α-glucosidase

MONDAY, July 15, 2024 -- Compared with other antidiabetic classes, metformin and sodium glucose co-transporter-2 inhibitors (SGLT2is) exhibit significantly lower dementia risk, according to a review published online May 3 in the American Journal of Preventive Medicine . Yongjun Sunwoo, from the College of Pharmacy at Kyung Hee University in Seoul, South Korea, and colleagues conducted a systematic review and meta-analysis to examine the risk for dementia and Alzheimer disease (AD) associated with antidiabetic medication classes. Data were included from 16 studies with 1,565,245 patients. The researchers found that the risks for dementia and AD were significantly lower with metformin and SGLT2is. Across diverse antidiabetics, metformin exhibited the lowest risk for dementia, while the highest risk was seen for α-glucosidase inhibitors. Across second-line antidiabetics, SGLT2is exhibited the lowest dementia risk. In the elderly (aged 75 years and older), a significantly higher dementia risk was seen with dipeptidyl peptidase-4 inhibitors, metformin, sulfonylureas, and thiazolidinediones compared with SGLT2is. Regardless of diabetic complication status or baseline hemoglobin A1c, dementia risk associated with metformin was substantially lower. "Optimal glycemic control with appropriate pharmacotherapy along with endorsement of routine cognitive status monitoring in diabetic patients are imperative to enhance prognoses associated with diabetes mellitus-related cognitive impairment," the authors write. Abstract/Full Text Whatever your topic of interest, subscribe to our newsletters to get the best of Drugs.com in your inbox.

MONDAY, July 15, 2024 -- Some diabetes drugs appear to lower the risk that people with type 2 diabetes will develop dementia or Alzheimer’s disease, a new evidence review says. The risk of dementia and Alzheimer’s is significantly lower in patients treated with metformin or a class of meds called "sodium glucose co-transporter-2 (SGLT-2) inhibitors", compared with other diabetes drugs, researchers report. Type 2 diabetes affects about 530 million people around the world, and there’s at least a 50% increased risk of cognitive impairment and dementia in these people, researchers said in background notes. “Our study contributes to the existing evidence by suggesting potential additional benefits of SGLT-2 inhibitors in mitigating dementia risk, thereby providing significant clinical implications for diabetes management,” lead researcher Yeo Jin Choi at Kyung Hee University in Seoul, South Korea, said in a news release. “Elderly patients aged 75 years or older may particularly benefit from these findings, since they often face greater cognitive health concerns,” Choi added. For their review, researchers analyzed data from 16 prior studies involving more than 1.5 million patients. The studies looked at six diabetic drug classes: DPP4 inhibitors, metformin, SGLT-2 inhibitors, sulfonylureas, alpha-glucosidase inhibitors and thiazolidinediones. The lowest risk of dementia and Alzheimer’s was found in patients taking metformin, results show. But SGLT-2 inhibitors were also associated with a lower risk of cognitive decline as well, and also provided heart health benefits, researchers said. These drugs include Farxiga (dapagliflozin) and Jardiance (empagliflozin). What's more, results show that SGLT-2 inhibitors performed better than all other drugs, including metformin, in reducing dementia risk in patients 75 and older. “We were quite surprised by the study results, particularly the potential cognitive benefits of SGLT-2 inhibitors over metformin and DPP-4 inhibitors in patients aged 75 years or older,” Choi said. “This finding is particularly notable given that SGLT-2 inhibitors are currently used for heart failure management as well.” Metformin works by decreasing the amount of glucose produced by the liver and by making muscle tissue more sensitive to insulin, the American Diabetes Association says. SGLT-2 inhibitors increase the amount of glucose that is excreted in urine, lowering blood sugar levels, the ADA says. The new study appears in the American Journal of Preventive Medicine . Whatever your topic of interest, subscribe to our newsletters to get the best of Drugs.com in your inbox.

WALTHAM, Mass., June 24, 2024 (GLOBE NEWSWIRE) -- Dyne Therapeutics, Inc. (Nasdaq: DYN), a clinical-stage muscle disease company focused on advancing innovative life-transforming therapeutics for people living with genetically driven diseases, today announced new preclinical data in a Pompe disease model demonstrating the potential of the FORCE™ platform to deliver enzyme replacement therapy to cardiac and skeletal muscle and the central nervous system (CNS). The data were presented at the New Directions in Biology and Disease of Skeletal Muscle Conference, being held June 23-26 in Fort Lauderdale, FL. “These preclinical data show for the first time the ability of FORCE to deliver enzymes to skeletal and cardiac muscle as well as the CNS, expanding the modularity of our platform beyond oligonucleotides. The data support the potential of FORCE to enable effective enzyme replacement therapy with the opportunity to substantially improve upon available treatments for Pompe disease,” Oxana Beskrovnaya, Ph.D., chief scientific officer of Dyne. “We look forward to continuing to explore this application of our platform as part of our mission to deliver life-transforming therapies for people with serious muscle diseases.” Pompe disease is a rare, severe neuromuscular disorder caused by deficiency of the lysosomal enzyme, acid alpha glucosidase (GAA). Lack of GAA leads to glycogen accumulation and increase in lysosomal size in muscle and subsequent weakness, cardiomyopathy and respiratory failure. Enzyme replacement therapy with GAA is the standard of care and increases survival but has inadequate efficacy in skeletal muscle. Pompe is also characterized by CNS manifestations, including behavioral and cognitive deficits due to glycogen accumulation in CNS cells, which are not addressed by the standard of care therapy. Dyne engineered FORCE-GAA by leveraging the FORCE platform and evaluated efficacy in vivo using hTfR1/6Neo mice, that were developed by crossing the well-established 6Neo mouse model of Pompe with mice expressing human transferrin receptor 1. Intravenous administration of FORCE-GAA cleared glycogen in muscle and the CNS and normalized lysosomal size in hTfR1/6Neo mice. FORCE-GAA reduced serum neurofilament light chain, a biomarker of axonal injury, providing evidence of benefit in the CNS. FORCE-GAA also displayed superior efficacy and dose potency compared to GAA alone. Additional data with FORCE-GAA showed the potential for monthly dosing which is less frequent than approved enzyme replacement therapies. The presentation entitled, “FORCE™ Platform for the Development of Targeted Therapeutics for Rare Muscle Diseases” is available in the Scientific Publications & Presentations section of Dyne’s website at . About Pompe Disease Pompe disease is a severe neuromuscular disorder caused by a deficiency of the lysosomal enzyme, acid alpha glucosidase (GAA). Lack of GAA causes glycogen accumulation in tissue leading to muscle weakness, cardiomyopathy, respiratory failure, and central nervous system (CNS) manifestations. Pompe disease belongs to a group of diseases known as the lysosomal storage disorders (LSDs). It can present as infantile-onset, the most severe form of the disease with early onset of symptoms in infancy that rapidly progress, or late-onset, which progressively damages muscles over time. An estimated 5,000 to 10,000 individuals worldwide are affected by Pompe. About the FORCE™ Platform The proprietary FORCE™ platform drives Dyne’s efforts to develop targeted, modern oligonucleotide therapeutics with the potential to be life-transforming for patients with serious muscle diseases. Dyne designed the FORCE platform using its deep knowledge of muscle biology and oligonucleotide therapeutics to overcome the current limitations in delivery to muscle tissue with the goal of stopping or reversing disease progression. The FORCE platform leverages the importance of transferrin receptor 1 (TfR1) in muscle biology as the foundation for its novel approach. TfR1, which is highly expressed on the surface of muscle cells, is required for iron transport into muscle cells. Dyne links therapeutic payloads to its TfR1-binding fragment antibody (Fab) to develop targeted therapeutics for muscle diseases. About Dyne Therapeutics Dyne Therapeutics is a clinical-stage muscle disease company focused on advancing innovative life-transforming therapeutics for people living with genetically driven diseases. With its proprietary FORCE™ platform, Dyne is developing modern oligonucleotide therapeutics that are designed to overcome limitations in delivery to muscle tissue. Dyne has a broad pipeline for serious muscle diseases, including clinical programs for myotonic dystrophy type 1 (DM1) and Duchenne muscular dystrophy (DMD) and a preclinical program for facioscapulohumeral muscular dystrophy (FSHD). For more information, please visit , and follow us on X, LinkedIn and Facebook. Forward-Looking Statements This press release contains forward-looking statements that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this press release, including statements regarding Dyne’s strategy, future operations, prospects and plans, objectives of management, the potential of the FORCE platform, the anticipated timelines for reporting additional data for FORCE-GAA, expectations regarding the initiation of additional preclinical studies or clinical trials of FORCE-GAA, and plans to provide future updates on pipeline programs, constitute forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. The words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “might,” “objective,” “ongoing,” “plan,” “predict,” “project,” “potential,” “should,” or “would,” or the negative of these terms, or other comparable terminology are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Dyne may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a result of various important factors, including: uncertainties inherent in the identification and development of product candidates, including the initiation and completion of preclinical studies and clinical trials; uncertainties as to the availability and timing of results from preclinical studies and clinical trials; the timing of and Dyne’s ability to enroll patients in clinical trials; whether results from preclinical studies and initial data from early clinical trials will be predictive of the final results of the clinical trials or future trials; whether Dyne’s cash resources will be sufficient to fund its foreseeable and unforeseeable operating expenses and capital expenditure requirements; as well as the risks and uncertainties identified in Dyne’s filings with the Securities and Exchange Commission (SEC), including the Company’s most recent Form 10-Q and in subsequent filings Dyne may make with the SEC. In addition, the forward-looking statements included in this press release represent Dyne’s views as of the date of this press release. Dyne anticipates that subsequent events and developments will cause its views to change. However, while Dyne may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do so. These forward-looking statements should not be relied upon as representing Dyne’s views as of any date subsequent to the date of this press release. Contacts: Investors Amy Reilly areilly@dyne-tx.com 857-341-1203 Media Stacy Nartker snartker@dyne-tx.com 781-317-1938