In an effort to improve the issue of radiotherapy treatments, we tested whether S-nitrosocaptopril, a molecule combining a NO donor and an angiotensin converting enzyme inhibitor (ACE inhibitor), could temporarily improve the hemodynamic status of experimental tumors. We monitored the effect of S-nitrosocaptopril in TLT tumors using non rinvasive magnetic resonance techniques. We identified a time window during which tumor oxygenation was improved, as a result of a combined effect on tumor blood flow and oxygen consumption. Consequently, the administration of S-nitrosocaptopril contributed to the increase in efficacy of radiation therapy, an effect that was not observed with captopril alone.
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http://dx.doi.org/10.1016/j.canlet.2010.01.016 | DOI Listing |
Molecules
December 2021
Nanjing Leechdom Biopharm Technology Co., Ltd., Nanjing 211500, China.
From unstable crystals to relatively stable monohydrate crystals, many researchers have been working on S-nitrosocaptopril for more than two decades. S-nitrosocaptopril monohydrate (Cap-NO·HO) is a novel crystal form of S-nitrosocaptopril (Cap-NO), and is not only a nitric oxide (NO) donor, but also an angiotensin-converting enzyme inhibitor (ACEI). Yet, a method for long-term storage has never been reported.
View Article and Find Full Text PDFDrug Discov Today
March 2021
Institute of Oceanography, Minjiang University, Fuzhou, Fujian 350108, China. Electronic address:
Pharmacol Res
January 2019
Cancer Metastasis Alert and Prevention Center, and Biopharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, 350116, China; Institute of Oceanography, Minjiang University, Fuzhou, 350108, China. Electronic address:
A perfect microenvironment facilitates the activated circulating tumor cells (CTCs) to spark the adhesion-invasion-extravasation metastatic cascade in their premetastatic niche. Platelet-CTC interaction contributes to the progression of tumor malignancy by protecting CTCs from shear stress and immunological assault, aiding CTCs entrapment in the capillary bed, enabling CTCs to successfully exit the bloodstream and enter the tissue, inducing epithelial-mesenchymal-like transition (EMT), and assisting in the establishment of metastatic foci. To prevent the cascade from sparking, we show that, the multifunctional S-nitrosocaptopril (CapNO) acts on both CTCs and platelets to interrupt platelet/CTCs interplay and adhesion to endothelium, thus inhibiting CTC-based pulmonary metastasis in vivo.
View Article and Find Full Text PDFFree Radic Biol Med
December 2018
Cancer Metastasis Alert and Prevention Center, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China; Institute of Oceanography, Minjiang University, Fuzhou, Fujian 350108, China. Electronic address:
S-nitrosocaptopril (CapNO) possesses dual capacities of both Captopril and an NO donor with enhanced efficacy and reduced side effects. CapNO crystals are difficult to make due to its unstable S-NO bond. Here, we report a novel stable S-nitrosocaptopril monohydrate (CapNO·HO) that is stabilized by intermolecular five-membered structure, where one H of HO forms a hydrogen bond with O of the stable resonance zwitterion Cap-S=N-O, and the O in HO forms the dipole-dipole interaction with S through two unpaired electrons.
View Article and Find Full Text PDFEur J Pharmacol
November 2016
Cancer Metastasis Alert and Prevention Center, and Biopharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fuzhou University, Fuzhou 350002, China. Electronic address:
Inflammatory cytokines can induce the expression of cell adhesion molecules (CAMs) in endothelial cells. The induction may play an important role in attracting circulating tumor cells (CTCs) to endothelial cells. S-nitrosocaptopril (CapNO) is known to produce vasorelaxation and interfere the hetero-adhesion of CTCs to vascular endothelium via down-regulating the expression of CAMs.
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