Tuning the Au(I)-mediated inhibition of cathepsin B through ligand substitutions

Gunatilleke, Shamila S.; Barrios, Amy

doi:10.1016/j.jinorgbio.2007.10.019

Cited by 30 publications

(24 citation statements)

References 36 publications

(81 reference statements)

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“…76 Recent studies have focused on understanding the mechanism of inhibition of cathepsin B by auranofin and in tuning the potency by changing the phosphine ligand. [76][77][78] Cathepsins K and S have been shown to play central roles in the inflammatory and erosive components of RA and a recent study 79 shows efficient inhibition of both these cathepsins by auranofin and aurothiomalate; a crystal structure of a cathepsins K/aurothiomalate complex shows linear S-Au-S coordination with Au bound to the active site Cys residue and a thiomalate ligand still coordinated. 79 At the transcription level Au(I) drugs downregulate a range of inflammatory genes by inhibiting transcription factors NF-kB and AP-1 (Jun/Fos).…”

Section: Targets For Gold Compounds In Rheumatoid Arthritismentioning

confidence: 99%

Gold compounds as therapeutic agents for human diseases

2011

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The application of gold in medicine is traceable for several thousand years and Au(i) compounds have been used clinically to treat rheumatoid arthritis since the last century. Recently research into gold-based drugs for a range of human diseases has seen a renaissance. Old as well as new Au(i) and Au(iii) compounds have been used and designed with an aim of targeting cellular components that are implicated in the onset or progression of cancers, rheumatoid arthiritis, viral and parasitic diseases. In addition, new disease targets have been found for gold compounds that have given insight into the mechanism of action of these compounds, as well as in the molecular pathophysiology of human diseases. Here we discuss the rationale for the design and use of gold compounds that have specific and selective targets in cells to alleviate the symptoms of a range of human diseases. We summarise the most recent findings in this research and our own discoveries to show that gold compounds can be developed to become versatile and powerful drugs for diseases caused by dysfunction of selenol and thiol containing proteins.

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Section: Targets For Gold Compounds In Rheumatoid Arthritismentioning

confidence: 99%

Gold compounds as therapeutic agents for human diseases

2011

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“…Infectious complications indicative of immunosuppression are not seen during auranofi n treatment [20] . Auranofi n is a moderate potency (low micromolar range) inhibitor of cathepsin B [21,22] . Since several rodent glioblastoma models have shown tumor aggressiveness to be proportional to the degree of cathepsin B overexpression [2,5,14,15,17] , these would be good fi delity models refl ecting human disease with a good predictive power of auranofi n eff ects on glioblastoma.…”

Section: Auranofi Nmentioning

confidence: 99%

Glioblastoma Invasion, Cathepsin B, and the Potential for Both to be Inhibited by Auranofin, an Old Anti-Rheumatoid Arthritis Drug

Re¹

2010

Cen Eur Neurosurg

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Section: Introductionmentioning

confidence: 99%

“…This is in part due to a long history of gold use in medicine [5]. For instance, gold sodium thiomalate and gold thioglucose, two antiarthritic gold(I) thiolates, have been in active clinical use for some time [5]. Further, the easy synthesis and surface chemistry, unique optical properties and existing safety data of gold in humans have more recently made GNPs an attractive choice for a wide range of nanomedical applications, including drug delivery [6] and photothermal cancer therapy [7].…”

Section: Introductionmentioning

confidence: 99%

Blood protein and blood cell interactions with gold nanoparticles: the need for in vivo studies

Shah

Bischof²

2013

BioNanoMaterials

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Gold nanoparticles (GNPs) have gained in prominence within the field of nanomedicine with recent advancement of several embodiments to clinical trials. To ensure their success in the clinic it has become increasingly clear that a deeper understanding of the biological interactions of GNPs is imperative. Since the majority of GNPs are intended for systemic intravenous use, an immediate and critical biological interaction is between the blood and the GNP. Blood is composed of plasma proteins and cells. Both of these components can induce downstream effects upon interacting with GNPs that ultimately influence their medical impact. For instance, proteins from the blood can cover the GNP to create a biological identity through formation of a protein corona that is quite different from the originally synthesized GNP. Once in the bloodstream this protein coated GNP evokes both positive and negative physiological responses such as biodistribution into tissue for therapy (i.e., cancer) and toxicity or off target accumulation in the reticuloendothelial system (RES) that must be controlled for optimal use. In this review, we summarize predominantly in vitro studies of GNP interactions with blood plasma proteins and blood cells and make the case that more in vivo study is urgently needed to optimal design and control GNP use in medicine. In some cases where no specific GNP blood studies exist, we draw the readers ' attention to studies conducted with other types of nanoparticles as reference.

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Tuning the Au(I)-mediated inhibition of cathepsin B through ligand substitutions

Cited by 30 publications

References 36 publications

Gold compounds as therapeutic agents for human diseases

Gold compounds as therapeutic agents for human diseases

Glioblastoma Invasion, Cathepsin B, and the Potential for Both to be Inhibited by Auranofin, an Old Anti-Rheumatoid Arthritis Drug

Blood protein and blood cell interactions with gold nanoparticles: the need for in vivo studies

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