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Organometallic Ru-arene complexes are promising as anticancer agents, but the lack of tumor uptake and poor solubility in the physiological medium impede their development. In order to deal with these challenges, we developed gold nanoparticles coated with Ru(arene)-functionalized PNVP-Py, where PNVP-Py is pyridine end-functionalized poly(N-vinylpyrrolidone). It is demonstrated that these particles exhibit higher anti-proliferative activity than the individual organometallic ruthenium(ii) complex of the type [Ru(η6-p-cymene)(NN)Cl]PF6, where NN is bis(4-methoxyphenylimino)acenaphthene, against colorectal adenocarcinoma cell lines. More specifically, a RuII(η6-p-cymene) complex containing a NN bidentate ligand has been prepared and characterized by spectral studies and X-ray crystallography. To tether the isolated complex onto the surface of the AuNPs, PNVP-Py, which contains a pyridine group at one end to coordinate to the Ru-complex and a suitable functional group at the other end to bind on the surface of the AuNPs, has been prepared and utilized to obtain the macromolecular complex [Ru(η6-p-cymene)(NN)(PNVP-Py)]Cl2. Next, stable Ru(p-cym)(NN)(PNVP-Py)@AuNPs were obtained via a ligand exchange reaction of citrate-stabilized AuNPs with a macromolecular complex by a direct 'grafting to' approach and characterized well. Despite the lower DNA cleavage activity, the nanoconjugate exhibits better cytotoxicity than the individual complex against HT-29 colorectal adenocarcinoma cells on account of its enhanced permeability across the cell membrane. The AO/EB staining assay revealed that the nanoconjugate is able to induce an apoptotic mode of cell death, which was further quantitatively evaluated by Annexin V-FITC/PI double assay. An immunofluorescence assay indicated the higher potency of the nanoconjugate to inhibit cyclin D1 gene expression that is required for cancer cell growth. To the best of our knowledge, this is the first report of the modification of an organometallic Ru(arene) complex into a Ru(arene)metallopolymer-gold nanoconjugate for the development of ruthenium-based nanomedicine for cancer treatment.

Herein, we have developed a novel aggregation-induced emission (AIE) probe and three-dimensional (3D) printed portable device for copper (Cu2+) sensing in an aqueous medium. A ubiquitous synthetic route has been employed to devise the anthracene-conjugated imidazo[1,5-a]pyridine (TL19) probe as a unique anchor for Cu2+ ions. The TL19 is meticulously characterized through pivotal spectroscopic techniques, and the satisfactory results were obtained. The solvatochromic analysis and density functional theory calculations cohesively reveal that the TL19 exhibits the intramolecular charge transfer transition upon photoexcitation. Intriguingly, the TL19 exhibits spherically shaped nanoaggregates and enhanced fluorescence in DMSO/water (10:90) mixtures. This fluorescent nanoaggregate instantaneously responded toward the detection of Cu2+ via a deaggregation mechanism. The detection limit is found to be 9 pM in an aqueous medium. Further, the detection of Cu2+ in the HeLa cells has also been achieved due to bright green fluorescence, photostability, and biocompatibility nature of TL19 aggregates. On the other hand, an internet of things (IoT)-embedded 3D printed portable device is constructed for the detection of Cu2+ ions in real water samples. The Cu2+ detection is achieved through an IoT device, and results were acknowledged through an android application in 3.32 s round-trip time. Thus, the IoT-enabled AIE probe could be a prospective device for Cu2+ detection in a constrained environment.

Herein, we have developed a tool for monitoring the outdoor performance of dye-sensitized solar cells. In this regard, a new dye consisting of an N-aryl-substituted imidazole with N-alkylated carbazole as the donor and cyanoacrylic acid as the acceptor has been designed. The overall power conversion efficiency of the designed dye reached ∼50%, with respect to that of the N719-based device (4%) under similar experimental conditions. Further, the device was interfaced with an IoT system, which measured the voltage and transmitted the device parameters to the user's mobile phone through a cloud channel. The developed IoT tool provides a resolution of 0.0315 mV and a round-trip delay time of

Overexpression of cysteine cathepsins proteases has been documented in a wide variety of cancers, and enhances the l-cysteine concentration in tumor cells. We report the synthesis and characterization of copper(ii) complexes [Cu(L1)2(H2O)](SO3CF3)2, 1, L1 = 3-phenyl-1-(pyridin-2-yl)imidazo[1,5-a]pyridine, [Cu(L2)2(SO3CF3)]SO3CF3, 2, L2 = 3-(4-methoxyphenyl)-1-pyridin-2-yl-imidazo[1,5-a]pyridine, [Cu(L3)2(H2O)](SO3CF3)2, 3, L3 = 3-(3,4-dimethoxy-phenyl)-1-pyridin-2-yl-imidazo[1,5-a]pyridine and [Cu(L4)2(H2O)](SO3CF3)2, 4, L4 = dimethyl-[4-(1-pyridin-2-yl-imidazo[1,5-a]pyridin-3-yl)phenyl]amine as 'turn-on' optical imaging probes for l-cysteine in cancer cells. The molecular structure of complexes adopted distorted trigonal pyramidal geometry (τ, 0.68-0.87). Cu-Npy bonds (1.964-1.989 A) were shorter than Cu-Nimi bonds (2.024-2.074 A) for all complexes. Geometrical distortion was strongly revealed in EPR spectra, showing g‖ (2.26-2.28) and A‖ values (139-163 × 10-4 cm-1) at 70 K. The d-d transitions appeared around 680-741 and 882-932 nm in HEPES, which supported the existence of five-coordinate geometry in solution. The Cu(ii)/Cu(i) redox potential of 1 (0.221 V vs. NHE) was almost identical to that of 2 and 3 but lower than that of 4 (0.525 V vs. NHE) in HEPES buffer. The complexes were almost non-emissive in nature, but became emissive by the interaction of l-cysteine in 100% HEPES at pH 7.34 via reduction of Cu(ii) to Cu(i). Among the probes, probe 2 showed selective and efficient turn-on fluorescence behavior towards l-cysteine over natural amino acids with a limit of detection of 9.9 × 10-8 M and binding constant of 2.3 × 105 M-1. The selectivity of 2 may have originated from a nearly perfect trigonal plane adopted around a copper(ii) center (∼120.70°), which required minimum structural change during the reduction of Cu(ii) to Cu(i) while imaging Cys. The other complexes, with their distorted trigonal planes, required more reorganizational energy, which resulted in poor selectivity. Probe 2 was employed for optical imaging of l-cysteine in HeLa cells and macrophages. It exhibited brighter fluorescent images by visualizing Cys at pH 7.34 and 37 °C. It showed relatively less toxicity for these cell lines as ascertained by the MTT assay.

A new pyrene Schiff base (KB-4) was synthesized and demonstrated as simple colorimetric chemosensor for carbon dioxide (CO2) gas activated by fluoride anion. The chemical structure of KB-4 was validated through pivotal characterization methods. A combined quantum chemical calculations and spectroscopic techniques were adopted to understand the photophysical properties of KB-4. The sensitivity of KB-4 chemosensor towards various anions is investigated and showed excellent selectivity towards F− anion with a distinct color change. The mechanism of F− anion sensing is due to the complete deprotonation of –NH proton in KB-4 as revealed by 1H NMR titration studies as well as DFT calculations. Subsequently, the in-situ deprotonated KB-4 is employed for CO2 gas sensing. Interestingly, deprotonated KB-4 is responded instantaneously to CO2 gas by exhibiting significant colorimetric and fluorimetric changes with a detection limit of 0.4 ml. Further, digital image based RGB analysis using smartphone is introduced for detection of CO2 gas. The digital images of CO2 gas induced fluorimetric changes are captured using smartphone and the RGB analysis of the images are processed using MATLAB. The intensity variation in the color components as an indicative measure for detection of CO2 gas is demonstrated.

D−π–A, D–A−π–A, and other configuration-based organic dyes have shown great potential in the field of dye-sensitized solar cells (DSCs). Compared with traditional configurations, D–D′–A offers several advantages such as enrichment of the electron-donating ability, absorption spectral region, and molar extinction coefficient and inhibits dye aggregation. Hence, in this work, a novel D–D′–A-type dye has been designed and synthesized for DSC applications. In this configuration, substituted imidazole has been used as a primary donor, phenothiazine as an auxiliary donor, and cyanoacetic acid as an acceptor/anchoring group. Structural characterizations of a D–D′–A-type dye were done by using NMR and electron ionization–mass spectrometry. Photophysical, electrochemical, and computational studies were systematically performed to evaluate its electronic transitions, light-harvesting property, highest occupied molecular orbital (HOMO)/lowest unoccupied molecular orbital (LUMO) levels, and redox behavior. The photop...

Platelet activation has been reported to play a major role in arterial thrombosis, cancer metastasis, and progression. Recently, we developed a novel Ir(III)-based compound, [Ir(Cp∗)1-(2-pyridyl)-3-(4-dimethylaminophenyl)imidazo[1,5-a]pyridine Cl]BF4or Ir-6 and assessed its effectiveness as an antiplatelet drug. Ir-6 exhibited higher potency against human platelet aggregation stimulated by collagen. Ir-6 also inhibited ATP-release, intracellular Ca2+mobilization, P-selectin expression, and the phosphorylation of phospholipase Cγ2 (PLCγ2), protein kinase C (PKC), v-Akt murine thymoma viral oncogene (Akt)/protein kinase B, and mitogen-activated protein kinases (MAPKs), in collagen-activated platelets. Neither the adenylate cyclase inhibitor SQ22536 nor the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one significantly reversed the Ir-6-mediated inhibition of collagen-induced platelet aggregation. Moreover, Ir-6 did not considerably diminish OH radical signals in collagen-activated platelets or Fenton reaction solution. At 2 mg/kg, Ir-6 markedly prolonged the bleeding time in experimental mice. In conclusion, Ir-6 plays a crucial role by inhibiting platelet activation through the inhibition of signaling pathways, such as the PLCγ2–PKC cascade and the subsequent suppression of Akt and MAPK activation, thereby ultimately inhibiting platelet aggregation. Therefore, Ir-6 is a potential therapeutic agent for preventing or treating thromboembolic disorders or disrupting the interplay between platelets and tumor cells, which contributes to tumor cell growth and progression.

Design and synthesis of a novel fluorescent probe for the detection of picric acid is a topic of an incessant research interest. In this context, we have developed a novel ‘Y’ shaped D-A-D type chromophore (TP171). Phenothiazine and methoxy phenyl groups are acting as donor whilst N-substituted imidazole as acceptor unit. As synthesized TP171 show an excellent fluorescent property with a quantum yield of 24%. Intriguingly, the TP171 fluorescent probe instantaneously responded towards the detection of picric acid with a concentration of 12 μM. The detection limit is found to be 7.95 nM.

Two novel pyrene-based Schiff base compounds 4-[(5-pyren-1-yl-thiophen-2-ylmethylene)-amino]-phenol (KSB-1) and 4-[(4-pyren-1-yl-benzylidene)-amino]-phenol (KSB-2) were designed and synthesized by a condensation reaction with a diminutive modification of π-spacers. The KSB-1 and KSB-2 molecules are thoroughly characterized by pivotal spectroscopic techniques. The prepared products were found to yield excellent quantity, and crystallographic data was also analyzed for KSB-1. Moreover, the antibacterial activities of the synthesized KSB-1 and KSB-2 were investigated against the two strains of Pseudomonas aeruginosa. BSA binding interaction with these pyrene-based Schiff bases was investigated by fluorescence quenching method, and the quenching of BSA followed a static type. The binding constant and number of binding modes were calculated.

A series of copper(I) complexes [Cu(L)(PPh3)2]NO3 (1–5) of bidentate ligands 2-pyridin-2-yl-quinoline (L1), 4-phenyl-2-pyridin-2-yl-quinoline (L2) 2-pyridin-2-yl-quinoxaline (L3), 6,7-dimethyl-2-(pyridin-2-yl)quinoxaline (L4), and 4-phenyl-2-pyridin-2-yl-quinazoline (L5) have been synthesized and characterized by elemental analysis, absorption, emission, IR, 1H, 13C, 31P NMR spectroscopies and redox method. Of these complexes [Cu(L1)(PPh3)2]NO3 (1), [Cu(L3)(PPh3)2]NO3 (3), and [Cu(L4)(PPh3)2]NO3 (4) are structurally characterized by single-crystal X-ray analysis. They exhibited distorted tetrahedral coordination geometries around the copper(I) center with τ4 values of 0.77–0.86. In the solid-state, all these complexes have exhibited emission in the range of 450–750 nm and their excited-state lifetimes were measured as of 1.9–8.9 μs. However, all the complexes were found to be weak emissive in solution due to the excited state structural rearrangement. Further, Time-dependent density-functional theory (TDDFT) calculations showed that the charge transfers are mainly caused by the contribution of HOMO-2 → LUMO, HOMO-1 → LUMO and HOMO → LUMO orbitals.

Herein, the two typical anchoring groups are tethered into the indole chromophore and studied their impact on the molecular orbital energy levels and titania sensitization. The synthesized indole derivatives were meticulously characterized. The photophysical and time dependent density functional theory results were revealed that the indole connected rhodanine-3-acetic acid group is an efficient light harvester. The favorable electronic excitation from the highest occupied molecular orbital to the lowest unoccupied molecular orbital indicated that the dye comprised with rhodanine-3-acetic acid could be used as a prospective material for dye-sensitized solar cell applications.

A series of mixed ligand copper(II) complexes, formulated as [Cu(L1-L5)(phen)(H2O)](ClO4)2 (1–5), where phen = 1,10-phenanthroline, L1 = 2-pyridin-2-yl-quinoline, L2 = 2-pyridin-2-yl-quinoxaline, L3 = 6,7-dimethyl-2-pyridin-2-yl-quinoxaline, L4 = 4-phenyl-2-pyridin-2-yl-quinoline, and L5 = 4-phenyl-2-pyridin-2-yl-quinazoline, were synthesized and characterized. The molecular structure of 3, which alone formed into appreciable crystals, was determined by single-crystal X-ray studies, and the coordination geometry around Cu(II) was nearly square pyramidal (τ, 0.092). DNA and protein binding, DNA cleavage and in vitro cytotoxicity of the mixed ligand complexes 1–5 were investigated and compared with their analogue bis-complexes [Cu(L1-L5)2H2O](ClO4)2 6–10. All five mixed ligand complexes exhibited efficient DNA and protein binding, wherein 5 was the most potent. DNA cleavage studies revealed that all mixed ligand complexes engage in self-activated DNA cleavage, with 2 producing full conversion of supercoiled DNA to nicked circular form. Complex 5, with the highest DNA- and protein-binding efficiencies, demonstrated the highest cytotoxicity to A549 non-small human lung carcinoma cell (IC50 = 3.85 μM), three times more potent than cisplatin. Metal-assisted reactive oxygen species (ROS) were found to be responsible for cytotoxicity of the complexes. Fluorescent staining assays showed that all complexes induce apoptotic cell death along with some degree of necrosis. Western blot analysis of caspase-3 expression of cells exposed to Cu(II) complexes 1 and 5 revealed that both promote apoptosis, with 5 demonstrating more potency. Thus, the mixed ligand copper complexes demonstrated efficient biological activity compared to bis-complexes, with 5 holding promise for future investigation towards development as a cancer therapeutic.

A series of organometallic Ru(II)-arene complexes of the type [(η6-p-cymene)Ru(L)Cl](BF4) 1–6, where L is 3-phenyl-1-pyridin-2-yl-imidazo[1,5-a]pyridine (L1), dimethyl-[4-(1-pyridin-2-yl-imidazo[1,5-a]pyridin-3-yl)phenyl]-amine (L2), diphenyl-[4-(1-pyridin-2-yl-imidazo[1,5-a]pyridin-3-yl)phenyl]amine (L3), 9-[4-(1-pyridin-2-yl-imidazo-[1,5-a]pyridin-3-yl)-phenyl]-9H-carbazole (L4), 9-ethyl-3-(1-pyridin-2-yl-imidazo-[1,5-a]pyridin-3-yl)-9H-carbazole (L5), and 10-ethyl-3-(1-pyridin-2-yl-imidazo[1,5-a]pyridin-3-yl)-10H-phenothiazine (L6), has been isolated and characterised by elemental analysis, ESI-MS, NMR and cyclic voltammetry. The photophysical properties of the complexes have been studied by electronic absorption and emission spectral techniques. All the ligands exhibit tuneable photoluminescence behaviour with the emission maximum spanning through the visible region (475–670 nm) in dichloromethane while all the complexes are emissive in acetonitrile. The single crystal X-ray structures of 2, 3 and 4 reveal that the complexes have a “piano stool” coordination geometry, comprising one π-bonded arene centroid, two σ-bonded nitrogen atoms from the chelating ligand and one Cl− ion. From DNA induced EthBr emission quenching experiments the apparent DNA binding constants of the complexes (Kapp) have been evaluated, which follows the order, 2 (1.3) 100 μM), exhibit in vitro cytotoxicity against A549 small lung cancer cell lines higher than cisplatin (∼69 μM), as revealed by both MTT (11.8–18.1 μM) and crystal violet staining (12.7–23.5 μM) assays, which is in agreement with their DNA and BSA binding affinity. Also, the complexes 3–6 cause higher cell death mainly through the apoptotic mode, as revealed by the observation of a higher percentage of apoptotic cells in AO/EB (36–43%) and Annexin V-Cy3 (36–45%) stained cancer cells.

A series of new copper complexes have been synthesized and completely characterized by pivotal analytical techniques. The coordination geometry around copper(I) complex was best described as distorted tetrahedral geometry. The binding of bovine serum albumin with Cu(I) complexes are also been investigated. The Stern–Volmer analysis on quenching data exhibits the presence of the static quenching mechanism. The binding constants were calculated using modified Stern-Volmer, Lineweaver–Burk and Scatchard plots. All the complexes exhibit the binding constants in the order of 104. Thus, these results can contribute to the development of Cu(I) based drugs.

Ruthenium metal complex has been shown to exert several chemical and biological activities. A series of three novel ruthenium derivatives (TQ 1, 2 and 4) were synthesized to evaluate the anti-inflammatory and hepatoprotective activities in lipopolysaccharide (LPS)-stimulated macrophages and mice liver injury. The hydroxyl radical (OH°) scavenging activity of these derivatives has also been evaluated. The results revealed that among the tested compounds, TQ-4 effectively attenuated LPS-induced abnormal alteration in liver histoarchistructure via reducing alanine transaminase (ALT) and aspartate transaminase (AST). This compound exhibited significant inhibition of inflammatory cytokines (TNF-α and IL-1β), inflammatory enzyme (iNOS), the component of NF-κB signaling pathway (p65) and JNK phosphorylation in LPS-induced mice liver tissues. In vitro results showed that TQ-4 had the best inhibition of NO production and iNOS expression in LPS-induced RAW 264.7 cells. Mechanistic approach indicated that TQ-4 inhibited the LPS-induced JNK phosphorylation, IκBα degradation, NF-κB p65 phosphorylation and its nuclear translocation, and hydroxyl radical (OH°) productions in RAW 264.7 cells. However, the compounds TQ-1 and 2 had no effects in this study. TQ-4 also inhibited LPS-induced OH° production. This study reveals the protective effect of TQ-4 against LPS-induced acute liver injury, inflammation, and oxidative reaction by destructing JNK/NF-κB signaling pathways. The result of this study may infer that TQ-4 might be a promising ruthenium metal derivative and/or therapeutic agent for treating liver injury.

Arterial thrombosis plays a key role in cardiovascular diseases. Hence, developing more effective antithrombotic agents is necessary. We designed a ruthenium (II)-derived complex, [Ru(η

Platelets play a major role in hemostatic events and are associated with various pathological events, such as arterial thrombosis and atherosclerosis. Iridium (Ir) compounds are potential alternatives to platinum compounds, since they exert promising anticancer effects without cellular toxicity. Our recent studies found that Ir compounds show potent antiplatelet properties. In this study, we evaluated the in vitro antiplatelet, in vivo antithrombotic and structure&ndash, activity relationship (SAR) of newly synthesized Ir complexes, Ir-1, Ir-2 and Ir-4, in agonists-induced human platelets. Among the tested compounds, Ir-1 was active in inhibiting platelet aggregation induced by collagen, however, Ir-2 and Ir-4 had no effects even at their maximum concentrations of 50 &mu, M against collagen and 500 &mu, M against U46619-induced aggregation. Similarly, Ir-1 was potently inhibiting of adenosine triphosphate (ATP) release, calcium mobilization ([Ca2+]i) and P-selectin expression induced by collagen-induced without cytotoxicity. Likewise, Ir-1 expressively suppressed collagen-induced Akt, PKC, p38MAPKs and JNK phosphorylation. Interestingly, Ir-2 and Ir-4 had no effect on platelet function analyzer (PFA-100) collagen-adenosine diphosphate (C-ADP) and collagen-epinephrine (C-EPI) induced closure times in mice, but Ir-1 caused a significant increase when using C-ADP stimulation. Other in vivo studies revealed that Ir-1 significantly prolonged the platelet plug formation, increased tail bleeding times and reduced the mortality of adenosine diphosphate (ADP)-induced acute pulmonary thromboembolism in mice. Ir-1 has no substitution on its phenyl group, a water molecule (like cisplatin) can replace its chloride ion and, hence, the rate of hydrolysis might be tuned by the substituent on the ligand system. These features might have played a role for the observed effects of Ir-1. These results indicate that Ir-1 may be a lead compound to design new antiplatelet drugs for the treatment of thromboembolic diseases.

In oncotherapy, ruthenium (Ru) complexes are reflected as potential alternatives for platinum compounds and have been proved as encouraging anticancer drugs with high efficacy and low side effects. Cardiovascular diseases (CVDs) are mutually considered as the number one killer globally, and thrombosis is liable for the majority of CVD-related deaths. Platelets, an anuclear and small circulating blood cell, play key roles in hemostasis by inhibiting unnecessary blood loss of vascular damage by making blood clot. Platelet activation also plays a role in cancer metastasis and progression. Nevertheless, abnormal activation of platelets results in thrombosis under pathological settings such as the rupture of atherosclerotic plaques. Thrombosis diminishes the blood supply to the heart and brain resulting in heart attacks and strokes, respectively. While currently used anti-platelet drugs such as aspirin and clopidogrel demonstrate efficacy in many patients, they exert undesirable side effects. Therefore, the development of effective therapeutic strategies for the prevention and treatment of thrombotic diseases is a demanding priority. Recently, precious metal drugs have conquered the subject of metal-based drugs, and several investigators have motivated their attention on the synthesis of various ruthenium (Ru) complexes due to their prospective therapeutic values. Similarly, our recent studies established that novel ruthenium-based compounds suppressed platelet aggregation via inhibiting several signaling cascades. Our study also described the structure antiplatelet-activity relationship (SAR) of three newly synthesized ruthenium-based compounds. This review summarizes the antiplatelet activity of newly synthesized ruthenium-based compounds with their potential molecular mechanisms.

The regulation of platelet function by pharmacological agents that modulate platelet signaling has proven to be a positive approach to the prevention of thrombosis. Ruthenium complexes are fascinating for the development of new drugs, as they possess numerous chemical and biological properties. The present study aims to evaluate the structure-activity relationship (SAR) of newly synthesized ruthenium (II) complexes, TQ-1, TQ-2 and TQ-3 in agonists-induced washed human platelets. Silica gel column chromatography, aggregometry, immunoblotting, NMR, and X-ray analyses were performed in this study. Of the three tested compounds, TQ-3 showed a concentration (1–5 μM) dependent inhibitory effect on platelet aggregation induced by collagen (1 μg/mL) and thrombin (0.01 U/mL) in washed human platelets; however, TQ-1 and TQ-2 had no response even at 250 μM of collagen and thrombin-induced aggregation. TQ-3 was effective with inhibiting collagen-induced ATP release, calcium mobilization ([Ca2+]i) and P-selectin expression without cytotoxicity. Moreover, TQ-3 significantly abolished collagen-induced Lyn-Fyn-Syk, Akt-JNK and p38 mitogen-activated protein kinases (p38 MAPKs) phosphorylation. The compound TQ-3 containing an electron donating amino group with two phenyl groups of the quinoline core could be accounted for by its hydrophobicity and this nature might be the reason for the noted antiplatelet effects of TQ-3. The present results provide a molecular basis for the inhibition by TQ-3 in collagen-induced platelet aggregation, through the suppression of multiple machineries of the signaling pathway. These results may suggest that TQ-3 can be considered a potential agent for the treatment of vascular diseases.

The geometry (twist vs. planar) of a dye is one of the most pivotal factors for determining intramolecular charge transfer (ICT), light harvesting and photovoltaic properties of dye-sensitized solar cells. In order to comprehend the role of dye geometry on the above properties, we have devised the pyrene based D–π–A dyes namely 2-cyano-3-(5-pyren-1-yl-furan-2-yl)-acrylic acid (PFCC) and 2-cyano-3-(5-pyren-1-ylethynyl-furan-2-yl)-acrylic acid (PEFCC). The synthesized pyrene dyes were well characterized by NMR and EI-MS spectrometry. In both the dyes, the donor (pyrene) and acceptor (cyanoacrylic acid) segments remained the same. The varied π-spacers were furan and ethynyl furan. The influences of the ethynyl spacer on the energy levels, light absorption, dynamics of excited states and photovoltaic properties of the DSCs were systematically investigated via theoretical calculations and spectroscopic measurements. UV-visible absorption spectral measurements indicated that the introduction of the ethynyl spacer enhances the molar absorptivity of a dye (PEFCC) in the order of 2, but does not shift the absorption range, which is consistent with the results obtained from density functional theory (DFT) calculations. The theoretical analysis indicated that the charge transfer transition is mainly constituted of the HOMO to the LUMO that were found to be located on donor and acceptor segments, respectively, which is supportive for efficient charge separation and electron injection processes. TDDFT calculations highlighted that the LUMO of the PEFCC dye is more stabilized by the incorporation of the ethynyl group between the pyrene and furan moieties that aid to inject electrons efficiently into TiO2 thereby resulting in an enhanced power conversion efficiency of 2.47% when compared to the PFCC dye. Notably, the overall conversion efficiency of the PEFCC dye reached 60% with respect to that of an N719-based device (4.12%) fabricated under similar conditions. Transient absorption kinetic studies demonstrated that a slower charge recombination rate is an essential factor behind enhanced efficiencies in PEFCC based cells.

New copper(II) complexes, [Cu(L1)2(H2O)](ClO4)2, 1 [L1 = 2-pyridin-2-yl-quinoline], [Cu(L2)2(H2O)](ClO4)2, 2 [L2 = 2-pyridin-2-yl-quinoxaline], [Cu(L3)2(H2O)](ClO4)2, 3 [L3 = 6,7-dimethyl-2-pyridin-2-yl-quinoxaline], [Cu(L4)2(H2O)](ClO4)2, 4 [L4 = 4-phenyl-2-pyridin-2-yl-quinoline] and [Cu(L5)2(H2O)](ClO4)2, 5 [L5 = 4-phenyl-2-pyridin-2-yl-quinazoline], were synthesized and characterized as catalysts for selective fixation of atmospheric CO2. The molecular structure of 2 was determined by single-crystal X-ray studies and shown to have an unusual trigonal bipyramid geometry (τ, 0.936) around the copper(II) center, with the coordination of two ligand units and a water molecule. The Cu–Nquin (2.040, 2.048 A) bonds are slightly longer than the Cu–Npyr (1.987 A) bonds but shorter than the Cu–Owater bond (2.117 A). Well-defined Cu(II)/Cu(I) redox potentials of around 0.352 to 0.401 V were observed for 1–5 in acetonitrile. The electronic absorption spectra of 1–5 showed ligand-based transitions at around 208–286 nm with a visible shoulder at around 342–370 nm. The d–d transitions appeared at around 750–800 and 930–955 nm in acetonitrile. The rhombic EPR spectra of 1–5 exhibited three different g values gx, 2.27–2.34; gy, 2.06–2.09; and gz, 1.95–1.98 at 70 K. Atmospheric CO2 was successfully fixed by 1–5 using Et3N as a sacrificial reducing agent, resulting in CO32−-bound complexes of type [Cu(L)CO3(H2O)] that display an absorption band at around 614–673 nm and a νst at 1647 cm−1. This CO32−-bound complex of 1 was crystallized from the reaction mixture and it displayed a distorted square pyramidal geometry (τ, 0.369) around the copper(II) center via the coordination of only one ligand unit, a carbonate group, and water molecules. Furthermore, treatment of the carbonate-bound Cu(II) complexes with one equivalent of H+ under N2 atmosphere resulted in the liberation of bicarbonate (HCO3−) and regenerated the parent complexes. These regenerated catalysts were active enough to fix CO2 in eight repeating cycles without any change in efficiency. The fixation of CO2 possibly occurs via the formation of Cu(I)-species, which is accompanied by the formation of an MLCT band at around 450–500 nm. The rates of Cu(I)-species formation, kobs, were determined and found to be 5.41–10.31 × 10−3 s−1 in the presence of Et3N in acetonitrile at 25 °C. Interestingly, the copper(I)-species of 3 has been successfully crystallized and displayed a distorted tetrahedral geometry through the coordination of two units of ligand L3.

Arterial thrombosis plays a key role in cardiovascular diseases. Hence, developing more effective antithrombotic agents is necessary. We designed a ruthenium (II)-derived complex, [Ru(η6-cymene)2-(1H-benzoimidazol-2-yl)-quinoline Cl]BF4 (TQ-6), as a new antiplatelet drug. TQ-6 (0.3 µM) exhibited extremely strong inhibitory activity against platelet aggregation, Src, and Syk phosphorylation stimulated by agonists in human platelets. In collagen-activated platelets, TQ-6 also inhibited ATP-release, [Ca+2]i, P-selectin expression, FITC-PAC-1 binding, and hydroxyl radical formation, as well as the phosphorylation of phospholipase Cγ2, protein kinase C, mitogen-activated protein kinases, and Akt. Neither FITC-JAQ1 nor FITC-triflavin binding or integrin β3 phosphorylation stimulated by immobilized fibrinogen were diminished by TQ-6. Furthermore, TQ-6 had no effects in cyclic nucleotide formation. Moreover, TQ-6 substantially prolonged the closure time in whole blood, increased the occlusion time of thrombotic platelet plug formation and bleeding time in mice. In conclusion, TQ-6 has a novel role in inhibiting platelet activation through the inhibition of the agonist receptors-mediated inside-out signaling such as Src-Syk-PLCγ2 cascade and subsequent suppression of granule secretion, leading to disturb integrin αIIbβ3-mediated outside-in signaling, and ultimately inhibiting platelet aggregation. Therefore, TQ-6 has potential to develop as a therapeutic agent for preventing or treating thromboembolic disorders.

In oncotherapy, ruthenium complexes are considered as potential alternatives for platinum compounds, and have been proved as promising anticancer drugs with high efficacy and lesser side effects. Platelet activation plays a major role in cancer metastasis and progression. Hence, this study explored the effect of a newly synthesized ruthenium complex, [Ru(η6-cymene)(L)Cl]BF4(TQ5), where L = 4-phenyl-2-pyridin-2-yl-quinazoline), on human platelet activation. TQ5 (3–5 µM) inhibited concentration-dependent collagen-induced platelet aggregation in washed human platelets. However, this compound only inhibited platelet aggregation at a maximum concentration of 500 and 100 µM against thrombin and 9,11-dideoxy-11α, 9α-epoxymethanoprostaglandin (U46619)-induced stimulation, respectively. TQ5 inhibited collagen-induced ATP release and calcium mobilization ([Ca2+]i), without inducing cell cytotoxicity. In addition, neither SQ22536, an adenylate cyclase inhibitor, nor 1H-[1,2,4] oxadiazolo [4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor, significantly reversed the TQ5-mediated inhibition of platelet aggregation. TQ5 inhibited the collagen-induced phosphorylation of protein kinase B (Akt) and c-Jun N-terminal kinase (JNK), but did not effectively inhibit extracellular signal-regulated kinase 1/2 (ERK1/2) and p38-mitogen-activated protein kinase (p38-MAPK) in human platelets. Additionally, TQ5 significantly prolonged the closure time in whole blood and increased the occlusion time of thrombotic platelet plug formation in mice. This study demonstrates, for the first time, that a newly synthesized ruthenium complex, TQ5, exhibits potent antiplatelet activity by hindering ATP release and [Ca2+]i, and by decreasing the activation of Akt/JNK signals. Together, these results suggest that TQ5 could be developed as a therapeutic agent that helps prevent or treat thromboembolic disorders, since it is found to be potently more effective than a well-established antithrombotic aspirin.

Pyrene derivatives show immense potential as sensitizers for dye-sensitized solar cells (DSCs). Therefore, this work focuses on the impact of π-spacers on the photophysical, electrochemical and photovoltaic properties of pyrene based D-π-A dyes, since the insertion of π-spacers is one of the doable strategies to improve the light harvesting properties of the dye. In this respect, three new pyrene based D-π-A dyes have been synthesized and characterized by 1H, 13C NMR, and elemental analyses and EI-MS spectrometry. The selected π-spacers are benzene, thiophene and furan. Compared with a benzene spacer, the introduction of a heterocyclic ring spacer reduces the band gap of the dye and brings about the broadening of the absorption spectra to the longer wavelength region through intramolecular charge-transfer (ICT). Combined experimental and theoretical studies were performed to investigate the ICT process involved in the pyrene derivatives. The profound solvatochromism with increased nonradiative rate constants (knr) has been construed in terms of ICT from the pyrene core to rhodanine-3-acetic acid via conjugated π-spacers. Electrochemical data also reveal that the HOMO and LUMO energy levels are fine-tuned by incorporating different π-spacers between pyrene and rhodanine-3-acetic acid. On the basis of the optimized DSC test conditions, the best performance was found for PBRA, in which a benzene group is the conjugated π-spacer. The divergence in the photovoltaic behaviors of these dyes was further explicated by femtosecond fluorescence and electrochemical impedance spectroscopy.