A new polyketide derivative koninginin H (1), has been isolated from the fungus Emericella nidulans, together with koninginin E (2), koninginin A (3), trichodermatide B (4), citrantifidiol (5), (4 S,5 R)-4-hydroxy-5-methylfuran-2-one (6), the glycerol derivatives gingerglycolipid B (7), (2 S)-bis[9 Z,12 Z]-1- O, 2- O-dilinoleoyl-3- O-[α-D-galactopyranosyl-(1″→6′)β-D-galactopyranosyl]glycerol (8), (2 S)-bis[9 Z,12 Z]-1- O, 2- O-dilinoleoyl-3- O-β-D-galactopyranosylglycerol (9), the cerebroside flavuside B (10), and the known sterols β-sitosterol glucoside and ergosta-5,7,22-trien-3-ol. Their structures were established by extensive NMR studies (¹H NMR, ¹³C NMR, DEPT, ¹H–¹H COSY, HSQC, HMBC) and mass spectrometry. The antibacterial, antimalarial, antifungal and antileishmanial activities of compounds 1–10 were examined and the results indicated that compound 4 showed good antifungal activity against Cryptococcus neoformans with an IC₅₀ value of 4.9 μg/mL.

The goal of this study was to assess the pharmacological effects of black tea (Camellia sinensis var. assamica) water extract on human kinin-forming enzymes in vitro. Tea is a highly consumed beverage in the world. Factor XII (FXII, Hageman factor)-independent- and -dependent activation of prekallikrein to kallikrein leads to the liberation of bradykinin (BK) from high-molecular-weight kininogen (HK). The excessive BK production causes vascular endothelial and nonvascular smooth muscle cell permeability, leading to angioedema. The prevalence of angiotensin-converting enzyme inhibitor (ACEI)-induced angioedema appears to be through BK. Both histamine and BK are potent inflammatory mediators. However, the treatments for histamine-mediated angioedema are unsuitable for BK-mediated angioedema. We hypothesized that long-term consumption of tea would reduce bradykinin-dependent processes within the systemic and pulmonary vasculature, independent of the anti-inflammatory actions of polyphenols. A purified fraction of the black tea water extract inhibited both kallikrein and activated FXII. The black tea water extracts inhibited factor XII-induced cell migration and inhibited the production of kallikrein on the endothelial cell line. We compared the inhibitory effects of the black tea water extract and twenty-three well-known anti-inflammatory medicinal herbs, in inhibiting both kallikrein and FXII. Surprisingly, arjunglucoside II specifically inhibited the activated factor XII (FXIIa), but not the kallikrein and the activated factor XI. Taken together, the black tea water extract exerts its anti-inflammatory effects, in part, by inhibiting kallikrein and activated FXII, which are part of the plasma kallikrein–kinin system (KKS), and by decreasing BK production. The inhibition of kallikrein and activated FXII represents a unique polyphenol-independent anti-inflammatory mechanism of action for the black tea.

Histone deacetylase (HDAC) inhibitors represent a promising class of anti-cancer agents that play a key role in both epigenetic and non-epigenetic regulation, leading to cancer cell death, apoptosis, and cell cycle arrest. This study synthesized novel bicyclic hydroxamic acid derivatives and evaluated their inhibitory and selectivity activity against class I and IIb HDACs. Our findings demonstrate that Compound 2e specifically inhibits HDAC10 with high selectivity over HDAC6, while shows no significant impact on class I HDACs. Compound 2a exhibited the most potant inhibitory activity against HDAC10, with IC₅₀ 0.41 ± 0.02 nM. In contrast, Compound 2f revealed a preference toward HDAC6, with an IC₅₀ value of 2.5 ± 0.3 nM. Compounds 2c and 2d demonstrated high selectivity toward class IIb over class I HDACs. Docking and molecular dynamics studies revealed that compound 2a fits well into the active site of HDAC10, forming stable and strong interactions with key residues F204, D94, W205, and E274 in HDAC10. In addition, we assessed the anti-proliferative activity these compounds against a panel of four human solid tumor cell lines. To evaluate their selectivity, non-cancerous kidney cell lines (LLC-PK1 and VERO) were employed to determine the effects of these compounds on normal cell proliferation.