Agonists induced transient heteromerization coupled to receptor internalization, while antagonists, especially plerixafor together with maraviroc, stabilized persistent surface-associated complexes. Molecular dynamics simulations in asymmetric bilayers resembling MDA-MB-231 and MCF-10A membranes identified cholesterol-enriched receptor interfaces that prolong CXCR4-CCR5 dimer lifetimes in MDA-like membranes. These results show that GPCR heteromerization is not an intrinsic fixed property of receptor pairs, but an emergent behavior shaped by cell state, lipid environment, and ligand input.

In our cohort, the incorporation of ASCT into multimodality therapy was feasible with resource-adapted strategies; however, this did not translate into a meaningful improvement in survival outcomes when compared with our historical non-transplant cohort.

Preclinical studies demonstrate that CXCR4 antagonists (e.g., plerixafor, LY2510924) suppress metastasis and, when combined with immune checkpoint inhibitors, can reverse the "cold" immune phenotype of microsatellite-stable CRC. We also discuss recent advances in the regulation of CXCL12/CXCR4 expression, the role of related receptors such as CXCR7, and emerging strategies targeting this axis for therapeutic intervention. Collectively, current evidence supports the CXCL12/CXCR4 axis as a promising biomarker and therapeutic target in metastatic CRC, and further elucidation of its regulatory network may facilitate the development of more effective precision treatment strategies.

Treatment with AMD3100, a CXCR4 antagonist, partially restored vascular abnormalities caused by VHL deletion in ECs. Additionally, publicly available single-cell RNA-sequencing data from ECs of patients with VHL syndrome supports our findings, indicating that VHL mutations in ECs contribute to abnormal angiogenesis through ectopic activation of the HIF-CXCR4 signaling axis.

In this randomized, double-blind, placebo-controlled phase II trial (NCT02502968; registered at ClinicalTrials.gov), 128 patients in first remission received high‑dose cytarabine (HiDAC) plus Motixafortide or placebo. Taken together, combining functional MRD profiling with biomarker-driven patient selection, such as CXCR4 expression, may enable more precise and effective post-remission interventions in AML. This clinical trial is registered at EudraCT number: 2014-002702-21.

Furthermore, this review positions mavorixafor within the broader CXCR4-targeted therapeutic landscape, identifying current research gaps and suggesting directions for future studies. In conclusion, by integrating mechanistic insights with preclinical and clinical findings, this article highlights mavorixafor's promise as a targeted therapy with the potential to transform treatment paradigms for CXCR4-driven diseases.

Collectively, our results indicate that PAMD-Ch17 has anti-leukemic effects against T-ALL cells but not healthy cells, likely mediated through a CXCR4 independent, mitochondrial based mechanism. These findings support further development of PAMDs as potential therapeutics for patients with T-ALL.

AMD3100 and si-CXCR4 can significantly inhibit the expression of Snail2...In summary, the CXCL12/CXCR4-Salil2-EMT signaling pathway is involved in the migration of gastric cancer cells promoted by periodontitis. This will uncover new insights into the mechanisms that might play a role in the development of gastric cancer and strategies for targeted therapy.

Therapeutic strategies include peptide antagonists (BL-8040, Balixafortide), radioligand therapies ([177Lu]Pentixather, [177Lu]Lu-BL02), small-molecule inhibitors (Plerixafor, WK1), and monoclonal antibodies (PF-06747143, Ulocuplomab, LY2624587). Key challenges include off-target uptake due to physiological CXCR4 expression and compensatory signaling via CXCR7. Future directions involve dual-receptor targeting, nanoparticle-based delivery, and integration into precision oncology for both hematologic and solid tumors.

We could achieve successful mobilization and stem cell collection with BR120 salvage therapy in two cases.

Therapeutic strategies targeting CXCR4 include small-molecule antagonists (e.g., AMD3100/plerixafor; balixafortide), anti-CXCR4 antibodies, and CXCL12 decoys, as well as imaging probes for patient selection and response monitoring (e.g., 68Ga-pentixafor PET). Preclinical and early clinical studies suggest that CXCR4 blockade can impair tumor growth, limit metastatic spread, and enhance chemotherapy and immunotherapy efficacy, although hematopoietic side effects and infection risk necessitate careful therapeutic design. This review synthesizes the molecular features, regulatory networks, and translational potential of CXCR4 in lung cancer and discusses future directions for precision therapy and biomarker-guided intervention.

Prophylactic use of CSFs to reduce the risk of febrile neutropenia is warranted when the risk of febrile neutropenia from chemotherapy is approximately 20% or higher and no other equally effective and safe regimen that does not require CSFs is available. For patients receiving chemotherapy with a <20% risk of febrile neutropenia, primary prophylaxis with a CSF may be warranted if patients are at a high risk of febrile neutropenia based on age, medical history, or disease characteristics. For stem-cell mobilization, CSFs may be used either alone, after chemotherapy, or in combination with plerixafor or motixafortide. The guideline also provides information about the dosing and selection of CSFs.Additional information is available at www.asco.org/supportive-care-guidelines.