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Abstract This article presents the synthesis and detailed structural investigation of a new palladium(II) heteroligand complex trans-[PdCl(CNXyl)2(C{CN(H)Xyl}2)]Cl, containing an acyclic diaminocarbene ligand and two isocyanide ligands. X-ray diffraction and NMR spectroscopy revealed that complex is stabilized both in the crystal and in solution by a system of N–H···Cl– hydrogen bonds formed between one chloride anion and two N–H groups of the diaminocarbene ligand (N–H···Cl–···H–N), with calculated energies of 3.8–5.4 kcal/mol. A Cambridge Structural Database search identified 22 other palladium(II) acyclic diaminocarbene complexes with similar N–H···X···H–N (X = Cl–, Br–, O=C<, O=S<, etc.) hydrogen-bonded systems. The complex demonstrated significant antiproliferative activity against the triple-negative breast cancer cell line MDA-MB-231, with an IC50 value of 5.55 ± 0.45 µM, which is four times higher than that of cisplatin. Show less

Immunotherapy represents a paradigm shift in oncology, rooted in a century of evolving scientific understanding and clinical application. From the pioneering use of Coley’s toxins in the late nineteenth century to the introduction of cytokine-based interventions, the trajectory of immunotherapeutic approaches has paralleled advancements in immunology and molecular biology. This review comprehensively examines the historical development and progressive refinement of immunotherapy for cancer, charting the transition from non-specific immune stimulation to targeted immune modulation. Central to this discussion are the sophisticated mechanisms by which tumour cells evade immune detection and destruction. These include downregulation of antigen presentation machinery, secretion of immunosuppressive cytokines, recruitment of regulatory T cells and myeloid-derived suppressor cells, and exploitation of immune checkpoint pathways, particularly CTLA-4 and PD-1/PD-L1 axes. The advent of immune checkpoint inhibitors has yielded durable clinical responses in diverse malignancies, substantiating their role as foundational agents in cancer therapy. Nonetheless, both primary and acquired resistance to immune checkpoint inhibition remain significant clinical obstacles. Resistance mechanisms are multifactorial, involving tumour-intrinsic genetic alterations, modulation of the tumour microenvironment, and adaptive changes in immune cell phenotypes. Contemporary research endeavors are directed at overcoming these barriers, including the optimization of combinatorial regimens, development of next-generation checkpoint modulators, tumour-specific vaccines, and the integration of adoptive cell therapies. Future directions in cancer immunotherapy are poised to leverage advances in systems biology, genomics, and single-cell technologies to individualize interventions and enhance therapeutic efficacy. Ultimately, a comprehensive delineation of tumour-immune interactions will underpin the next generation of rational, effective, and durable cancer immunotherapies. Show less

High-Grade Serous Ovarian Cancer (HGSOC) is the most common and lethal subtype of ovarian cancer, known for its high aggressiveness and extensive genomic alterations. Typically diagnosed at an advanced stage, HGSOC presents formidable challenges in drug therapy. The limited efficacy of standard treatments, development of chemoresistance, scarcity of targeted therapies, and significant tumor heterogeneity render this disease incurable with current treatment options, highlighting the urgent need for novel therapeutic approaches to improve patient outcomes. In this study we report a straightforward and stereoselective synthetic route to novel Pd(II)-vinyl and -butadienyl complexes bearing a wide range of monodentate and bidentate ligands. Most of the synthesized complexes exhibited good to excellent in vitro anticancer activity against ovarian cancer cells. Particularly promising is the water-soluble complex bearing two PTA (1,3,5-triaza-7-phosphaadamantane) ligands and the Pd(II)-butadienyl fragment. This compound combines excellent cytotoxicity towards cancer cells with substantial inactivity towards non-cancerous ones. This derivative was selected for further studies on ex vivo tumor organoids and in vivo mouse models, which demonstrate its remarkable efficacy with surprisingly low collateral toxicity even at high dosages. Moreover, this class of compounds appears to operate through a ferroptotic mechanism, thus representing the first such example for an organopalladium compound. Show less

The coordination capacity of thiosemicarbazone ligands and their synergism with palladium(II) ions modulate their reactivity, allowing custom design. Using thiosemicarbazones with two potential stable tautomeric forms and imidazole as bioisosteres, we studied how the substitution in the N4 group of the thiosemicarbazone by the p-chlorophenyl group modifies their hydrophilic properties, integrity in solution, and interactions toward their potential targets. The coordination to Pd(II) affects the bioactivity of the ligands, resulting in either improved or reduced antiproliferative effects depending on the cell type (cancerous versus bacterial, respectively). Show less

In the frame of our research aiming to develop efficient triplet-emitting materials, we are exploring the role of the second coordination sphere in enhancing the rigidity of structures and its controlling aspect over the extents of excited state distortions. We thus synthesised three N^C^N cyclometalated complexes [M(LBn)Cl] (M = Pt, Pd, and Ni), where the two ortho-positions of the pyridyl moieties in 1,3-di(2-pyridyl)-benzene are benzyl substituted (Bn) forming a tight binding pocket for the metal and the Cl− ancillary ligand. The molecular structures from single-crystal X-ray diffraction show a markedly distorted square planar M(II) coordination with τ4 values of around 0.4. UV-vis absorption spectra show long-wavelength bands in the range 350 to 5400 nm with the energies increasing along the series Ni < Pt < Pd. The Pt(II) complex emits in solution at 298 K (λmax = 544 nm) and displays aggregated emission within poly(methyl methacrylate) (PMMA) films at various concentrations at 298 K. The Pd(II) derivative exhibits a broad emission band at 77 K in a frozen glassy 2-MeTHF matrix, peaking at 530 nm. Very different from the Pt(II) and Pd(II) spectra, the Ni(II) sample showed a broad emission with λmax = 699 nm at 77 K, with a quantum yield of 20% and ms lifetime. TD-DFT calculated decomposition of the assumed emissive T1 state showed similar 3MLCT character of about 30% for all three complexes, but marked differences in LC character of about 38% for Pd and Pt and only 5% for Ni. In turn, for Ni the by far the highest MC character (42%) was calculated which strongly speaks against triplet photoluminescence from the Ni(II) complex. Show less

PT-112 is a novel small molecule exhibiting promising clinical activity in patients with solid tumors. PT-112 kills malignant cells by inhibiting ribosome biogenesis while promoting the emission of immunostimulatory signals. Accordingly, PT-112 is an authentic immunogenic cell death (ICD) inducer and synergizes with immune checkpoint inhibitors in preclinical models of mammary and colorectal carcinoma. Moreover, PT-112 monotherapy has led to durable clinical responses, some of which persisting after treatment discontinuation. Mitochondrial outer membrane permeabilization (MOMP) regulates the cytotoxicity and immunogenicity of various anticancer agents. Here, we harnessed mouse mammary carcinoma TS/A cells to test whether genetic alterations affecting MOMP influence PT-112 activity. As previously demonstrated, PT-112 elicited robust antiproliferative and cytotoxic effects against TS/A cells, which were preceded by the ICD-associated exposure of calreticulin (CALR) on the cell surface, and accompanied by the release of HMGB1 in the culture supernatant. TS/A cells responding to PT-112 also exhibited eIF2α phosphorylation and cytosolic mtDNA accumulation, secreted type I IFN, and exposed MHC Class I molecules as well as the co-inhibitory ligand PD-L1 on their surface. Acute cytotoxicity and HMGB1 release caused by PT-112 in TS/A cells were influenced by MOMP competence. Conversely, PT-112 retained antiproliferative effects and its capacity to drive type I IFN secretion as well as CALR, MHC Class I and PD-L1 exposure on the cell surface irrespective of MOMP defects. These data indicate a partial involvement of MOMP in the mechanisms of action of PT-112, suggesting that PT-112 is active across various tumor types, including malignancies with MOMP defects. Show less

Abstract Transition metal complexes have been widely utilized as cellular imaging tools. To impart organelle specificity, ligand architecture is usually modified to modulate properties like overall charge and lipophilicity. In many such designs, the metal identity and its intrinsic properties are often ignored. To address this gap, in this study, we explored the effects of changing the metal center on the localization patterns of isostructural complexes. To this end, we employed the thiosemicarbazone Dp44mT to synthesize coumarin‐conjugated complexes of Au(III), Pt(II), and Pd(II). Although the metal centers in these compounds share a formal d 8 configuration, they differ in properties such as ionic radius, charge density, and ligand exchange rates, which can affect their subcellular localization patterns. In addition, we synthesized a second set of analogous complexes using BODIPY as the conjugating fluorophore to assess the influence of using a different dye on the cellular distribution. Confocal imaging revealed that the complexes exhibited distinct intracellular distributions. For instance, while the coumarin‐conjugated Pt(II) complex localized specifically in lysosomes, the corresponding lipophilic Pd(II) complex lacked this specificity and instead followed a diffusely cytosolic distribution. Similarly, the more lipophilic BODIPY conjugated complexes were non‐specific in their cellular distribution as well. Overall, the findings of this study highlight the interplay of metal identity and lipophilicity in determining the localization patterns of Dp44mT‐based metal complexes, offering fresh insights into the design of new metal‐based imaging tools. Show less

Platinum-based drugs are a mainstay in chemotherapy, with traditional forms exerting their work directly on DNA. In recent years, it has been observed that platinum complexes had the potential to induce immunogenic cell death (ICD) and effectively trigger antitumor immune responses. Herein, to obtain novel platinum complexes with chemo-immunological properties, a series of Pt(ΙΙ)-N-heterocyclic carbene (Pt(ΙΙ)-NHC) complexes derived from 4,5-diarylimidazoles were synthesized. Among them, the dominant complex 3f was proved to exhibit better anti-liver cancer capacity compared to cisplatin and oxaliplatin. Complex 3f showed the ability to cause DNA damage by binding to DNA. In addition, it triggered intracellular reactive oxygen species (ROS) generation, affected the function of mitochondria, and blocked cells in G0/G1 phase, ultimately induced apoptosis in liver cancer cells. Furthermore, complex 3f activated endoplasmic reticulum stress (ERS) which promoted the release of damage-associated molecular patterns (DAMPs), induced ICD and dendritic cells (DCs) maturation. Interestingly, complex 3f also upregulated PD-L1, consequently converted "cold tumors" into "hot tumors". Overall, complex 3f had the potential to be regarded as a promising chemoimmunotherapy for the treatment of liver cancer. Show less

Protein Arginine Methyltransferases (PRMTs) are a family of enzymes regulating protein arginine methylation, which is a post-translational modification crucial for various cellular processes. Recent studies have highlighted the mechanistic role of PRMTs in cancer pathogenesis, immunotherapy, and drug resistance. PRMTs are involved in diverse oncogenic processes, including cell proliferation, apoptosis, and metastasis. They exert their effects by methylation of histones, transcription factors, and other regulatory proteins, resulting in altered gene expression patterns. PRMT-mediated histone methylation can lead to aberrant chromatin remodeling and epigenetic changes that drive oncogenesis. Additionally, PRMTs can directly interact with key signaling pathways involved in cancer progression, such as the PI3K/Akt and MAPK pathways, thereby modulating cell survival and proliferation. In the context of cancer immunotherapy, PRMTs have emerged as critical regulators of immune responses. They modulate immune checkpoint molecules, including programmed cell death protein 1 (PD-1), through arginine methylation. Drug resistance is a significant challenge in cancer treatment, and PRMTs have been implicated in this phenomenon. PRMTs can contribute to drug resistance through multiple mechanisms, including the epigenetic regulation of drug efflux pumps, altered DNA damage repair, and modulation of cell survival pathways. In conclusion, PRMTs play critical roles in cancer pathogenesis, immunotherapy, and drug resistance. In this overview, we have endeavored to illuminate the mechanistic intricacies of PRMT-mediated processes. Shedding light on these aspects will offer valuable insights into the fundamental biology of cancer and establish PRMTs as promising therapeutic targets. Show less

Dihydroorotate dehydrogenase (DHODH)-mediated ferroptosis defense is a targetable vulnerability in cancer. Currently, only a few DHODH inhibitors have been utilized in clinical practice. To further enhance DHODH targeting, we introduced the mitochondrial targeting group triphenylphosphine (TPP) to brequinar (BRQ), a robust DHODH inhibitor, resulting in the creation of active molecule B2. This compound exhibits heightened anticancer activity, effectively inhibiting proliferation in various cancer cells, and restraining tumor growth in melanoma xenografts in mice. B2 achieves these effects by targeting DHODH, triggering the formation of reactive oxygen species (ROS), promoting mitochondrial lipid peroxidation, and inducing ferroptosis in B16F10 and A375 cells. Surprisingly, B2 significantly downregulates PD-L1 and alleviates immune suppression. Importantly, B2 exhibits no apparent adverse effects in mice. Collectively, these findings highlight that enhancing the mitochondrial targeting capability of the DHODH inhibitor is a promising therapeutic approach for melanoma treatment. Show less

Mono or bis(tetrazole–thiolato) Pd(II) or Pt(II) complexes were obtained from the reactions of dialkyl Pd(II) or Pt(II) complexes with organic tetrazole–thiones (1-aryl- or 1-alkyl-1H-tetrazole-5-thiones) via deprotonation. In contrast, equimolar reactions of zerovalent Pt(0) or Pd(0) complexes with organic tetrazole–thiones afforded hydrido or bis(tetrazole–thiolato) Pt(II) and Pd(II) complexes, and cyclometallated Pt(II) or Pd(II) complexes bearing a tetrazole–thiolato moiety via oxidative addition, depending on the organic substituents on the tetrazole–thiones. In particular, variable (time and temperature)-dependent 1H-NMR spectra of the hydrido Pt(II) tetrazole–thiolates reveal an upfield shift of the hydride signal, suggesting N,S-coordination behavior of the tetrazole–thiolato ligand. Additionally, the N-CH2 signal corresponds to the six-membered ring of platinacycle or palladacycle exhibiting geminal coupling with multiple protons and PR3 ligands; these coupling values were further determined using 1H{31P} experiments. Finally, treatment of the alkyl Pd(II) tetrazole–thiolate or Pd(II) bis(tetrazole–thiolates) with organic tert-butyl isocyanide, thiophenol, and organic halides caused the selective insertion of the isocyanide into the Pd–C bond or deprotonation to afford a Pd(II) disulfide complex and substitution to afford new organic tetrazolyl sulfides. Show less

Pd–aryl complexes bearing a wide range of disphosphine, aryl and halide ligands were synthesized. Their remarkable in vitro and ex vivo anticancer activity seems to involve DNA as the main biotarget and an intrinsic apoptotic cell death mechanism. Show less

To date, a general approach for the direct α-acyloxylation of cyclic 1,3-dicarbonyls remains challenging. Herein, we report a Pd-catalyzed α-acyloxylation of cyclic 1,3-dicarbonyl-derived hypervalent iodine compounds with highly abundant carboxylic acids. Our approach utilizes a commercially available Pd(OAc)₂ catalyst, which exhibits mild reaction conditions, scalability, operational simplicity, and robustness against moisture and air. Importantly, our approach eliminates the need for excess carboxylic acids (only 1 equiv) and the use of explosive peroxides and is compatible with diverse complex substrates (e.g., glycyrrhetinic acid and celastrol). The power of this method is further demonstrated through significantly simplifying a previous synthesis. Show less

The stepwise, one-pot synthesis of heterobimetallic carbene gold(i) platinum(ii) complexes from readily available starting materials is presented. The protecting group free methodology is based on the graduated nucleophilicities of aliphatic and aromatic amines as linkers between both metal centers. This enables the selective, sequential installation of the metal fragments. In addition, the obtained complexes were tested as potential anticancer agents and directly compared to their gold(i) palladium(ii) counterparts. Show less

We describe the synthesis of a triazolyl-pyridine-based aminophosphine, N-(diphenylphosphaneyl)-6-(1-phenyl)-1H-(1,2,3-triazol-4-yl)pyridine-2-amine [2,6-{(PPh2)-N(H)(C5H3N)(C2HN3C6H5)}] [1, PN(H)N hereafter], and its palladium and platinum complexes and their catalytic application. The reaction of 1 with [M(COD)Cl2] (M = Pd or Pt) afforded the cationic complex [(MCl){PN(H)N}-κ3-P,N,N]Cl [M = Pd (2) or Pt (3)]. Alternatively, compounds 2 and 3 were also synthesized by treating [2,6-{H2N(C5H3N)(C2HN3C6H5)}] (A) with [M(COD)Cl2] (M = Pd or Pt), followed by the addition of stoichiometric amounts of PPh2Cl and Et3N. The neutral, dearomatized complexes [(MCl){PNN}-κ3-P,N,N] [M = Pd (4) or Pt (5)] were prepared by the deprotonation of the NH of 2 and 3 with 1 equiv of tBuOK. Compounds 4 and 5 were also synthesized stepwise by treating [2,6-{H2N(C5H3N)(C2HN3C6H5)}] (A) with [M(COD)Cl2] (M = Pd or Pt) to give intermediate complexes [{MCl2}2,6-{NH2(C5H3N)(C2HN3C6H5)-κ2-N,N}] [M = Pd (B) or Pt (C)], which were subsequently phosphinated. The in situ-generated PNN ligand-stabilized Pd nanoparticles from compound 2 catalyzed the annulation of o-bromobenzaldehyde with alkynes to yield indenone derivatives. Mechanistic investigations suggested that the reaction was catalyzed by Pd nanoparticles (Pd@2) generated from compound 2 and proceeded through sequential oxidative addition, alkyne insertion, and reductive elimination steps to produce indanone products. Show less

The biological activity of Pd(II) and Pt(II) complexes toward three different cancer cell lines as well as inhibition of selenoenzyme thioredoxin reductase (TrxR) was modulated in an unexpected way by the introduction of triazolate as a "protective group" to the inner metal coordination sphere using the iClick reaction of [M(N₃)(terpy)]PF₆ [M = Pd(II) or Pt(II) and terpy = 2,2':6',2″-terpyridine] with an electron-poor alkyne. In a cell proliferation assay using A549, HT-29, and MDA-MB-231 human cancer cell lines, the palladium compound was significantly more potent than the isostructural platinum analogue and exhibited submicromolar activity on the most responsive cell line. This difference was also reflected in the inhibitory efficiency toward TrxR with IC₅₀ values of 0.1 versus 5.4 μM for the Pd(II) and Pt(II) complexes, respectively. UV/Vis kinetic studies revealed that the Pt compound binds to selenocysteine faster than to cysteine [k = (22.9 ± 0.2)·10^-3 vs (7.1 ± 0.2)·10^-3 s^-1]. Selective triazolato ligand exchange of the title compounds with cysteine (Hcys) and selenocysteine (Hsec)─but not histidine (His) and 9-ethylguanine (9EtG)─was confirmed by ¹H, ⁷⁷Se, and ¹⁹⁵Pt NMR spectroscopy. Crystal structures of three of the four ligand exchange products were obtained, including [Pt(sec)(terpy)]PF₆ as the first metal complex of selenocysteine to be structurally characterized. Show less

Dimethyl fumarate (DMF) is an antioxidative and anti-inflammatory drug approved for treatment of multiple sclerosis and psoriasis; however, beneficial effects of DMF have also been found in other inflammatory diseases and cancers. DMF is a prodrug that is immediately hydrolysed to monomethyl fumarate (MMF) in vivo. Both fumarates activate the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway, and Nrf2 is a key transcription factor of the antioxidant response. The immunosuppressive and anti-inflammatory actions of DMF occur through several mechanisms: via inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway and by downregulation of aerobic glycolysis and pyroptosis in activated myeloid and lymphoid cells. MMF is also an agonist of hydroxycarboxylic acid receptor 2 (HCAR2). Differences in the strength of effects and mechanisms of action of both fumarates are discussed. The aim of this review was to analyse and compare the neuroprotective, antioxidative and anti-inflammatory effects of DMF and its active metabolite, MMF, in cellular (in vitro) and animal models of neurodegenerative diseases (NDs), other than multiple sclerosis. There are more than twenty studies that currently represent this field. Most of the studies are concerned with cellular or animal models of Alzheimer's disease (AD) and Parkinson's disease (PD), one utilized a mouse model of Huntington's disease (HD) and one clinical trial was carried out with amyotrophic lateral sclerosis (ALS) patients. The discrepancies in the results of the various studies are discussed, and issues requiring further research have been identified. Show less

The term ‘magic bullet’ is a scientific concept proposed by the German Nobel laureate Paul Ehrlich in 1907, describing a medicine that could specifically and efficiently target a disease without harming the body. Oncologists have been looking for a magic bullet for cancer therapy ever since. However, the current therapies for cancers—including chemotherapy, radiation therapy, hormone therapy, and targeted therapy—pose either pan-cytotoxicity or only single-target efficacy, precluding their ability to function as a magic bullet. Intriguingly, niclosamide, an FDA-approved drug for treating tapeworm infections with an excellent safety profile, displays broad anti-cancer activity in a variety of contexts. In particular, niclosamide inhibits multiple oncogenic pathways such as Wnt/β-catenin, Ras, Stat3, Notch, E2F-Myc, NF-κB, and mTOR and activates tumor suppressor signaling pathways such as p53, PP2A, and AMPK. Moreover, niclosamide potentially improves immunotherapy by modulating pathways such as PD-1/PDL-1. We recently discovered that niclosamide ethanolamine (NEN) reprograms cellular metabolism through its uncoupler function, consequently remodeling the cellular epigenetic landscape to promote differentiation. Inspired by the promising results from the pre-clinical studies, several clinical trials are ongoing to assess the therapeutic effect of niclosamide in cancer patients. This current review summarizes the functions, mechanism of action, and potential applications of niclosamide in cancer therapy as a magic bullet. Show less

Mitochondrial uncoupling proteins (UCP) are a part of the large family of mitochondrial solute carriers (SLC25s), concentrated in the inner mitochondrial membrane that carries protons from intermembrane space to the matrix. Further, some UCPs are also involved in the transportation of the fatty acid anions and catalyzed the proton transport by fatty acid cycling across the membrane. Out of the 5 UCPs, UCP 2, 4, and 5 are localized in the central nervous system (CNS), and alteration within the expression of these UCPs results in neuronal dysfunction and, ultimately, death of neurons. UCPs play a vital role in regulating mitochondrial membrane potential, preventing reactive oxygen species (ROS) production, alteration in neuronal activity, and the regulation of calcium homeostasis that ultimately results in the prevention of neuronal loss. These changes in mitochondria impact the function and survival of neurons playing a critical role in the progression of neurodegenerative diseases, particularly Alzheimer's disease (AD) and Parkinson's disease (PD). Additionally, UCP2 regulates the microglia response towards neuroinflammation by modulating microglia's M1 and M2 phenotypes. These microglia cells are further involved in regulating inflammatory response and synaptic functions. Moreover, UCP2, 4, and 5 are ubiquitously present in all brain regions that negatively regulate ROS production and inflammation, leading to the prevention of neuronal cell death. Increased ROS production is a common symptom reported in neurodegenerative diseases that affect several pathways concerned with neuronal death, either apoptosis or autophagy. These accumulating evidence suggested UCPs as a possible therapeutic target for the management of neurodegenerative diseases. Show less

A new diaminocarbene cis-palladium(II) complex containing a 2-aminobenzoxazole ligand was synthesized by reacting cis-[PdCl2(CNCy)2] and 2-aminobenzoxazole. The structure and composition of the obtained complex were proven by NMR spectroscopy and high-resolution mass spectrometry. The cytotoxicities of the obtained complex and structurally similar palladium(II) complexes containing a 2-aminothiazole ligand were tested against human cancer cells of various histogenesis (MCF-7, HL60, HeLa, DLD1, A431). The activities of several complexes against cancer cells were higher than those of the reference drug cisplatin and the free ligands, i.e., 2-aminooxazole and substituted 2-aminothiazoles. Show less

Pd(II)-compounds are presently regarded as promising anticancer drugs, as an alternative to Pt(II)-based drugs (e.g., cisplatin), which typically trigger severe side-effects and acquired resistance. Dinuclear Pd(II) complexes with biogenic polyamines such as spermine (Pd2Spm) have exhibited particularly beneficial cytotoxic properties, hence unveiling the importance of understanding their impact on organism metabolism. The present study reports the first nuclear magnetic resonance (NMR)-based metabolomics study to assess the in vivo impact of Pd2Spm on the metabolism of healthy mice, to identify metabolic markers with possible relation to biotoxicity/side-effects and their dynamics. The changes in the metabolic profiles of both aqueous and lipophilic extracts of mice kidney, liver, and breast tissues were evaluated, as a function of drug-exposure time, using cisplatin as a reference drug. A putative interpretation was advanced for the metabolic deviations specifically triggered by Pd2Spm, this compound generally inducing faster metabolic response and recovery to control levels for all organs tested, compared to cisplatin (except for kidney lipid metabolism). These results constitute encouraging preliminary metabolic data suggestive of potential lower negative effects of Pd2Spm administration. Show less

Abstract A series of palladium(II) complexes with 1H- and 2H-tetrazole ligands (2-isopropyl-5-R-2H-tetrazoles and 1H-tetrazol-1-ylcarboxylic acids) was synthesized. Structure of the obtained compounds was confirmed by 1H and 13C NMR spectroscopy, high-resolution mass spectrometry, and single crystal X-ray diffraction analysis. According to the spectrophotometry data, the complexes are weakly bound to DNA. The cytotoxic activity of the obtained palladium complexes was studied in vitro. Show less

Water soluble Pd(ii) and Pt(ii)–ADC species synthesized via the metal-mediated coupling of isocyanides and 1,2-diaminobenzene have demonstrated antitumor potential.

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A new dinuclear Pd(I) complex coordinating two bis(NHC) ligands revealed an unsuspected stability despite the unsaturation of the two metal centres. Even more surprisingly, the compound showed high and selective antiproliferative activity against different cancer cell lines and ovarian cancer tumoroids, and the mechanism of action was different from that of cisplatin. Show less