Herein, we first present synthesis, structures, luminescent properties, and electrochemistry of gold(III)‐N‐heterocyclic carbene (NHC) complexes fasten with 2,2′‐bipyridine (bpy) or 1,10′‐phenanthroline (phen). Starting from the proligand 3‐[pyridin‐3‐yl]imidazo[1,5‐a]pyridin‐4‐ylium hexafluorophosphate (1·HPF6), two novel complexes, namely, [Au(1)(bpy)Cl][PF6]2 (2) and [Au(1)2(phen)][PF6]3 (3), have been synthesized and characterized by several spectroscopic techniques. Finally, the solid‐state structures of 2, 3, and precursors [Au(bpy)Cl2][PF6] and [Au(phen)Cl2][PF6] have been determined by single‐crystal X‐ray diffraction studies. The absorption, emission, and lifetime properties of 2 and 3 have been compared with the precursors [Au(bpy)Cl2][PF6] and [Au(phen)Cl2][PF6] to observe the influence of NHC. Though the precursors [Au(bpy)Cl2][PF6] and [Au(phen)Cl2][PF6] are non‐luminescent, yet complexes 2 and 3 are luminescent. A combination of the chromophoric and π‐acid bpy/phen ligand in Au(III) complexes with the strong σ‐donor NHC ligand significantly enhanced the emission properties of the complexes. The blue emission of 2 and 3 in 390–500 nm regions has been tentatively ascribed to arise from intraligand and metal‐to‐ligand charge transfer (MLCT) transitions; also, partial contributions are expected from hydrogen‐bonding interactions. Cyclic voltammetric studies revealed Au(III) → Au(I) and Au(I) → Au(0) reductions at ~ −0.35 to ‐0.29 V and ~ −1.20 to ‐1.15 V, and the potentials are compared with precursors.

The design and synthesis of a cleft-shaped bis-diarylurea receptor for chloride anion transport is reported in this work. The receptor is based on the foldameric nature of N,N′-diphenylurea upon its dimethylation. The bis-diarylurea receptor exhibits a strong and selective affinity for chloride over bromide and iodide anions. A nanomolar quantity of the receptor efficiently transports the chloride across a lipid bilayer membrane as a 1:1 complex (EC50 = 5.23 nm). The work demonstrates the utility of the N,N′-dimethyl-N,N′-diphenylurea scaffold in anion recognition and transport.

We report the design and synthesis of a new cleft-shaped bis-urea receptor for the recognition of tetrahedral oxyanions from a foldameric N,N′-dimethyl-N,N′-diphenylurea scaffold. The receptor forms 3:1 host–guest complexes with sulfate, phosphate, and arsenate anions in the solid state by readily binding them through hydrogen bonding. 1H NMR analysis of binding events in a competitive medium (DMSO-d 6/H2O, 90:10) revealed that the receptor has a strong and selective affinity for arsenate (K a(3:1) = 2.41 (±0.79) × 108 M–3) in comparison with phosphate and no affinity for sulfate. The receptor extracts the three oxyanions from water into chlorinated organic solvents when the tetra-n-butyl ammonium ion is used as a cationic support. The receptor also crystallizes out the arsenate anion from water with faster kinetics in acetonitrile solution with a similar cationic support.

Leishmaniasis is a group of neglected tropical diseases (NTDs) caused by about 20 species of obligate intracellular protozoan parasites of the genus Leishmania, which occurs in cutaneous, mucocutaneous, and visceral forms. Many researchers have sought to utilize natural products for novel and effective treatments to combat many infectious diseases, including leishmaniasis. Holarrhena pubescens Wall. ex G. Don (Apocynaceae) bark is a rich source of bioactive steroidal alkaloids. The total alkaloidal extract (IC50 6.12 ± 0.117 μg/mL), and the isolated alkaloid, holanamine, showed significant antileishmanial activity (IC50 2.66 ± 0.112 μM against AG83 and 3.80 ± 0.126 μM against BHU-575) against the Leishmania donovani parasite, better than miltefosine (IC50 19.61 ± 0.093 μM against AG83 and 23.20 ± 0.094 μM against BHU-575). Holanamine inhibited the L. donovani topoisomerase 1B (LdToP1B) in a non-competitive manner (IC50 2.81 ± 0.105 μM), indicating that it interacts with the free enzyme and enzyme–DNA complex without inhibiting human topoisomerase. Hydrogen bonding and hydrophobic interactions of holanamine with the N-terminal and hinge region of the large subunit of LTop1B is responsible for its potent antileishmanial activity, as shown by docking studies. Treatment with holanamine causes apoptotic-like cell death by generating cellular and mitochondrial reactive oxygen species, disrupting the mitochondrial membrane potential and inducing ultrastructural alterations in the promastigotes. Holanamine effectively clears intracellular amastigotes but minimally affects host macrophages with no significant cytotoxicity in HEK 293 and L929 cell lines. Thus, our studies show that holanamine can further be used to develop effective antileishmanial agents against evolving drug-resistant parasites.