo). [1]

Importantly, these findings show the relevance of Spherix's newly completed study involving its drug candidate D-tagatose and LDLR-/- mice, which are predisposed to developing atherosclerosis and mimic the pathogenesis of atherosclerosis in humans. Similar to what was found in the human study, infrared spectrometric imaging of diseased vascular samples from mice given an atherogenic diet containing high amounts of sucrose showed increases in macrophages and reductions in collagen and elastin content. The mice fed an atherogenic diet containing D-tagatose but not sucrose showed significantly fewer plaques and infrared spectrometric imaging of the plaques that developed revealed fewer macrophages, and more collagen and elastin. These results suggest that D-tagatose not only reduces the number of plaques formed, but also may stabilize atherosclerotic plaques.

LDL cholesterol particles imbedded within atherosclerotic plaques have been reported to attract circulating monocytes into the lesion, thereby leading to the accumulation of macrophages in the plaque and weakening of atherosclerotic lesions.[2] Diets high in fat, cholesterol and carbohydrates promote the development of atherosclerosis in both animals and humans by increasing triglycerides and LDL cholesterol in the blood. Robert Lodder, M.D., president of Spherix remarked, "We know that our drug candidate, SPX-106T, significantly reduces the number of atherosclerotic plaques in animal models. These new results, however, are very exciting because they not only support Spherix's previous findings, but also open the door to new therapeutic opportunities."

"It is encouraging to note that D-tagatose has a beneficial effect on atherosclerosis and Spherix is successfully providing experimental evidence that our two drug candidates in combination therapy, SPX-106T, work synergistically to produce the desired therapeutic activity needed to advance SPX-106T through clinical and regulatory development," said Claire Kruger, M.D., Spherix's CEO. "SPX-106T is consistent with our business strategy to develop combination drugs that affect multiple pathways to disease."

For more information: www.spherix.com

References:

[1]. Finn AV, Nakano M, Narula J, Kolodgie FD, Virmani R, "Concept of vulnerable/unstable plaque,"
Arterioscler. Thromb. Vasc. Biol. 30 (7): 1282-92, July 2010.

[2]. Kreuzer J, Denger S, Jahn L, Bader J, Ritter K, von Hodenberg E, Kubler W, "LDL Stimulates
Chemotaxis of Human Monocytes Through a Cyclooxygenase-Dependent Pathway, Arteriosclerosis,
Thrombosis, and Vascular Biology," 16:1481-1487, 1996.

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