Ciclopirox olamine

A review.Pyridine-based ring structures are widely employed in drug design due to their significant impact on pharmacol. activity, resulting in the development of various broad-spectrum therapeutics.The US FDA approves 95 pharmaceuticals derived from pyridine, including isoniazid and ethionamide for tuberculosis, delavirdine for HIV/AIDS, abiraterone acetate for prostate cancer, tacrine for Alzheimers, ciclopirox for ringworm and athletes foot, crizotinib for cancer, nifedipine for Raynauds syndrome and premature birth, piroxicam for arthritis, and nilvadipine for hypertension.Moreover, pyridine derivatives act as an excellent candidate for targeted anticancer agents.However, pyridine anti-cancer therapies continue to encounter hurdles, including poor response rates and drug resistance.Researchers are exploring pyridine derivatives as a potential treatment for targeted anticancer therapies.To further the development of targeted anti-cancer therapies, we analyzed pyridine-targeted drugs based on target categorization.We have covered all researchers of the last six years (2019-2024) investigating pyridine derivatives as targeted anticancer treatments.The highlights of pyridine-containing drugs and their targets are listed, as well as most promising drug candidates in clin. trials containing pyridine are also discussed.This review also included explanatory insights and viewpoints from several groups involved in the creation of targeted anticancer pyridine derivatives, with an emphasis on the structure-activity relationship (SAR).We hope that the current review provides insights and perspectives for the research and development of pyridine-containing anti-cancer drugs.

While iron (Fe) is essential for life and plays important roles for almost all growth related processes, it can trigger cell death in both animals and plants. However, the underlying mechanisms for Fe-induced cell death in plants remain largely unknown. S-nitrosoglutathione reductase (GSNOR) has previously been reported to regulate nitric oxide homeostasis to prevent Fe-induced cell death within root meristems. Here, we found that in the absence of GSNOR , exposure to high Fe treatment results in DNA damage–dependent cell death specifically in vascular stem cells in root meristems within 48 h. Through a series of time-course transcriptomic analyses, we unveil that in the absence of GSNOR , mitochondrial dysfunction emerges as the most prominent response to high Fe treatment. Consistently, the application of mitochondrial respiratory inhibitors leads to stem cell death in root meristems, and pharmacological blockage of the voltage-dependent anion channel that is responsible for the release of mitochondrial-derived molecules into the cytosol or genetic changes that abolish the ANAC017- and ANAC013-mediated mitochondrial retrograde signaling effectively eliminate Fe-induced stem cell death in gsnor root meristems. We further identify the nuclear transcription factor ANAC044 as a mediator of this mitochondrial retrograde signaling. Disruption of ANAC044 completely abolishes the GSNOR-dependent, Fe-induced stem cell death in root meristems, while ectopic expression of ANAC044 causes severe root stem cell death. Collectively, our findings reveal a mechanism responsible for initiating Fe-induced stem cell death in the root meristem, which is the ANAC044-mediated GSNOR-regulated mitochondrial stress signaling pathway.