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Formation of the NiCo2O4 (NCO) nanoparticle with the simultaneous reduction of GO and growth of MoS2 by a two step hydrothermal process results in a 2D RGO-MoS2 (R-MoS2) cocatalyst layer with intimate interfacial contact with NCO. The phase purity, chemical coupling and morphology of the synthesized materials are established through X-ray diffraction, Raman and X-ray photoelectron spectroscopy studies. The ternary composite, RGO-MoS2-NiCo2O4 (RM-NCO), shows excellent electrocatalytic performance toward solar driven water splitting with 3.08% solar to hydrogen (STH) conversion efficiency, photocurrent density of 5.36 mA cm–2, injection efficiency of 97% at 1 V (vs Ag/AgCl) and long-term stability. The photo degradation (95%) of Rhodamine B under visible light irradiation is obtained in 90 min by the ternary composite (RM-NCO). The improved performance of the ternary composite, RM-NCO, over bare NCO and MoS2, toward photocatalytic activity is achieved through the dual charge transfer pathway between interfacial layer of NCO and MoS2 to RGO, which leads to generation of more photoinduced charge carriers and suppression of electron–hole recombination process.

To overcome chemical limitations of camptothecin (CPT), we report design, synthesis, and validation of a quinoline-based novel class of topoisomerase 1 (Top1) inhibitors and establish that compound 28 (N-(3-(1H-imidazol-1-yl)­propyl)-6-(4-methoxyphenyl)-3-(1,3,4-oxadiazol-2-yl)­quinolin-4-amine) exhibits the highest potency in inhibiting human Top1 activity with an IC50 value of 29 ± 0.04 nM. Compound 28 traps Top1–DNA cleavage complexes (Top1ccs) both in the in vitro cleavage assays and in live cells. Point mutation of Top1-N722S fails to trap compound 28-induced Top1cc because of its inability to form a hydrogen bond with compound 28. Unlike CPT, compound 28 shows excellent plasma serum stability and is not a substrate of P-glycoprotein 1 (permeability glycoprotein) advancing its potential anticancer activity. Finally, we provide evidence that compound 28 overcomes the chemical instability of CPT in human breast adenocarcinoma cells through generation of persistent and less reversible Top1cc-induced DNA double-strand breaks as detected by γH2AX foci immunostaining after 5 h of drug removal.

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