Search

Cocrystal, ionic salt, and coordination polymer had prompted the development of propellants, explosives, and pyrotechnics. However, the difference between their formation based on the same coformer has rarely been studied. 5,5′-Bis(trinitromethyl)-3,3′-bi-1H-1,2,4-triazole (BTNMBT) is perchlorate-free, favorable to scale-up, and a green energetic oxidizer with high physical performance (oxygen balance: +18.4%, IS: 22.5 J, FS: 252 N, D: 9073 m s–1, P: 36.2 GPa). To investigate the influence of different coformers on the formation of BTNMBT’s cocrystal, ionic salt, and metal–organic framework, organic acid as well as organic and inorganic bases with different dissociation constants (pKa) were theoretically studied. In this work, two energetic cocrystals, energetic ionic salt, and energetic metal–organic framework were synthesized based on BTNMBT. For their formation, the basic principle is found as follows: (i) when the pKavalue of organic base is far lower than both pKavalues of hydrogen-protons in organic acid, the reaction systems are prone to forming cocrystals; (ii) if the pKavalue of the selected organic base is higher than that of one of the hydrogen-protons in organic acid but lower than that of the other one, a 1:1 energetic ionic salt appears; (iii) the 1:2 type of energetic ionic salt (or coordination polymer) can form when the pKavalue of corresponding base is higher than values of both hydrogen-protons in organic acid. Among these shapes of derivatives, the coordination polymer form of BTNMBT not only exhibits good detonation performance (D: 8872 m s–1), but also shows positive oxygen balance (+18.2%) and high thermal stability (Td: 180 °C) comparable to those of AP and superior to those of ADN. These discoveries can assist the design and preparation of other promising energetic materials toward future high-performing energy applications.

The effectiveness of hydroxycinnamic acids (HCAs), that is, caffeic acid (CaA), chlorogenic acid (ChA), sinapic acid (SA), ferulic acid (FA), 3‐hydroxycinnamic acid (3‐HCA), and 4‐hydroxycinnamic acid (4‐HCA), as pBR322 plasmid DNA‐cleaving agents in the presence of CuIIions was investigated. Compounds bearing o‐hydroxy or 3,5‐dimethoxy groups on phenolic rings (CaA, SA, and ChA) were remarkably more effective at causing DNA damage than the compounds bearing no such groups; furthermore, CaA was the most active among the HCAs examined. The involvement of reactive oxygen species (ROS) and CuIions in the DNA damage was affirmed by the inhibition of the DNA breakage by using specific scavengers of ROS and a CuIchelator. The interaction between CaA and CuIIions and the influence of ethylenediaminetetraacetic acid (EDTA), the solvent, and pH value on the interaction were also studied to help elucidate the detailed prooxidant mechanism by using UV/Vis spectroscopic analysis. On the basis of these observations, it is proposed that it is the CaA phenolate anion, instead of the parent molecule, that chelates with the CuIIion as a bidentate ligand, hence facilitating the intramolecular electron transfer to form the corresponding CaA semiquinone radical intermediate. The latter undergoes a second electron transfer with oxygen to form the corresponding o‐quinone and a superoxide, which play a pivotal role in the DNA damage. The intermediacy of the semiquinone radical was supported by isolation of its dimer from the CuII‐mediated oxidation products. Intriguingly, CaA was also the most cytotoxic compound among the HCAs toward human promyelocytic leukemia (HL‐60) cell proliferation. Addition of exogenous CuIIions resulted in an effect dichotomy on cell viability depending on the concentration of CaA; that is, low concentrations of CaA enhanced the cell viability and, conversely, high concentrations of CaA almost completely inhibited the cell proliferation. On the other hand, when superoxide dismutase was added before, the two stimulation effects of exogenous CuIIions were significantly ameliorated, thus clearly indicating that the oxidative‐stress level regulates cell proliferation and death. These findings provide direct evidence for the antioxidant/prooxidant mechanism of cancer chemoprevention.