Manchester, NH, United States

Boston Therapeutics
Manchester, NH, United States
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LAWRENCE, Mass., June 19, 2017 (GLOBE NEWSWIRE) -- Mr. Carl Rausch, CEO of Boston Therapeutics, Inc. (OTCQB:BTHE) and its Asian partner Advance Pharmaceutical Company Limited, Hong Kong had data presented from the proof of concept trial (Protocol Code: SG01) conducted by the Chinese University of Hong Kong (CUHK). Presentation is made this June 2017 in a presentation at the ADA’s 77th scientific sessions (Abstract: Hyperglycemia in High-Risk Chinese Subjects with Prediabetes) in San Diego, California (June 9-13). A copy of the abstract is printed in the Scientific Sessions Abstract Book (June 2017), supplement to the journal Diabetes. This 16-week, phase 2, double blind, randomized, placebo-controlled, POC study in Chinese subjects with pre-diabetes examined for the glucose-management effects of BTI320 and the demonstration of the safety as well as the positive drug effect of BTI320 on postprandial hyperglycemia in the selected population. Both the clinical report and manuscript are under preparation for submission to competent authorities for review with the goal of supporting the on-going clinical development of the compound. Clinical findings of the trial have been posted on (NCT02358668) as of Jan 2017. Type 2 diabetes is a multi-factorial disease and the biggest challenge in maintaining healthy blood sugar level is the management of post-prandial (after meal) sugar spikes. Targeting post-meal plasma glucose is an important strategy for achieving optimal glycemic control in the long run. Given the clinical significance on the development and progression of diabetes and related metabolic syndromes, special focus for intervention including personalized diets to control postprandial glucose excursion (PPGE) and glycemic variability for modification in subsequent metabolic consequences were considered in this POC study in high risk pre-diabetic Chinese subjects. Results show that BTI320 significantly reduced postprandial hyperglycemia and glycemic variability, as measured by CGMS in subjects at high risk for diabetes. No significant differences were detected (normal range fructosamine) in subjects treated with BTI320 and placebo, nonetheless, significant attenuation of postprandial hyperglycemia and multiple CGM glycemic variability parameters were observed in subjects receiving BTI320 (4g) compared with placebo. It is also noted that treatment with 4g BTI320 significantly reduced post-prandial glucose AUC at 1, 2 and 3 hours post meal and modestly reduced body weight. We believe that this may be the optimal dose in terms of delaying glucose absorption in the GI tract. Overall, BTI320 was well tolerated and these positive findings suggest that BTI320 works by predominately suppressing postprandial glucose excursion, slowing down the rate of glucose excursion, as well as reducing the absolute amount absorbed, thereby preventing hyperglycemia without the risk of hypoglycemia. As such, BTI320, if approved, may potentially slow down and possibly delay diabetes progression. Given the ease of administration and high levels of tolerance, BTI320 has the potential to be used as an adjunct to lifestyle modification for diabetes prevention. SugarDown® The Company also developed and markets SugarDown®, a sugar blocker dietary food supplement designed to support glycemic health. More information is available at SugarDown® in its present formulation is a natural sugar blocker dietary supplement product made entirely from a non-digestible sugar molecule that can help people maintain healthier weight levels and is the first chewable tablet of its kind. In a previous study, SugarDown® demonstrated significant reduction of glucose and insulin Area Under the Curve (AUC) when taken with Jasmine rice, a food with a glycemic index of about 90 compared to glucose, which is 100.  Sugary soft drinks that also have high glycemic index, include sucrose and maltose which is also found in beer. More information can be found on About Boston Therapeutics, Inc. Boston Therapeutics, headquartered in Lawrence MA, (OTCQB:BTHE) is an innovator in designing compounds using complex carbohydrate chemistry. The company's product pipeline is focused on developing and commercializing therapeutic molecules that address diabetes and inflammatory diseases, including: BTI-320, a non-systemic chewable therapeutic compound designed to reduce HbA1 . Forward Looking Statement This press release includes forward-looking statements. These statements may be identified by words such as “feel,” “believes,” “expects,” “estimates,” “projects,” “intends,” “should,” “is to be,” or the negative of such terms, or other comparable terminology. Forward-looking statements are statements that are not historical facts. Such forward-looking statements are subject to risks and uncertainties, which could cause actual results to differ materially from the forward-looking statements contained herein. Factors that could cause actual results to differ materially include, but are not limited to: our limited operations and need to expand in the near future; risks associated with obtaining regulatory approval of our products; the ability to protect our intellectual property; the potential lack of market acceptance of our products; potential competition; our inability to retain key members of our management team; our inability to raise additional capital to fund our operations and business plan; our ability to continue as a going concern; our liquidity and other risks and uncertainties and other factors discussed from time to time in our filings with the Securities and Exchange Commission (“SEC”), including our annual report on Form 10-K filed with the SEC. Boston Therapeutics expressly disclaims any obligation to publicly update any forward-looking statements contained herein, whether as a result of new information, future events or otherwise, except as required by law.

Sullivan E.,Massachusetts General Hospital | Hudson J.,Boston Therapeutics
Orthopaedic Nursing | Year: 2017

Most psychologists treat the mind as disembodied, a phenomenon with little or no connection to the physical body. Conversely most physicians treat the body with no regard to the mind or the emotions. But the body and mind are not separate, and we cannot treat one without the other. © 2017 by National Association of Orthopaedic Nurses.

Roberto M.,Scripps Research Institute | Cruz M.T.,Scripps Research Institute | Gilpin N.W.,Scripps Research Institute | Sabino V.,Scripps Research Institute | And 11 more authors.
Biological Psychiatry | Year: 2010

Background: Corticotropin-releasing factor (CRF) and gamma-aminobutyric acid (GABA)ergic systems in the central amygdala (CeA) are implicated in the high-anxiety, high-drinking profile associated with ethanol dependence. Ethanol augments CeA GABA release in ethanol-naive rats and mice. Methods: Using naive and ethanol-dependent rats, we compared electrophysiologic effects and interactions of CRF and ethanol on CeA GABAergic transmission, and we measured GABA dialyzate in CeA after injection of CRF1 antagonists and ethanol. We also compared mRNA expression in CeA for CRF and CRF1 using real-time polymerase chain reaction. We assessed effects of chronic treatment with a CRF1 antagonist on withdrawal-induced increases in alcohol consumption in dependent rats. Results: CRF and ethanol augmented CeA GABAergic transmission in naive rats via increased GABA release. Three CRF1 receptor (CRF1) antagonists decreased basal GABAergic responses and abolished ethanol effects. Ethanol-dependent rats exhibited heightened sensitivity to CRF and CRF1 antagonists on CeA GABA release. Intra-CeA CRF1 antagonist administration reversed dependence-related elevations in GABA dialysate and blocked ethanol-induced increases in GABA dialyzate in both dependent and naive rats. Polymerase chain reaction studies indicate increased expression of CRF and CRF1 in CeA of dependent rats. Chronic CRF1 antagonist treatment blocked withdrawal-induced increases in alcohol drinking by dependent rats and tempered moderate increases in alcohol consumption by nondependent rats in intermittent testing. Conclusions: These combined findings suggest a key role for specific presynaptic CRF-GABA interactions in CeA in the development and maintenance of ethanol dependence. © 2010 Society of Biological Psychiatry.

Claria J.,Boston Therapeutics | Nguyen B.T.,Harvard University | Madenci A.L.,Harvard University | Keith Ozaki C.,Harvard University | Serhan C.N.,Boston Therapeutics
American Journal of Physiology - Cell Physiology | Year: 2013

Adipose tissue is a heterogeneous organ with remarkable variations in fat cell metabolism depending on the anatomical location. However, the pattern and distribution of bioactive lipid mediators between different fat depots and their relationships in complex diseases have not been investigated. Using LC-MS/MS-based metabolo-lipidomics, here we report that human subcutaneous (SC) adipose tissues possess a range of specialized proresolving mediators (SPM) including resolvin (Rv) D1, RvD2, protectin (PD) 1, lipoxin (LX) A4, and the monohydroxy biosynthetic pathway markers of RvD1 and PD1 (17-HDHA), RvE1 (18-HEPE), and maresin 1 (14-HDHA). The "classic" eicosanoids prostaglandin (PG) E2, PGD2, PGF2α, leukotriene (LT) B4, 5-hydroxyeicosatetraenoic acid (5-HETE), 12-HETE, and 15-HETE were also identified in SC fat. SC fat from patients with peripheral vascular disease (PVD) exhibited a marked deficit in PD1 and 17-HDHA levels. Compared with SC, perivascular adipose tissue displayed higher SPM levels, suggesting an enhanced resolution capacity in this fat depot. In addition, augmented levels of eicosanoids and SPM were observed in SC fat surrounding foot wounds. Notably, the profile of SC PGF2α differed significantly when patients were grouped by body mass index (BMI). In the case of peri-wound SC fat, BMI negatively correlated with PGE2. In this tissue, proresolving mediators RvD2 and LXA4 were identified in lower levels than the proinflammatory LTB4. Collectively, these findings demonstrate a diverse distribution of bioactive lipid mediators depending on the localization of human fat depots and uncover a specific SPM pattern closely associated with PVD. © 2013 the American Physiological Society.

Yuan K.,University of Sichuan | Yuan K.,University of North Dakota | Huang C.,University of Sichuan | Fox J.,University of North Dakota | And 6 more authors.
Journal of Cell Science | Year: 2012

Intracellular bacteria have been shown to cause autophagy, which impacts infectious outcomes, whereas extracellular bacteria have not been reported to activate autophagy. Here, we demonstrate that Pseudomonas aeruginosa, a Gram-negative extracellular bacterium, activates autophagy with considerably increased LC3 punctation in both an alveolar macrophage cell line (MH-S) and primary alveolar macrophages. Using the LC3 Gly120 mutant, we successfully demonstrated a hallmark of autophagy, conjugation of LC3 to phosphatidylethanolamine (PE). The accumulation of typical autophagosomes with double membranes was identified morphologically by transmission electron microscopy (TEM). Furthermore, the increase of PE-conjugated LC3 was indeed induced by infection rather than inhibition of lysosome degradation. P. aeruginosa induced autophagy through the classical beclin-1-Atg7-Atg5 pathway as determined by specific siRNA analysis. Rapamycin and IFN-γ (autophagy inducers) augmented bacterial clearance, whereas beclin-1 and Atg5 knockdown reduced intracellular bacteria. Thus, P. aeruginosa-induced autophagy represents a host protective mechanism, providing new insight into the pathogenesis of this infection. © 2012.

Relias V.,Boston Therapeutics | Saif M.W.,Boston Therapeutics
Journal of the Pancreas | Year: 2014

Ampullary adenocarcinomas have unique biologic and clinical features that result in its improved prognosis versus adenocarcinomas that arise from the distal bile ducts and pancreas. However the histological differentiation and identification of these tumors is not easily accomplished. Two abstracts at this year's ASCO Annual Meeting describe attempts to identify unique methods for distinguishing these tumors. Abstract 4141 described a 92 gene RT-PCR assay that was used for molecular classification of patients with ampullary adenocarcinomas while abstract e15175 looked at mutational status of K-ras in patients with these tumors. The results of their abstracts will be discussed.

Kesselheim A.S.,Boston Therapeutics | Shiu N.,Boston Therapeutics
Clinical Pharmacology and Therapeutics | Year: 2014

Patents are commonly granted for the use of biomarkers in making medical decisions. However, the US Supreme Court recently changed the landscape with a unanimous decision that patents cannot cover discoveries of basic correlations in nature, such as those relating biomarkers to particular clinical outcomes. Subsequent court decisions have overturned patents on genetic and other diagnostic methods involving purely mental processes, but processes integrating biomarkers in practical clinical steps can still earn intellectual property protections.

Dalli J.,Boston Therapeutics | Chiang N.,Boston Therapeutics | Serhan C.N.,Boston Therapeutics
Proceedings of the National Academy of Sciences of the United States of America | Year: 2014

Upon infection and inflammation, tissue repair and regeneration are essential in reestablishing function. Here we identified potent molecules present in self-limited infectious murine exudates, regenerating planaria, and human milk as well as macrophages that stimulate tissue regeneration in planaria and are proresolving. Characterization of their physical properties and isotope tracking indicated that the bioactive structures contained docosahexaenoic acid and sulfido-conjugate (SC) of triene double bonds that proved to be 13-glutathionyl, 14-hydroxy-docosahexaenoic acid (SCI) and 13-cysteinylglycinyl, 14-hydroxy-docosahexaenoic acid (SCII). These molecules rescued Escherichia coli infectionmediated delay in tissue regeneration in planaria, improving regeneration intervals from ∼4.2 to ∼3.7 d. Administration of SCs protected mice from second-organ reflow injury, promoting repair via limiting neutrophil infiltration, up-regulating Ki67, and Roof plate-specific spondin 3. At nanomolar potencies these conjugates also resolved E. coli infections by limiting neutrophil infiltration and stimulating bacterial phagocytosis and clearance as well as efferocytosis of apoptotic cells. Together, these findings identify previously undescribed conserved chemical signals and pathways in planaria, mouse, and human tissues that enhance host responses to contain infections, stimulate resolution of inflammation, and promote the restoration of function.

Boston Therapeutics | Date: 2014-03-14

The present disclosure relates to the use of polymers to coat bitter-tasting active pharmaceutical ingredients in a manner that masks the bitter taste of these compounds. Taste masked pharmaceutical formulations in which the particles of pharmaceutically active ingredients are coated with polymers or ion exchange resins are disclosed. The formulations provide taste masked pharmaceutical formulations in which the rapid disintegration of tablets is preserved. A method for preparing such coated particles in a fluidized bed coating process is disclosed. The polymer coating may include a combination of low molecular and high molecular weight water in-soluble polymers, plasticizer and fillers, which provides for a chewable dosage form having a pleasing taste thereby improving patient compliance.

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