## 1 Introduction  
Neuroblastoma (NB) is a cancer of the sympathetic nervous system [1]. It is the most common and deadly tumor of infancy accounting for 15% of all childhood cancer-related deaths [2]. NB almost exclusively occur in young children and the median age for diagnosis is 18 months [3]. Approximately 40% of the patients are younger than 1 year at diagnosis whereas less than 5% are older than 10 years [4]. Clinically, NB manifests as a primary tumor anywhere along with the sympathetic nervous system, with >50% occurring in the adrenal medulla [5]. It develops from cells in the neural crest, a fragile structure made up of multipotent stem cells active in the early stages of embryonic development that arise along the borders of the closing neural tube [6]. Numerous other cell types, including neurons and glial cells in the peripheral nervous system, mesenchymal, pigment and secretory cells, as well as bone and cartilage cells for the facial area, develop from neural crest cells [7]. Massive transcriptional alterations caused by abnormal Myccoprotein [8] levels result in hundreds, if not thousands, of increased and decreased genes, which collectively regulate a number of malignant cells' distinguishing characteristics [9]. Patients diagnosed with low-risk neuroblastoma (NB) experience a positive outlook, with a survival rate exceeding 90% over a span of five years. Various treatment alternatives have been explored, including the utilization of nonsteroidal anti-inflammatory drugs (NSAIDs) [10; 11] and vitamin A derivatives [12]. However, a significant portion, amounting to 60% of patients are afflicted with high-risk NB. Unfortunately, the prognosis for these patients following treatment remains unfavorable [13]. Treatment for high-risk NB involves several stages, including induction chemotherapy, localized control, consolidation, and maintenance therapy. To enhance and tailor treatment approaches, it is imperative to conduct additional research and clinical trials. Studies have explored various inhibitors that target activated signaling pathways in neuroblastoma, including the p53-MDM2, RAS-MAPK, PI3K/Akt/mTOR, and MDM2 pathways [14; 15; 16]. Some of these studies emphasize the importance of combination therapies that involve existing inhibitors to enhance therapeutic efficacy [17]. We headed to marine pharmacognosy, supporting a new strategy using sponge-derived alkaloids to find an effective treatment with fewer side effects. The first multicellular metazoan animals are marine sponges (_Porifera_), sessile organisms that effectively filter nutrients from the surrounding water [18]. They inhabit an oligotrophic, anoxic habitat with high salinity, high pressure and low light sensitivity [19]. Researchers have looked into marine sponges as potential sources of lead compounds for biomedical applications [20]. As one of the most common marine sponges in tropical and subtropical oceans, the sponges of the genus _Agelas_, including _Agelas oroides_ S. and _Agelas nakamurai_ H. have emerged as unique and yet under-investigated pools for discovery of natural products with fabulous molecular diversity and myriad interesting biological activities [21]. Pyrrole-imidazole alkaloids (PIAs) and simple pyrrole alkaloids represent a specific structural class of compounds isolated from sponges including those from the genus _Agelas_. These were proposed in this study on the basis of their unique chemical structures, particularly the bromopyrrole alkaloids [22], their anticancer activity by targeting key pathways associated with tumor growth and metastasis [23], and the specific needs of neuroblastoma therapy. These compounds can potentially reduce tumor burden and prevent the spread of neuroblastoma cells, making them worthy candidates for further research and development. This research seeks to evaluate in silico--the inhibition effect of five _Agelas_ sp. alkaloids, on six neuroblastoma targets.