plerixafor

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 our real-life study, we confirmed the strong negative impact of lenalidomide on PBSC collection by comparing lenalidomide-treated patients with a control cohort of thalidomide-treated subject, also showing a more frequent use of plerixafor to mitigate these effects, thereby reducing the reliance on cyclophosphamide, that was associated with lower risk of prolonged apheresis sessions. Indeed, we showed that lenalidomide use significantly impaired stem cell collection, with prolonged apheresis sessions and lower CD34+ cell collection on day 1, while post-transplant outcomes did not significantly differ between groups. Our real-life bi-center experience is of great interest in the era of daratumumab-based regimens as first-line therapy for autologous stem cell transplantation-eligible MM patients, because the concomitant use with lenalidomide might negatively affect PBSC mobilization, urging for more tailored PBSC collection strategies.

Although Dara-VTd induction is associated with impaired mobilization kinetics, successful steady-state mobilization remains feasible. On-demand plerixafor use overcomes mobilization deficits, supporting this approach in patients receiving CD38-based quadruplet induction therapy. Furthermore, follow-up analysis of stem cell graft utilization demonstrates a high proportion of collected but unused stem cell grafts in both cohorts.

P3, N=10, Recruiting, Fondazione Telethon | Not yet recruiting --> Recruiting

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.

The first-day CD34⁺ cell count provides a robust, real-time tool for guiding apheresis. HD-Ara-C-based mobilisation should be considered the preferred regimen for fit patients, with steady-state mobilisation as an alternative for selected cases.

Antagonistic peptides AMD3100 (Plerixafor), LY2510924, and POL6326, as well as their therapeutic potential. 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.