Quorum sensing is a communication system among bacteria to sense the proper time to express their virulence factors. Quorum sensing inhibition is a therapeutic strategy to block bacterial mechanisms of virulence. The aim of this study was to synthesize and evaluate new bioisosteres of N-acyl homoserine lactones as Quorum sensing inhibitors in Chromobacterium violaceum CV026 by quantifying the specific production of violacein. Five series of compounds with different heterocyclic scaffolds were synthesized in good yields: thiazoles, 16a–c, thiazolines 17a–c, benzimidazoles 18a–c, pyridines 19a–c and imidazolines 32a–c. All 15 compounds showed activity as Quorum sensing inhibitors except 16a. Compounds 16b, 17a–c, 18a, 18c, 19c and 32b exhibited activity at concentrations of 10 µM and 100 µM, highlighting the activity of benzimidazole 18a (IC₅₀ = 36.67 µM) and 32b (IC₅₀ = 85.03 µM). Pyridine 19c displayed the best quorum sensing inhibition activity (IC₅₀ = 9.66 µM). Molecular docking simulations were conducted for all test compounds on the Chromobacterium violaceum CviR protein to gain insight into the process of quorum sensing inhibition. The in-silico data reveal that all 15 the compounds have higher affinity for the protein than the native AHL ligand (1). A strong correlation was found between the theoretical and experimental results.

Two novel water-soluble polynuclear Cu(ii)–risedronate complexes were synthesized, described structurally by single-crystal X-ray diffraction, and studied as antiparasitic agents against Trypanosoma cruzi and Leishmania mexicana.

In this work, we performed anti-proliferative assays for the compound N-(2-hydroxyphenyl)-2-propylpentanamide (HO-AAVPA) on breast cancer (BC) cells (MCF-7, SKBR3, and triple-negative BC (TNBC) MDA-MB-231 cells) to explore its pharmacological mechanism regarding the type of cell death associated with G protein-coupled estrogen receptor (GPER) expression. The results show that HO-AAVPA induces cell apoptosis at 5 h or 48 h in either estrogen-dependent (MCF-7) or -independent BC cells (SKBR3 and MDA-MB-231). At 5 h, the apoptosis rate for MCF-7 cells was 68.4% and that for MDA-MB-231 cells was 56.1%; at 48 h, that for SKBR3 was 61.6%, that for MCF-7 cells was 54.9%, and that for MDA-MB-231 (TNBC) was 43.1%. HO-AAVPA increased the S phase in MCF-7 cells and reduced the G2/M phase in MCF-7 and MDA-MB-231 cells. GPER expression decreased more than VPA in the presence of HO-AAVPA. In conclusion, the effects of HO-AAVPA on cell apoptosis could be modulated by epigenetic effects through a decrease in GPER expression.

Background/Objectives: Tamsulosin extended-release (ER) formulations minimize peak-related vasodilatory adverse events in benign prostatic hyperplasia (BPH) treatment. This study assessed the pharmacokinetics and bioequivalence of a generic tamsulosin 0.4 mg ER formulation against the innovator under fasting and fed conditions. Methods: Two randomized, open-label, four-period crossover, single-dose trials were conducted in healthy Mexican males. Subjects received treatment following a 10 h fast or a high-fat meal, with a 7-day washout. Plasma tamsulosin was quantified over 72 h via LC-MS/MS. An exploratory in vitro–in vivo correlation (IVIVC) analysis was also performed. Results: Analyses included 32 (fasting) and 58 (fed) subjects. In both states, 90% confidence intervals for C_max, AUC_0-t, and AUC_0-∞ geometric mean ratios fell entirely within the 80.00–125.00% bioequivalence limits. The formulations showed comparable dissolution (f₂ = 92.47), with numerical deconvolution proving most predictive in exploratory IVIVC. Notably, the pharmacokinetic profile of the test formulation was consistent with maintained controlled drug release under both dietary conditions and showed no pharmacokinetic evidence of food-induced dose dumping. Both formulations were well-tolerated; all adverse events were mild, with no clinically significant orthostatic hypotension observed. Conclusions: The generic tamsulosin 0.4 mg ER formulation is bioequivalent to the reference product in both fasting and fed states. Its structural robustness prevents dose dumping, ensuring a favorable hemodynamic safety profile. Comparable dissolution and IVIVC findings further support their reliability in vivo performance and therapeutic interchangeability. ClinicalTrials.gov identifiers: NCT07698288 and NCT07698275.