A bioinspired manganese(II)-creatine coordination polymer with anti-inflammatory potential: supramolecular framework, periodic-DFT calculations and spectroscopic study.

The synthesis, structural characterization, spectroscopic features, solubility, and anti-inflammatory properties of a novel manganese(II)-creatine coordination polymer, {[Mn(μ2-CRN)2(H2O)2](NO3)2·2H2O}n (CRN = creatine), are reported. Single-crystal X-ray diffraction revealed a one-dimensional coordination polymer crystallizing in the triclinic system (P1¯), in which the Mn2+ center resides on a crystallographic inversion center and adopts a regular octahedral geometry defined by four carboxylate oxygen atoms from four syn-syn μ2-bridging CRN ligands and two trans-aqua ligands; adjacent Mn2+ centers are doubly bridged along the crystallographic a axis (Mn⋯Mn = 4.7085 Å). Hirshfeld surface analysis demonstrated that the framework is dominated by O⋯H/H⋯O and N⋯H/H⋯N contacts, yielding compact packing with only 6.37% void volume. Periodic density functional theory calculations supported the assignment of Raman and infrared vibrational modes. Thermal analyses revealed a three-stage decomposition (25-400 °C) involving sequential loss of lattice water, coordinated water, nitrate, and organic ligand. In vitro anti-inflammatory evaluation against lipopolysaccharide-stimulated RAW 264.7 macrophages showed no cytotoxicity up to 50 μM and an inverse concentration-dependent inhibition of nitric oxide production (maximal reduction of 25 ± 2% at 0.78 μM). Cell-free control experiments confirmed that nitrate counterions do not contribute to nitrite generation or interfere with the Griess reaction, validating the biological origin of the observed inhibition. Aqueous solubility was determined experimentally as 1.00 mM (0.514 g/L) at 25 °C, and in silico pharmacokinetic parameters indicate low gastrointestinal absorption, absence of P-glycoprotein substrate behavior, and no cytochrome inhibition, positioning this bioinspired compound for further mechanistic investigation of inflammatory pathways.