Chemotherapy is limited by its poor selectivity towards cancer cells over normal cells. Herein, we designed half-sandwich ruthenium imino-pyridyl complexes [(η-bz)Ru(N^N)Cl]PF to achieve selective cytotoxicity to cancer cells. This kind of ruthenium complex has unique characteristics and is worthy of further exploration in the design of new anticancer drugs.

Two half-sandwich RuII diimine complexes combine features of bioimaging, anticancer and antimetastasis properties into one molecule. The complexes target mitochondria and damage mitochondrial integrity.

Poor selectivity between cancer cells and normal cells is one of the major limitations of cancer chemotherapy. Lysosome-targeted ruthenium-based complexes target tumor cells selectively, only displaying rather weak cytotoxicity or inactivity toward normal cells. Confocal microscopy was employed for the first time to determine the cellular localization of the half-sandwich Ru complex.

COVID‐19 has become a pandemic and it has already spread to at least 171 countries/regions. Chronic kidney disease (CKD) is a global public health problem with a total of approximately 850 million patients with CKD worldwide and 119.5 million in China. Severe COVID‐19 infection may damage the kidney and cause acute tubular necrosis, leading to proteinuria, hematuria and elevated serum creatinine. Since the SARS‐CoV‐2 enters the cells by binding to the angiotensin‐converting enzyme 2 receptor, some doctors question its ability to increase the risk and severity of developing COVID‐19. Neither clinical data nor basic scientific evidence supports this assumption. Therefore, patients who take angiotensin‐converting enzyme inhibitor or angiotensin receptor blocker are not advised to change their therapy. Patients with CKD are generally the elderly population suffering from multiple comorbidities. Moreover, some patients with CKD might need to take glucocorticoids and immunosuppressants. Dialysis patients are recurrently exposed to a possible contaminated environment because their routine treatment usually requires three dialysis sessions per week. Considering all the above reasons, patients with CKD are more vulnerable to COVID‐19 than the general population. The development of COVID‐19 may worsen the impaired kidney function and further lead to rapid deterioration of kidney function and even death. Strict comprehensive protocols should be followed to prevent the spread of COVID‐19 among patients with CKD. In this review, we provide some practical management recommendations for health care providers, patients with CKD, dialysis patients and dialysis facilities.

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Fifteen organometallic Ir(III) half-sandwich complexes (1A-5C) having the general formula [(η 5 -Cp x )Ir(N^N)Cl]PF 6 (Cp x = Cp*, tetramethyl(phenyl) cyclopentadienyl (Cp xph ) or tetramethyl(biphenyl)cyclopentadienyl (Cp xbiph ); N^N = diamine) have been synthesized and characterized. The molecular structure of 1A was determined using single-crystal X-ray diffraction analysis.The hydrolysis of 1A-5C was monitored using UV-visible spectra. Complexes 3A-3C showed catalytic activity for the oxidation of NADH to NAD + , where 3C showed the highest turnover number of 29.9 within 450 min. Cytotoxicity examination by MTT assay was carried out against two human cancer cell lines (HeLa and A549) after 24 or 48 h drug treatment. The complexes showed high potency, where the most potent complex (3C; IC 50 = 3.4 μM) was six times more active than cisplatin against A549 cells after 24 h drug exposure. Cytotoxic potency towards A549 cells increased with phenyl substitution on Cp ring: Cp xbiph > Cp xph > Cp*. In addition, the biological studies showed that 3C caused cell apoptosis and cell cycle arrest at G 1 phase in A549 cancer cells.Moreover, 3C increased the level of reactive oxygen species markedly after 24 h, which may provide an important basis for killing cancer cells. Confocal laser scanning microscopy was used to track 3C in A549 cells. The cellular localization experiment showed that 3C targeted lysosomes and caused lysosomal damage.

It is known that the proposed biologically active form of ruthenium is its oxidation state II other than oxidation state III, and ruthenium complexes offer the potential of a novel mechanism of action, reduced toxicity. Herein, three half‐sandwich RuII complexes [(η6‐p‐cym)Ru(N^N)Cl]PF6 were designed and synthesized. Lysosomes are involved in various aspects of cancer cell immortalization and cell death. Thus, lysosomes are attractive pharmacological targets for selective killing of cancer cells. We demonstrated that Ru2 can accumulate in lysosomes. In addition, A549 cell viability remained at 87.81 % after exposure to Ru2 for 24 h at the working concentration. Meanwhile, Ru2 exhibited relatively high photostability and suitability for long‐term tracking. At increased concentration after 24 h of exposure to the complex toward A549 cell line, Ru2 induced a high apoptotic rate, cell cycle arrest, mitochondrial membrane potential loss, and reactive oxygen species overload. Ru2 integrated the anticancer properties and imaging capabilities and is expected to be developed as a dual functional theranostic agent.

Organometallic half-sandwich Ir complexes of the type [(η-Cp)Ir(N^N)Cl]PF 1-6, where Cp = CMe (Cp*), CMeCH (Cp), CMeCHCH (Cp), N^N is imionopyridine chelating ligand, were prepared and characterized. The X-ray crystal structure of complex 1 has been determined. Four compounds displayed higher anticancer potency than clinically used anticancer drug cisplatin against A549 cancer cells, especially complex 3 which is 8 times more active than cisplatin. No hydrolysis was observed by NMR and UV-Vis for complexes 3 and 6; however, these complexes show big differences in nucleobase binding, mainly decided by the imionopyridine chelating ligand. Complex 3 is stable in the presence of glutathione, but 6 reacted rapidly with glutathione. The octanol/water partition coefficients (log P) of 3 and 6 have been determined. In addition, these complexes display effective catalytic activity in converting coenzyme NADH to NAD by accepting hydride to form an Ir hydride adduct. The mechanism of actions of these complexes involves apoptosis induction, cell cycles arrest, and significant increase of reactive oxygen species levels in A549 cancer cells.