Motixafortide
(Redirected from Aphexda)
Motixafortide is a novel therapeutic agent that is being investigated for its potential use in various medical conditions, particularly in oncology and hematology. It is a synthetic peptide that functions as a high-affinity antagonist of the CXCR4 receptor, which plays a crucial role in the tumor microenvironment and hematopoiesis.
Mechanism of Action[edit | edit source]
Motixafortide binds to the CXCR4 receptor, inhibiting its interaction with its natural ligand, stromal cell-derived factor-1 (SDF-1), also known as CXCL12. This inhibition disrupts the CXCR4/CXCL12 axis, which is involved in the homing and retention of hematopoietic stem cells (HSCs) in the bone marrow. By blocking this pathway, motixafortide mobilizes HSCs into the peripheral blood, making them more accessible for collection and subsequent hematopoietic stem cell transplantation.
Clinical Applications[edit | edit source]
Oncology[edit | edit source]
In the field of oncology, motixafortide is being studied for its potential to enhance the efficacy of chemotherapy and immunotherapy. The CXCR4/CXCL12 axis is known to contribute to tumor growth, metastasis, and tumor resistance to therapy. By inhibiting this pathway, motixafortide may help to sensitize tumors to treatment and inhibit their progression.
Hematology[edit | edit source]
Motixafortide is also being investigated for its role in hematopoietic stem cell transplantation. By mobilizing HSCs from the bone marrow into the peripheral blood, it facilitates their collection for transplantation procedures. This can be particularly beneficial for patients requiring autologous or allogeneic stem cell transplants.
Development and Research[edit | edit source]
Motixafortide is currently undergoing clinical trials to evaluate its safety and efficacy in various indications. Preliminary results have shown promise, particularly in the mobilization of HSCs and in combination with other therapeutic agents in cancer treatment.
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References[edit | edit source]
External Links[edit | edit source]
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