In recent years, many preclinical studies have focused on the use of biologically derived compounds, particularly those extracted from snake and scorpion venoms, to destroy solid tumors in mouse models. These studies have demonstrated the potential to develop new anticancer therapies capable of acting through multiple mechanisms, reducing tumor size, and minimizing systemic toxicity compared to conventional chemotherapy.

One notable study utilized the peptide Smp24, isolated from the venom of the scorpion Scorpio maurus palmatus, in mice bearing solid Ehrlich carcinoma (SEC). The peptide was injected into mice with subcutaneous tumors. Results showed a significant reduction in tumor volume, near normalization of hematological and liver enzyme parameters, decreased levels of MDA and NO, and increased antioxidant enzyme activities such as GSH, SOD, and CAT. Histological analysis revealed marked apoptosis through increased expression of caspase-3 and Bax, while Ki-67 and VEGF levels were reduced, indicating inhibition of cell proliferation and angiogenesis. These findings confirm that Smp24 exerts a potent anticancer effect on solid tumor models in mice.

Another important study investigated the venom of the Egyptian snake Walterinnesia aegyptia combined with silica nanoparticles (WEV-NPs) in mice bearing breast and prostate tumors. Injection of this composite resulted in a marked reduction in tumor volume compared with controls. The venom induced the generation of reactive oxygen species (ROS), disrupted mitochondrial membrane potential, activated caspase-3, -8, and -9, and upregulated pro-apoptotic genes such as Bax and Bak, while downregulating anti-apoptotic proteins including Bcl-2, Mcl-1, and Bcl-XL. Additionally, WEV-NPs inhibited growth factor signaling pathways (IGF-1/EGF) and chemokines associated with metastasis (CXCL9/10/12/13/16), thereby suppressing tumor cell migration. The use of nanoparticles improved venom stability, selectivity, and penetration into solid tumor tissue, significantly enhancing therapeutic efficacy.

A separate study used L-amino acid oxidase (LAAO) derived from king cobra (Ophiophagus hannah) venom on mice bearing prostate cancer (PC-3) xenografts. The enzyme generated hydrogen peroxide (H₂O₂) within the tumor microenvironment, causing oxidative stress that led to apoptosis of cancer cells. Tumor size was markedly reduced in LAAO-treated mice, while healthy tissues remained largely unaffected, indicating a degree of biological selectivity.

Another approach involved using recombinant cystatin from snake venom to inhibit tumor angiogenesis. In mice with hepatocellular carcinoma (HCC) and B16F10 lung tumors, cystatin reduced microvessel density (MVD) and decreased VEGF-A165 and bFGF expression, leading to tumor hypoxia and progressive shrinkage. This mechanism is especially relevant to solid tumors, where blood vessel formation is essential for tumor growth and survival.

Some studies have also explored combining venom-derived peptides or enzymes with traditional chemotherapeutic agents such as doxorubicin or cisplatin to enhance efficacy while reducing systemic toxicity. In mice bearing H22 liver tumors, combination therapy reduced tumor mass by over 60%, compared with around 35% in chemotherapy-only groups.

Collectively, these studies demonstrate that venom-derived compounds from snakes and scorpions can effectively eliminate solid tumors in mice through multiple biological pathways, including oxidative stress induction, apoptosis activation, inhibition of proliferation and angiogenesis, and suppression of metastasis. However, these investigations remain at the preclinical stage. Issues such as systemic toxicity, optimal dosing, delivery methods, tumor selectivity, and clinical translation to humans require further in-depth research before clinical trials can be initiated.