Pinocembrin as a novel anti-cancer agent: Exploring preclinical evidence along with therapeutic potential

Figure 1 Atom-numbered chemical structure of pinocembrin (5,7-dihydroxyflavanone). The hydroxyl groups at carbon positions C-5 and C-7 are shown explicitly, which are critical sites for phase II metabolic conjugation such as glucuronidation and sulfation. The absence of substituents on the B-ring is also highlighted, a feature that contributes to both its pharmacological profile and metabolic lability.

Figure 2 Cellular and molecular mechanisms of pinocembrin’s anticancer activity. This schematic illustrates how pinocembrin (PB) enters cancer cells and triggers mitochondrion-mediated apoptosis through upregulation of Bax, downregulation of Bcl-2, and subsequent activation of caspase-9 and caspase-3. Concurrently, PB reduces intracellular reactive oxygen species levels, destabilizing the metabolic balance required for tumor growth and inhibiting phosphoinositol-3 kinase/protein kinase B signaling. Additionally, PB’s anti-inflammatory effects mediated by nuclear factor-kappa B inhibition decrease cyclooxygenase-2 and inducible nitric oxide synthase expression, further impeding cancer cell survival and proliferation. AKT: Protein kinase B; COX-2: Cyclooxygenase-2; iNOS: Inducible nitric oxide synthase; NF-κB: Nuclear factor-kappa B; PI3K: Phosphoinositol-3 kinase; ROS: Reactive oxygen species.