Molecules

Dielectric relaxation of n-propanol and isopropanol was examined by radio-frequency measurements at seven fixed frequencies (0.3–32 MHz) over +20 to −160 °C and by openCOSMO-RS calculations. Apparent characteristic times were assigned from dielectric-loss maxima and analyzed with Arrhenius and Eyring formalisms. Nine temperature scans were available for each sample, obtained with three independent measuring capacitors and three repeat scans per capacitor. Capacitor-specific Arrhenius fits gave apparent activation energies of 21.30 ± 0.16 kJ mol⁻¹ (SD; 95% CI of the mean 20.91–21.69) for n-propanol and 21.99 ± 0.16 kJ mol⁻¹ (95% CI 21.60–22.38) for isopropanol. A conservative Welch comparison of the three independent-capacitor estimates gave ΔE_a = 0.687 kJ mol⁻¹ (95% CI 0.332–1.042, p = 0.0058). Although this sub-kJ difference is statistically distinguishable in the cell-level analysis, it is not considered to have mechanistic significance because systematic temperature uncertainty and unresolved spectral overlap are not included in that comparison. Eyring activation enthalpies are 19.60 ± 0.15 and 20.23 ± 0.15 kJ mol⁻¹ (SD), respectively. Entropy and Gibbs-energy values are reported only as apparent quantities under κ = 1. openCOSMO-RS yields liquid-to-n-hexane infinite-dilution transfer enthalpies of 30.5 and 28.0 kJ mol⁻¹. These transfer quantities include hydrogen bonding and nonspecific solvation, dispersion, and packing contributions and are therefore not identified with hydrogen-bond enthalpies. Literature calorimetry gives lower neat-alcohol hydrogen-bonding enthalpy magnitudes of approximately 17 kJ mol⁻¹. Kirkwood factors above unity indicate strong static orientational correlation. Because the seven-frequency window does not independently resolve the Debye and structural α processes, the kinetic parameters are interpreted as effective descriptors of the dominant dielectric-loss process rather than mode-specific barriers.

Cannabidiol (CBD) is a highly lipophilic phytocannabinoid whose low aqueous solubility, variable oral absorption, extensive first-pass metabolism, and chemical instability motivate advanced delivery strategies. Carbon nanodots (CNDs) have tunable surface chemistry and photoluminescence and have been investigated as carriers for multiple therapeutic cargos. This review critically evaluates whether the literature supports a specific CBD–CND delivery advantage. A structured narrative search of PubMed and targeted publisher websites was conducted. Evidence was classified as direct CBD–CND evidence, indirect CND-platform evidence, or indirect CBD-nanoformulation evidence. No direct study was identified that characterized CBD loading on CNDs and then demonstrated release, pharmacokinetics, safety, or therapeutic efficacy. Existing support is therefore indirect: CNDs can carry other drugs, whereas lipid, polymeric, micellar, and transdermal systems can improve selected CBD formulation or preclinical endpoints. Consequently, improved solubility, targeting, lower toxicity, enhanced bioavailability, and therapeutic synergy remain hypotheses for CBD–CND systems. The review retains a broad discussion of possible applications while clearly separating demonstrated evidence from proposed uses and defining the analytical, comparative, pharmacokinetic, biodistribution, and toxicological studies needed to validate the platform.

Chronic low-grade inflammation (metaflammation) is a key contributor to obesity-associated metabolic disorders and their cardiovascular complications. This study investigated the effects of CXT29, a novel dual cyclooxygenase-2 (COX-2) inhibitor and thromboxane prostanoid receptor (TP) antagonist, in comparison with its parent compound etodolac, in a murine model of diet-induced metabolic dysfunction. Four-week-old male C57BL/6 mice were fed either a standard diet or a high-fat diet for 18 weeks and subsequently treated with etodolac (20 mg/kg/day) or CXT29 (25 mg/kg/day) by oral gavage for 5 weeks. High-fat-diet-fed mice developed increased body weight, impaired glucose tolerance, altered circulating metabolic hormones, liver dysfunction, steatosis, inflammatory cell infiltration, and systemic inflammation. Both treatments attenuated systemic inflammation and improved the metabolic alterations induced by the obesogenic diet. Notably, CXT29, but not etodolac, attenuated the increase in circulating plasminogen activator inhibitor-1 (PAI-1), a biomarker associated with cardiovascular risk. These findings indicate that pharmacological inhibition of COX-2 improves metabolic dysfunction associated with diet-induced obesity. Furthermore, the additional TP antagonism provided by CXT29 does not compromise the metabolic benefits associate with COX-2 inhibition, while displaying a distinct effect on circulating PAI-1, supporting further investigation of this dual-target approach in obesity-associated metabolic dysfunction.