Gold nanoparticles (AuNPs) have shown great potential for use in nanomedicine and nanotechnologies due to their ease of synthesis and functionalization. However, their apparent biocompatibility and biodistribution is still a matter of intense debate due to the lack of clear safety data. To investigate the biodistribution of AuNPs, monodisperse 14-nm dual-radiolabeled [¹⁴C]citrate-coated [¹⁹⁸Au]AuNPs were synthesized and their physico-chemical characteristics compared to those of non-radiolabeled AuNPs synthesized by the same method. The dual-radiolabeled AuNPs were administered to rats by oral or intravenous routes. After 24 h, the amounts of Au core and citrate surface coating were quantified using gamma spectroscopy for ¹⁹⁸Au and liquid scintillation for the ¹⁴C. The Au core and citrate surface coating had different biodistribution profiles in the organs/tissues analyzed, and no oral absorption was observed. We conclude that the different components of the AuNPs system, in this case the Au core and citrate surface coating, did not remain intact, resulting in the different distribution profiles observed. A better understanding of the biodistribution profiles of other surface attachments or cargo of AuNPs in relation to the Au core is required to successfully use AuNPs as drug delivery vehicles.

Isoflavone derivatives were prepared from benzoylbenzofuran precursors. The synthesized compounds were analyzed by 1D and 2D nuclear magnetic resonance (NMR) spectroscopy, as well as high-resolution mass spectrometry (HRMS) to confirm their structures. The benzoylbenzofuran and isoflavone analogues were evaluated for inhibition of sirtuin 1 (SIRT1) and cell proliferation in MDA-MB-231 triple-negative breast cancer (TNBC) cells. Several isoflavone and benzoylbenzofuran derivatives exhibited potent antiproliferative effects against the MDA-MB-231 cancer cell line. Most of the isoflavone derivatives attenuated SIRT1 activity to below 50%. The most active compounds were the isoflavone quinones 38, 39, and 40, at IC₅₀ values of 5.58 ± 0.373, 1.62 ± 0.0720, and 7.24 ± 0.823 μM, respectively. Importantly, the most active compound, 6-methoxy-4',6'-dimethylisoflavone-2',5'-quinone (39) displayed SIRT1 inhibitory activity comparable to that of the reference compound, suramin. The in silico docking simulations in the active site of SIRT1 further substantiated the experimental results and explored the binding orientations of potent compounds in the active site of the target.

In the study, ultraperformance liquid chromatography–quadrupole time-of-flight–mass spectrometry analysis of Leucosidea sericea leaf and stem extracts led to the identification of various classes of compounds. Further chromatographic purifications resulted in the isolation of 22 compounds that consisted of a new triterpenoid named leucosidic acid A (1), an acetophenone derivative 2, a phloroglucinol derivative 3, three chromones 4–6, seven pentacyclic triterpenoids 7–13, a phytosterol glucoside 14, a flavonoid 15, and seven flavonoid glycosides 16–22. Nineteen of these compounds including the previously undescribed triterpenoid 1 are isolated for the first time from L. sericea. The structures of the isolated compounds were assigned based on their high-resolution mass spectrometry and nuclear magnetic resonance data. Some of the isolated triterpenoids were evaluated for inhibitory activity against α-amylase, α-glucosidase, and pancreatic lipase. Of the tested compounds, 1-hydroxy-2-oxopomolic acid (7) and pomolic acid (13) showed higher potency on α-glucosidase than acarbose, which is used as a positive control in this study. The two compounds inhibited α-glucosidase with IC₅₀ values of 192.1 ± 13.81 and 85.5 ± 6.87 μM, respectively.