## 1 Introduction
Pharmacokine studies have reported single-dose administration (10 to 30 mg) in healthy human adult males, a time to reach maximum plasma concentration (0.08-0.21 uM) (Tmax) ranging from 15 to 33 h post-ingestion, with a half-life varying between 28 and 62 h and volume of distribution varying from 250 to 800 L, indicating prolonged retention in the body [16; 18]. These parameters can be influenced by factors including the food matrix, presence of dietary fats, and individual variations in metabolism [16; 18]. Understandingthese pharmacokinetic characteristics is essential for optimizing lycopene's therapeutic applications and determining appropriate dosing regimens. Lycopene has gained significant attention for its broad spectrum of pharmacological activities. Its principal mechanisms of action include potent antioxidant, anti-inflammatory, and anti-proliferative effects, which collectively contribute to its therapeutic potential across a range of diseases in humans [7, 19, 20, 21, 22]. As a strong antioxidant, lycopene efficiently scavenges reactive oxygen species (ROS), thereby protecting cells from oxidative damage, a critical factor in the pathogenesis of cardiovascular diseases, cancers, and neurodegenerative disorders [7, 19, 20]. Lycopene modulates inflammatory responses by inhibiting pro-inflammatory cytokines and promoting negative feedback mechanisms that suppress chronic inflammation. This anti-inflammatory effect plays a vital role in conditions such as cardiovascular disease, where lycopene improves vascular function and reduces oxidative stress [23, 24]. Neuroprotective effects have also been observed, with lycopene helping preserve cognitive function by mitigating oxidative damage and neuroinflammation in disorders like [PERSON]'s and Parkinson's disease [25, 26]. In cancer prevention, lycopene interferes with growth factor receptor signalling and cell cycle progression, particularly in prostate cancer cells, without inducing toxicity or apoptosis [7, 19]. It also impacts pathways such as the mevalonate pathway and Ras activation, further supporting its antitumor activity [27]. In metabolic disorders, lycopene improves insulin sensitivity, lowers blood glucose levels, and protects pancreatic \(\beta\)-cells from oxidative stress, indicating benefits in diabetes and metabolic syndrome [28, 29]. At the molecular level, lycopene interacts with a variety of human targets, modulating key signalling pathways including _MAPKs_, _PI3K/Akt_, and _NF-\(\kappa\)B_[30, 31]. It inhibits IxB kinase to suppress _NF-\(\kappa\)B_ signalling and activates _PPAR\(\gamma\)_, a nuclear receptor involved in glucose and lipid metabolism [32, 33, 34]. Lycopene also influences _EGFR_ and Protein Kinase C (_PKC_), affecting cell growth and gene expression [20, 35, 36]. Despite numerous studies highlighting the beneficial effects of lycopene, the precise molecular mechanisms and biological targets underlying its therapeutic actions still have considerable scientific gaps. Traditional pharmacological approaches have identified some pathways influenced by lycopene; however, a comprehensive, systems-level understanding of lycopene pharmacology is lacking. Network pharmacology, which integrates systems biology and computational tools, offers a holistic framework to elucidate the complex interactions between bioactive compounds and biological systems. By constructing and analysing networks of protein-protein interactions (PPIs), we can identify key molecular targets and pathways modulated by compounds like lycopene. In this study, we employed network pharmacology methodologies to systematically explore the molecular mechanisms and biological targets of lycopene in humans. By integrating data from open-access databases, we identified lycopene-associated proteins and constructed a PPI network (based on hydrogen bond formation) to discern critical targets and pathways.