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AZD2693, a PNPLA3 antisense oligonucleotide, for the treatment of MASH in 148M homozygous participants: two randomized phase I trials.
J Hepatol
January 2025
MASLD Research Center, Division of Gastroenterology and Hepatology, University of California at San Diego, La Jolla, CA, USA.
Background & Aims: A common genetic variant (rs738409) encoding isoleucine to methionine at position 148 in the PNPLA3 protein is a determinant of hepatic steatosis, inflammation, fibrosis, cirrhosis, and liver-related mortality. AZD2693 is a liver-targeted antisense oligonucleotide against PNPLA3 mRNA. We evaluated the safety, tolerability, pharmacokinetics, and pharmacodynamics in single ascending dose (SAD) and multiple ascending dose (MAD) studies.
View Article and Find Full Text PDFEfficient Encapsulation and Controlled Release of the Pesticide Emamectin Benzoate in Polylactic Acid Microspheres Prepared by Modified Solvent Evaporation.
Molecules
December 2024
Key Laboratory of Biopesticide and Chemical Biology, Ministry of Education, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Emamectin benzoate (EB) is a highly effective broad-spectrum insecticide and acaricide. However, because EB is easily degraded, the conventional formulations of EB are often overapplied. In this study, polylactic acid (PLA)-based microspheres were prepared using the modified solvent evaporation method for the controlled release of EB.
View Article and Find Full Text PDFElevated cell-free hemoglobin: A novel early biomarker following traumatic injury.
J Trauma Acute Care Surg
December 2024
From the Department of Surgery (J.T.R.), and Blood, Heart, Lung, and Immunology Research Center (J.T.R., K.E.R.), University Hospitals Cleveland Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio; Department of Surgery (A.J.R., A.B., A.R.B., R.A.C.), University of California Davis, Sacramento, California; Department of Anesthesia and Critical Care (A.M., N.N.), Pontchaillou University Hospital of Rennes, Rennes, France; Department of Anesthesiology and Perioperative Medicine (J.D.R.), University Hospitals Cleveland Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio; and Division of Pulmonary Critical Care Medicine, Department of Medicine (K.E.R.), University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Background: Cell-free hemoglobin (CFH) and free heme are potent mediators of endotheliopathy and organ injury in sepsis, but their roles in other hemolytic pathologies are not well-defined. A prime example is trauma where early hemolysis may initiate damage and predict outcome. Here, we investigated the presence of plasma CFH, heme, and their major scavengers after traumatic injury.
View Article and Find Full Text PDFNRH, a potent NAD enhancer, improves glucose homeostasis and lipid metabolism in diet-induced obese mice though an active adenosine kinase pathway.
Metabolism
December 2024
Department of Pharmacology, Weill Cornell Medicine, New York, NY 10021, United States of America.
Aims: NAD deficiency underlies obesity-induced metabolic disturbances. This study evaluated dihydronicotinamide riboside (NRH), a potent NAD enhancer, in lean and obese mice and explored whether NRH operates through a unique mechanism involving adenosine kinase (ADK), an enzyme critical for NRH-driven NAD synthesis.
Methods: Pharmacokinetic and pharmacodynamic analyses were performed following a single 250 mg/kg intraperitoneal injection of NRH in healthy mice.
HDAC6 inhibitor-loaded brain-targeted nanocarrier-mediated neuroprotection in methamphetamine-driven Parkinson's disease.
Redox Biol
December 2024
Department of Biopharmaceutical Convergence, Sungkyunkwan University, Suwon, 16419, Republic of Korea; School of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea. Electronic address:
The dynamic equilibrium between acetylation and deacetylation is vital for cellular homeostasis. Parkinson's disease (PD), a neurodegenerative disorder marked by α-synuclein (α-syn) accumulation and dopaminergic neuron loss in the substantia nigra, is associated with a disruption of this balance. Therefore, correcting this imbalance with histone deacetylase (HDAC) inhibitors represents a promising treatment strategy for PD.
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