Glioblastoma (GBM) is an extremely aggressive form of brain cancer that remains challenging to treat, especially owing to the lack of effective targeting and drug delivery concerns. Due to its anatomical advantages, the nose-to-brain strategy is an interesting route for drug delivery. Nanoengineering has provided technological tools and innovative strategies to overcome biotechnological limitations, which is promising for improving the effectiveness of conventional therapies. Herein, we designed a biomimetic multifunctional nanostructure produced by polymeric poly(d,l-lactic-co-glycolic) acid (PLGA) core loaded with Temozolomide (TMZ) coated with cell membrane isolated from glioma cancer cells. The developed nanostructures (NP-MB) were fully characterized, and their biological performance was investigated extensively. The results indicate that NP-MB could control TMZ release and promote TMZ permeation in the ex vivo nasal porcine mucosa. The higher cytotoxicity of NP-MB in different glioma cell lines, particularly against U251 cells, reinforces their potential for homotypic targeting. The chicken chorioallantoic membrane assay revealed a tumor size reduction and antiangiogenic activity. In vivo biodistribution studies showed that NP-MB effectively reaches the brain following nasal administration. These findings suggest that NP-MB holds promise as a biomimetic nanoplatform for effective targeting and homotypic recognition in GBM therapy with high potential for clinical translation.

Four new Cu/PPh₃/naphtoquinone complexes were synthesized, characterized (IR, UV/visible, 1D/2D NMR, mass spectrometry, elemental analysis, and X-ray diffraction), and evaluated as anticancer agents. We also investigated the reactive oxygen species (ROS) generation capacity of complex 4, considering the well-established photochemical property of naphthoquinones. Therefore, employing the electron paramagnetic resonance (EPR) “spin trap”, 5,5-dimethyl-1-pyrroline N-oxide (DMPO) technique, we identified the formation of the characteristic •OOH species (hydroperoxyl radical) adduct even before irradiating the solution containing complex 4. As the irradiation progressed, this radical species gradually diminished, primarily giving rise to a novel species known as •DMPO-OH (DMPO + •OH radical). These findings strongly suggest that Cu(I)/PPh₃/naphthoquinone complexes can generate ROS, even in the absence of irradiation, potentially intensifying their cytotoxic effect on tumor cells. Interpretation of the in vitro cytotoxicity data of the Cu(I) complexes considered their stability in cell culture medium. All of the complexes were cytotoxic to the lung (A549) and breast tumor cell lines (MDA-MB-231 and MCF-7). However, the higher toxicity for the lung (MRC5) and breast (MCF-10A) non-tumoral cells resulted in a low selectivity index. The morphological analysis of MDA-MB-231 cells treated with the complexes showed that they could cause decreased cell density, loss of cell morphology, and loss of cell adhesion, mainly with concentrations higher than the inhibitory concentration of 50% of cell viability (IC₅₀) values. Similarly, the clonogenic survivance of these cells was affected only with concentrations higher than the IC₅₀ values. An antimigratory effect was observed for complexes 1 and 4, showing around 20–40% of inhibition of wound closure in the wound healing experiments.

Herein, we report on the synthesis and characterization of ruthenium compounds with the general formula [RuCl(AA-H)(NO)(dppb]PF₆, where AA = glycine (1), L-alanine (2), L-phenylalanine (3) and L-valine (4), and dppb = 1,4-bis(diphenylphosphine)butane. The complexes were characterized using elemental analysis, UV/Vis and infrared spectroscopies, ¹H, ¹³C, ³¹P NMR techniques, and cyclic voltammetry. Furthermore, the structures of the compounds (1) and (3) were determined using single-crystal X-ray diffraction. In vitro evaluation of the Ru(II)/nitrosyl/amino acid complexes revealed their cytotoxic activities against triple-negative MDA-MB-231 breast cancer cells, and against the non-tumor murine fibroblast cells. All the compounds decreased the percentage of viable cells, inducing cell death by apoptosis. Additionally, the Ru(II) complexes inhibited the migration of MDA-MB-231 cells at concentrations lower than 35 µM, after 48 h of exposure. Thus, these complexes may be promising agents for the treatment of triple-negative MDA-MB-231 breast cancer.

Manganese is a bioessential element that plays a crucial role in biological systems. Four Mn(II) complexes with different 1,10‐phen skeletons were synthesized, characterized, and their purity was confirmed by elemental analysis. The solid structure of cis ‐[Mn(phenOne) ₂ Cl ₂ ] ( 3 ) where phenOne is 1,10‐phenanthroline‐5,6‐dione, was determined by x‐ray diffraction. All complexes are stable in aqueous media and interact with human serum albumin, an important behavior for a good pharmacokinetic profile. All complexes were tested against Mycobacterium tuberculosis, Trypanosoma cruzi , and Leishmania amazonensis . Furthermore, their cytotoxicity was investigated on breast (MDA‐MB‐231 and MCF‐10A) and lung (A549 and MRC‐5) human cell lines. The effect of complex 3 , the most promising complex, on the morphology of MDA‐MB‐231 breast cancer cells was further studied at different concentrations. The cytotoxic effect was confirmed by fluorescence microscopy using Hoechst/PI dyes. Viscosity, circular dichroism, fluorescence experiments, and electrophoresis indicated that DNA is not the main target for this compound. Overall, manganese(II)–phenanthroline complexes represent a promising scaffold for medicinal applications.