Manual Organoiron Compounds, Part B: Mononuclear Compounds 11

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1. Introduction

RSS Feeds. Chemistry World. Education in Chemistry. Open Access. Historical Collection. You do not have JavaScript enabled. Please enable JavaScript to access the full features of the site or access our non-JavaScript page. Issue 21, Previous Article Next Article. From the journal: Dalton Transactions.

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Michael S. You have access to this article. Please wait while we load your content Something went wrong. Try again? Cited by. Back to tab navigation Download options Please wait Two possible mechanisms of resistance have been proposed. One is that the mutation to the larger methionine residue prevents TKIs accessing the drug binding site. The results of a phase III trial recently published in the New England Journal of Medicine found that median progression-free survival of patients taking osimertinib was nearly doubled at The U.

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The background image is a detail from a Creative Commons licensed illustration depicting the life cycle of a cancer cell. In contrast, P. Vivax malaria used to be officially known as "benign" malaria in contrast to the "malignant" variety caused by P. Thanks to the work of Austrian psychiatrist Julius Wagner-Jauregg — , from until the advent of penicillin antibiotics in the s, it was widely used as a treatment for tertiary syphilis the end-phase of the disease in which the Treponema pallidum bacteria attacks the brain and nervous system.

Around half of the patients treated with P. Although it is still not known exactly how the treatment worked, it seems that the prolonged high fevers it induced helped the patients' immune systems to fight off the bacteria. Wagner-Jauregg was awarded the Nobel Prize in Physiology or Medicine for his discovery although in later years his reputation suffered through his support for eugenics and forced sterilisation of the mentally ill and criminal, as well as his sympathies for the Nazi party.

The term "benign malaria" is no longer used, for the reality is that vivax malaria is anything but benign. Just like falciparum malaria, it causes the classic malaria symptoms of alternating fever, chills and sweats along with headaches and muscle pain. While P. This can make vivax infections difficult to diagnose. Furthermore, unlike P.

While an initial P. It is this form that enables P.

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Weeks or months later, the parasite re-emerges and the disease flares up again. Commonly recurring times a year, each bout of the disease causes sufferers to become gradually more anaemic. Fighting off each flare-up of the disease makes sufferers more vulnerable to other diseases as well as to problems resulting from malnutrition and poverty — they are unable to work while they are ill.

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In turn, other diseases, including falciparum malaria, seem to trigger relapses of vivax malaria. Vivax malaria infection is consequently a significant factor in many deaths [1]. Until recently, primaquine was the only treatment available to clear the parasites hiding in the liver and so prevent the relapse of vivax malaria. However, it needs to be taken for 14 days and common side effects include nausea, stomach pain, and vomiting. Consequently, many patients who feel better after just a few days stop taking the pills, allowing the parasite to awaken at a later date.

At the Walter Reed Army Institute of Research , a compound synthesised in which was coded as WR ,, later named etaquine but which now has the International Nonproprietary Name tafenoquine CHEBI was investigated as a radical cure against relapsing vivax malaria, but for many years the development work was not given high priority [3]. In the last 30 years, however, tafenoquine has been the subject of more than 30 clinical trials and found to be effective against the major malaria parasites at all stages of the parasites' life cycle and to have very little potential to trigger the development of resistance.

In contrast to primaquine, a single mg dose is all that is required to clear P. It is the first new treatment for vivax malaria to be approved in over 60 years. The background image is a detail of a Creative Commons licensed thin film micrograph showing a red blood cell containing two ring-form P. The red blood cells are normal, to 1. PLoS Med. The researchers used x-ray crystallography and kinase-inhibitor specificity profiling to show that curcumin binds to a kinase enzyme known as dual-specificity tyrosine-regulated kinase 2 DYRK2.

This binding inhibits the activity of the enzyme, reducing the DYRK2-mediated phosphorylation of the 26S proteasome a large multi-protein complex involved in the regulated degradation of unwanted or damaged proteins in cells , leading to reduced proteasome activity and impaired cell proliferation. The team found that when curcumin was used in combination with the proteasome inhibitor carfilzomib against the aggressive triple-negative breast cancer TBNC cell line, there was a strong synergistic effect — curcumin induced a much higher degree of cancer cell death.

An added bonus was that this combination treatment showed little or no cytotoxicity to non-cancerous cells. While curcumin has demonstrated the "proof of concept", it is unlikely be the final agent of choice. For in a recent review of the medicinal chemistry of curcumin [3], researchers led by Prof. Its structure was finally established some five decades later, as a result of the studies of Swiss chemist Alfred Werner — into the isomerisation of inorganic complexes [2]. It was the research of Professor Barnett Rosenberg — and co-workers that would finally raise the status of cisplatin to chemical superstar.

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In the mids, they found that the complex prevented bacteria from dividing normally [3]. Subsequent testing on cancer cells showed that it was biologically active. After undergoing animal and clinical trials, cisplatin was approved for treatment of testicular and ovarian cancers in the late s [4]. Cisplatin is administered as an intravenous injection — it's ineffective when given orally — and enters into cancer cells from the bloodstream.

In turn, the water can be replaced by one of the N -heterocyclic bases on DNA, particularly guanine.

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Cross-linking to the DNA can then occur through displacement of the remaining chloride by another guanine group, interfering with mitosis. The cancer cells recognise something is wrong and initiate apoptosis programmed cell death [5]. Even though five other platinum drugs with structures based on that of cisplatin have been developed since, cisplatin is still one of the most widely used anticancer agents.

However, cisplatin is by no means a perfect drug. Its use is associated with a number of particularly unpleasant side-effects. The best known are probably severe nausea and vomiting, which are so bad that development work was nearly stopped when the drug was first tested on people; it was only approved following the invention of effective anti-nausea drugs [6]. Other side effects of cisplatin include nephrotoxicity kidney damage , electrolyte disturbance, including hypomagnesaemia and hypokalaemia , and ototoxicity hearing loss. The damage particularly affects hearing high frequency sounds, so can be devastating for young children who have not developed speech, — consonants such as 'f', 'h', and 's' are heard at high frequencies and even mild hearing damage is likely to affect their speech development, learning, and general quality of life.

It has been known since the s that sodium thiosulfate Na 2 S 2 O 3 , STS can reduce the cytotoxicity and nephrotoxicity of cisplatin [7]. Subsequent nonclinical studies and phase 1 and phase 2 trials have shown that STS has a potential otoprotective effect [8,9]. It inactivates platinum complexes by binding the electophilic platinum with thiol , forming a non-cytotoxic covalent complex that is rapidly excreted. Last year, a group of researchers suggested a reason for cisplatin's ototoxicity: they found that in both mice and humans, while cisplatin is eliminated from most organs in the body within a few days or weeks, it is retained in and damages the cochlea for months or even years after the treatment [10].

Now, a multi-national team led by Penelope Brock, paediatric consultant at the Great Ormond Street Hospital in London, has reported on a 7-year study of children suffering from hepatoblastoma , a rare liver cancer 1. The study group was enrolled at 52 centres in 12 countries from The children were either given the standard treatment involving cisplatin chemotherapy, or cisplatin followed by STS six hours later giving the cisplatin some time to work before being deactivated the the STS.

Importantly, the six hour delay between administering the cisplatin and the STS treatment was long enough for the cisplatin to work — the new treatment was just as effective as the traditional 'cisplatin alone' treatment. Almost 40 years after the ototoxicity of cisplatin was discovered, it seems that a big step forward has been made. Sodium thiosulfate tradename Pedmark is now being reviewed for a licence for use in hepatoblastoma treatment in Europe and the US.