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

Table 1 Mapping of pinocembrin’s mechanistic actions to experimental cancer models

Experimental model	Mechanism targeted	Key findings	Ref.
Human cancer cell lines (in vitro)	Mitochondrion-mediated apoptosis	PB stabilized mitochondrial membrane potential, downregulated Bcl-2, promoted Bax translocation, and triggered cytochrome C release. This led to the activation of caspase-9 and caspase-3, resulting in apoptotic cell death	Kumar et al[40], 2007
Cancer cell lines (in vitro)	ROS modulation and mitochondrial function	PB reduced intracellular ROS levels and preserved mitochondrial integrity. By limiting oxidative stress, it disrupted the energy balance necessary for tumor cell proliferation	Gong[41], 2021
Cancer cell lines (in vitro)	Anti-inflammatory and antioxidant pathways	PB inhibited nuclear factor-kappa B activation, which lowered cyclooxygenase-2 and inducible nitric oxide synthase expression. Concurrently, it upregulated endogenous antioxidant enzymes, thereby reducing prostaglandin and nitric oxide production, which support tumor progression	Zhou et al[38], 2015
Animal models and cell assays	Integrated safety, apoptosis, and signaling	Across multiple preclinical models, PB showed minimal toxicity and a broad therapeutic window. It combined pro-apoptotic effects (via the mitochondrial pathway) with anti-inflammatory and antioxidant actions, supporting further development	Elbatreek et al[42], 2023

PB: Pinocembrin; ROS: Reactive oxygen species.