C-X-C chemokine receptor type 4 (CXCR4) antagonism in precision oncology: Clinical applications and future directions – Research

Physiologically, the C-X-C chemokine receptor type 4 (CXCR4) signalling pathway regulates key aspects of tumor behavior (growth, metastasis, and immune evasion) and modulates immune system function. Anticancer researchers have identified peptide-based CXCR4 antagonists as promising candidates due to their high targeting specificity and favorable safety profiles. This review provides an analytical examination of CXCR4 antagonistic peptides,the selective Mavorixafor (X4P-001), an advanced, selective CXCR4 inhibitor. When Mavorixafor binds to the same location as C-X-C motif chemokine ligand 12 (CXCL12), it disrupts the CXCR4 protein receptor, stopping signals that help cancer grow and spread, as well as the formation of new blood vessels. Mavorixafor blocks cancer cell progression and metastatic growth in different tumor models while enhancing chemotherapy, radiotherapy, and immune checkpoint inhibitor efficacy. Antagonistic peptides AMD3100 (Plerixafor), LY2510924, and POL6326, as well as their therapeutic potential. Mavorixafor is a promising option for cancer treatments that combine different therapies because it stays attached to its target for a long time and can be taken by mouth. Clinical studies have demonstrated that Mavorixafor produces promising outcomes when combined with chemotherapy or immune checkpoint inhibitors during the treatment of both hematological malignancies and solid tumors. Mavorixafor is promising for cancer treatment because it works well with other therapies, such as immune checkpoint inhibitors and chemotherapy, as well as targeted therapies and radiation therapy. Future research on Mavorixafor will focus on two main areas: personalized medicine development, new delivery systems and their broad medical applications extending beyond oncology. As a potential CXCR4 antagonist, Mavorixafor shows promise as a transformative tool in cancer care because it regulates the tumor microenvironment (TME) while increasing the degree of therapeutic benefits.