Related Experiment Video
Updated: Sep 25, 2026

The Synthesis, Characterization and Reactivity of a Series of Ruthenium N-triphosPh Complexes
Published on: April 10, 2015
Antiangiogenic properties of selected ruthenium(III) complexes that are nitric oxide scavengers
L Morbidelli1, S Donnini, S Filippi
1Department of Molecular Biology, University of Siena, Via Aldo Moro 2, 53100 Siena, Italy.
Abstract:
The nitric oxide synthase (NOS) pathway has been clearly demonstrated to regulate angiogenesis. Increased levels of NO correlate with tumour growth and spreading in different experimental and human cancers. Drugs interfering with the NOS pathway may be useful in angiogenesis-dependent tumours. The aim of this study was to pharmacologically characterise certain ruthenium-based compounds, namely NAMI-A, KP1339, and RuEDTA, as potential NO scavengers to be used as antiangiogenic/antitumour agents. NAMI-A, KP1339 and RuEDTA were able to bind tightly and inactivate free NO in solution. Formation of ruthenium-NO adducts was documented by electronic absorption, FT-IR spectroscopy and (1)H-NMR. Pretreatment of rabbit aorta rings with NAMI-A, KP1339 or RuEDTA reduced endothelium-dependent vasorelaxation elicited by acetylcholine. This effect was reversed by 8-Br-cGMP. The key steps of angiogenesis, endothelial cell proliferation and migration stimulated by vascular endothelial growth factor (VEGF) or NO donor drugs, were blocked by NAMI-A, KP1339 and RuEDTA, these compounds being devoid of any cytotoxic activity. When tested in vivo, NAMI-A inhibited angiogenesis induced by VEGF. It is likely that the antitumour properties previously observed for ruthenium-based NO scavengers, such as NAMI-A, are related to their NO-related antiangiogenic properties.
Insights
Ruthenium compounds NAMI-A, KP1339, and RuEDTA effectively scavenge nitric oxide (NO), inhibiting angiogenesis and showing potential as anti-cancer agents by blocking tumor growth and spread.
Area of Science:
- Biochemistry
- Pharmacology
- Cancer Research
Background:
- The nitric oxide synthase (NOS) pathway regulates angiogenesis, with elevated nitric oxide (NO) linked to tumor progression.
- Targeting the NOS pathway offers potential therapeutic strategies for angiogenesis-dependent tumors.
Purpose of the Study:
- To pharmacologically characterize ruthenium-based compounds (NAMI-A, KP1339, RuEDTA) as potential nitric oxide (NO) scavengers for antiangiogenic and antitumour applications.
Main Methods:
- In vitro assessment of NO scavenging by ruthenium compounds using spectroscopy (electronic absorption, FT-IR, 1H-NMR).
- Evaluation of effects on endothelium-dependent vasorelaxation in rabbit aorta rings.
- Inhibition assays for vascular endothelial growth factor (VEGF)-stimulated endothelial cell proliferation and migration.
- In vivo studies using NAMI-A to assess angiogenesis inhibition.
Main Results:
- NAMI-A, KP1339, and RuEDTA demonstrated potent NO scavenging capabilities, forming stable ruthenium-NO adducts.
- These compounds inhibited endothelium-dependent vasorelaxation, an effect reversible by 8-Br-cGMP.
- Ruthenium compounds effectively blocked VEGF- or NO-stimulated endothelial cell proliferation and migration without exhibiting cytotoxicity.
- NAMI-A significantly inhibited VEGF-induced angiogenesis in vivo.
Conclusions:
- Ruthenium-based compounds NAMI-A, KP1339, and RuEDTA function as effective NO scavengers.
- Their NO-scavenging activity underlies their antiangiogenic and potential antitumour properties, particularly in angiogenesis-dependent cancers.
Related Concept Videos
Mechanism of Angiogenesis
Nitric Oxide Signaling Pathway
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Regulation of Angiogenesis and Blood Supply

