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The first fifty years of the chemistry of 2,2′-bipyridine are reviewed from its first discovery in 1888 to the outbreak of the second global conflict in 1939. The coordination chemistry and analytical applications are described and placed in the context of the increasingly sophisticated methods of characterization which became available to the chemist in this time period. Many of the “simple” complexes of 2,2′-bipyridine reported in the early literature have been subsequently shown to have more complex structures.

Methicillin-resistant (MRSA) infections have become arduous to treat due to their capacity to form biofilms, develop persistence, and exhibit significant antimicrobial resistance. These factors contribute to the complexity of managing MRSA infections and highlight the urgent need for innovative treatment strategies. This endeavor aims to evaluate the safety of 2,2'-Bipyridine (2,2'-Bipy) derivatives and their antimicrobial, anti-biofilm, and anti-persister activities in treating MRSA Infections. Six derivatives were screened for their ADMET properties and tested for minimum inhibitory concentrations against various bacterial strains using agar well diffusion and broth dilution. Safety studies were conducted through hemolysis tests, cell viability assays, and acute oral toxicity examinations. Bactericidal mechanisms and biofilm disruption effects were analyzed using crystal violet staining and confocal microscopy assays. The murine thigh infection model was also used to investigate the efficacy. All derivatives exhibited favorable physicochemical profiles and ADMET properties and are predicted to be safe based on their drug-like properties. studies demonstrated that derivatives are non-toxic to 3T3 L1, and studies confirmed their safety in mice at a dose of 300 mg/kg and their non-hemolytic nature against rabbit red blood cells. All compounds showed potent antibacterial activity against the tested bacteria, including the resistant MRSA strain 831. They inhibited biofilm formation and eradicated biofilms in a dose-dependent manner against MTCC 737 and MRSA 831, and they effectively eliminated MRSA persister cells, outperforming the reference antibiotic vancomycin. These derivatives were found to depolarize the mitochondrial membrane and accumulate intracellular reactive oxygen species. These derivatives significantly reduced the bacterial load in the murine thigh infection model. The study concluded that 2,2'-Bipy derivatives possess significant antimicrobial activity, are non-toxic, and are effective in inhibiting biofilm formation and killing persister cells.

The syntheses of 4,4′-bis(4-dimethylaminophenyl)-6,6′-dimethyl-2,2′-bipyridine (1), 4,4′-bis(4-dimethylaminophenylethynyl)-6,6′-dimethyl-2,2′-bipyridine (2), 4,4′-bis(4-diphenylaminophenyl)-6,6′-dimethyl-2,2′-bipyridine (3), and 4,4′-bis(4-diphenylaminophenylethynyl)-6,6′-dimethyl-2,2′-bipyridine (4) are reported along with the preparations and characterisations of their homoleptic copper(I) complexes [CuL2][PF6] (L = 1–4). The solution absorption spectra of the complexes exhibit ligand-centred absorptions in addition to absorptions in the visible region assigned to a combination of intra-ligand and metal-to-ligand charge-transfer. Heteroleptic [Cu(5)(Lancillary)]+ dyes in which 5 is the anchoring ligand ((6,6′-dimethyl-[2,2′-bipyridine]-4,4′-diyl)bis(4,1-phenylene))bis(phosphonic acid) and Lancillary = 1–4 have been assembled on fluorine-doped tin oxide (FTO)-TiO2 electrodes in dye-sensitized solar cells (DSCs). Performance parameters and external quantum efficiency (EQE) spectra of the DSCs (four fully-masked cells for each dye) reveal that the best performing dyes are [Cu(5)(1)]+ and [Cu(5)(3)]+. The alkynyl spacers are not beneficial, leading to a decrease in the short-circuit current density (JSC), confirmed by lower values of EQEmax. Addition of a co-absorbent (n-decylphosphonic acid) to [Cu(5)(1)]+ lead to no significant enhancement of performance for DSCs sensitized with [Cu(5)(1)]+. Electrochemical impedance spectroscopy (EIS) has been used to investigate the interfaces in DSCs; the analysis shows that more favourable electron injection into TiO2 is observed for sensitizers without the alkynyl spacer and confirms higher JSC values for [Cu(5)(1)]+.

Alzheimer’s disease (AD) is a complex multifactorial neurodegenerative disease. Metal ion dyshomeostasis and Aβ aggregation have been proposed to contribute to AD progression. Metal ions can bind to Aβ and promote Aβ aggregation, and ultimately lead to neuronal death. Bifunctional (metal chelation and Aβ interaction) compounds are showing promise against AD. In this work, eleven new 3,3’-diamino-2,2’-bipyridine derivatives 4a-4k were synthesized, and evaluated as bifunctional agents for AD treatment. In vitro Aβ aggregation inhibition assay confirmed that most of the synthesized compounds exhibited significant self-induced Aβ1−42 aggregation inhibition. Among them, compound 4d displayed the best inhibitory potency of self-induced Aβ1−42 aggregation with IC50 value of 9.4 µM, and it could selectively chelate with Cu2+ and exhibited 66.2% inhibition of Cu2+-induced Aβ1−42 aggregation. Meanwhile, compound 4d showed strong neuroprotective activity against Aβ1−42 and Cu2+-treated Aβ1−42 induced cell damage. Moreover, compound 4d in high dose significantly reversed Aβ-induced memory impairment in mice.

Nine manganese(II) complexes with a series of non-steroidal anti-inflammatory drugs (namely sodium diclofenac, diflunisal, flufenamic acid, sodium meclofenamate, mefenamic acid, and tolfenamic acid) were prepared in the presence of diverse nitrogen donors, i.e., pyridine, 1,10–phenanthroline, 2,2′–bipyridine and neocuproine, as co-ligands and were characterized with spectroscopic techniques and single-crystal X-ray crystallography. The biological profile of the resultant complexes was investigated regarding their antioxidant potency and their interaction with DNA and serum albumins. The complexes interact with calf–thymus DNA in an intercalative mode and bind tightly and reversibly to human and bovine serum albumins studied. In order to assess the antioxidant activity of the Mn(II) complexes, their ability to scavenge 2,2′–azinobis(3–ethylbenzothiazoline–6–sulfonic acid) free radicals was monitored.

Collismycin A (CMA), a microbial product, has anti-proliferative activity against cancer cells, but the mechanism of its action remains unknown. Here, we report the identification of the molecular target of CMA by ChemProteoBase, a proteome-based approach for drug target identification. ChemProteoBase profiling showed that CMA is closely clustered with di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone, an iron chelator. CMA bound to both Fe(II) and Fe(III) ions and formed a 2:1 chelator-iron complex with a redox-inactive center. CMA-induced cell growth inhibition was completely canceled by Fe(II) and Fe(III) ions, but not by other metal ions such as Zn(II) or Cu(II). Proteomic and transcriptomic analyses showed that CMA affects the glycolytic pathway due to the accumulation of HIF-1α. These results suggest that CMA acts as a specific iron chelator, leading to the inhibition of cancer cell growth.

Photoredox catalysis and organocatalysis represent two powerful fields of molecule activation that have found widespread application in the areas of inorganic and organic chemistry, respectively. We merged these two catalysis fields to solve problems in asymmetric chemical synthesis. Specifically, the enantioselective intermolecular α-alkylation of aldehydes has been accomplished using an interwoven activation pathway that combines both the photoredox catalyst Ru(bpy)₃Cl₂ (where bpy is 2,2′-bipyridine) and an imidazolidinone organocatalyst. This broadly applicable, yet previously elusive, alkylation reaction is now highly enantioselective and operationally trivial.

Azamethiphos (AZA) is an insecticide and neurotoxic agent that causes the inhibition of acetylcholinesterase (AChE). AChE is a vital enzyme for neurotransmission because it metabolizes acetylcholine neurotransmitter at the synaptic cleft and terminates synaptic transmission. It is worth mentioning that organophosphates and carbamates inhibit AChE. These AChE inhibitors bind to the active site of the enzyme and inactivate it, leading to paralysis and death. Herein, for the first time, we develop a sensitive, low-cost, and rapid electrogenerated chemiluminescence (ECL) system for the detection of AZA. The designed ECL sensor was applied for the highly sensitive detection of AZA with a wide dynamic range (from 0.1 μM to 1000 μM) and low detection limit of 0.07 μM (S/N = 3). The practical utility of the sensor demonstrates high recoveries (96–102%) in real samples of lake water and wastewater.

Five new nucleoside antibiotics, named streptcytosines A–E (1–5), and six known compounds, de-amosaminyl-cytosamine (6), plicacetin (7), bamicetin (8), amicetin (9), collismycin B (10), and SF2738 C (11), were isolated from a culture broth of Streptomyces sp. TPU1236A collected in Okinawa, Japan. The structures of new compounds were elucidated on the basis of their spectroscopic data (HRFABMS, IR, UV, and 2D NMR experiments including 1H-1H COSY, HMQC, HMBC, and NOESY spectra). Streptcytosine A (1) belonged to the amicetin group antibiotics, and streptcytosines B–E (2–5) were derivatives of de-amosaminyl-cytosamine (6), 2,3,6-trideoxyglucopyranosyl cytosine. Compound 1 inhibited the growth of Mycobacterium smegmatis (MIC = 32 µg/mL), while compounds 2–5 were not active at 50 µg/disc. Bamicetin (8) and amicetin (9) showed the MICs of 16 and 8 µg/mL, respectively.

Three novel gold(III) complexes (1–3) of general composition [Au(Bipydc)(S2CNR2)]Cl2 (Bipydc = 2,2′-bipyridine-3,3′-dicarboxylic acid and R = methyl for dimethyldithiocarbamate (DMDTC), ethyl for diethyldithiocarbamate (DEDTC), and benzyl for dibenzyldithiocarbamate (DBDTC)) have been synthesized and characterized by elemental analysis, FTIR and NMR spectroscopic techniques. The spectral results confirmed the presence of both the Bipydc and dithiocarbamate ligands in the complexes. The in vitro cytotoxic studies demonstrated that compounds 1–3 were highly cytotoxic to A549, HeLa, MDA-231, and MCF-7 cancer cells with activities much higher (about 25-fold) than cisplatin. In order to know the possible mode of cell death complex 2, [Au(Bipydc)(DEDTC)]Cl2 was further tested for induction of apoptosis towards the MCF-7 cells. The results indicated that complex 2 induces cell death through apoptosis.