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SPX-106T Arrests Development of Atherosclerotic Plaques in Mouse Model of Cardiovascular Disease
Date:3/7/2012

evented body weight gain. These data also support Spherix's other findings that SPX-106T reduced atherosclerotic lesion areas in the aortic arches of LDL receptor-deficient mice fed fructose and glucose.

"As we continue the development program for SPX-106T, we are gaining valuable insight into the therapeutic potential for SPX-106T. We are looking forward to bringing SPX-106T into human clinical trials in 2012," noted Dr. Claire Kruger, CEO of Spherix.

LDL-cholesterol is a known risk factor for the development of atherosclerosis in humans.(4) Spherix has previously shown that LDL-cholesterol is reduced in LDL receptor-deficient mice treated with SPX-106T.

"This is a very exciting time for Spherix," remarked Dr. Robert Lodder, Spherix's President. "We have now tested SPX-106T in two different genetic models and are looking into the underlying mechanisms by which SPX-106T prevents plaque development in the apolipoprotein E-deficient mice. We are also expanding the applications of SPX-106T to other indications where dyslipidemia may be a primary risk factor."

About Spherix
Spherix Incorporated was launched in 1967 as a scientific research company under the name Biospherics Research.  The Company now leverages its scientific and technical expertise and experience through its two subsidiaries – Biospherics Incorporated and Spherix Consulting, Inc.  Biospherics is dedicated to developing and licensing/marketing proprietary therapeutic products for treatment of diabetes, metabolic syndrome and atherosclerosis.  Biospherics is actively seeking a pharmaceutical partner to continue the development of its Phase 3 compound for the treatment of diabetes, D-tagatose, while exploring new drugs and combinations for treatment of high triglycerides, a risk factor for atherosclerosis, myocardial infarction, and stroke.  Spherix's Consulting subsidiary provides scientific and strategic support for suppliers, manufacture
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