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Hydroxyl-based acid-hypersensitive acetal ester bond: Design, synthesis and the application potential in nanodrugs.
Eur J Med Chem
February 2025
State Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. Electronic address:
Article Synopsis
- Targeted drug delivery systems are utilizing the acidic environment of tumors to improve drug stability and reduce toxicity through modifications like hydroxyl groups.
- A newly developed "acetal ester bond" offers a highly sensitive and easy-to-synthesize linkage that allows for efficient drug release specifically in acidic conditions while maintaining stability in healthy physiological environments.
- The acetal ester bond-based paclitaxel conjugate (PTX-COU) demonstrated superior tumor growth inhibition in experiments, suggesting its potential for enhancing targeted drug delivery and minimizing systemic side effects.
DNMT3a Downregulation Ttriggered Upregulation of GABA Receptor in the mPFC Promotes Paclitaxel-Induced Pain and Anxiety in Male Mice.
Adv Sci (Weinh)
December 2024
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Institute of Neuroscience, Translational Medicine Institute, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, P. R. China.
Chemotherapeutic agents, such as paclitaxel (PTX), induce neuroplastic changes and alter gene expression in the prefrontal cortex (PFC), which may be associated with chemotherapy-induced pain and negative emotions. Notably, DNA methylation undergoes adaptive changes in neurological disorders, emerging as a promising target for neuromodulation. In this study, systemic administration of PTX leads to a decrease in the expression of the DNA methyltransferase DNMT3a, while concurrently upregulating the expression of Gabrb1 mRNA and its encoded GABARβ1 protein in the medial PFC (mPFC) of male mice.
View Article and Find Full Text PDFAssessing Outcomes of Tapering 12-Hour and 6-Hour Dexamethasone Prior to Paclitaxel Infusions in Patients With Breast Cancer.
Clin Breast Cancer
November 2024
Nebraska Medicine, Department of Pharmacy Practice and Science, Omaha, NE.
Background: Paclitaxel has a boxed warning for causing severe hypersensitivity reactions, however, the majority (95%) of these reactions occur during the first or second infusion. Corticosteroids can reduce the incidence of paclitaxel hypersensitivity reactions from 30% to around 1%-3% but are not without adverse effects. Current practice at our institution is to prescribe dexamethasone 20 mg to be given orally 12 and 6 hours prior to paclitaxel infusion, however, some medical oncology providers have elected to decrease or omit dexamethasone premedication.
View Article and Find Full Text PDFIncreased keratinocyte activity and PIEZO1 signaling contribute to paclitaxel-induced mechanical hypersensitivity.
Sci Transl Med
December 2024
Department of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Recent work demonstrates that epidermal keratinocytes are critical for normal touch sensation. However, it is unknown whether keratinocytes contribute to touch-evoked pain and hypersensitivity after tissue injury. Here, we used a mouse model of paclitaxel treatment to determine the extent to which keratinocyte activity contributes to the severe neuropathic pain that accompanies chemotherapy.
View Article and Find Full Text PDFThe cannabinoid CB agonist LY2828360 suppresses neuropathic pain behavior and attenuates morphine tolerance and conditioned place preference in rats.
Neuropharmacology
March 2025
Program in Neuroscience, Indiana University, Bloomington, IN, USA; Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA; Gill Institute for Neuroscience, Indiana University, Bloomington, IN, USA. Electronic address:
Cannabinoid CB agonists show promise as analgesics because they lack unwanted side effects associated with direct activation of CB receptors. CB receptor activation suppresses pathological pain in animal models, but the types of pain that best respond to CB agonists are incompletely understood. This gap in knowledge may contribute to failures in clinical translation.
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