mercaptopurine

In particular, pharmacogenetic markers for the following drugs were analyzed: anthracyclines (doxorubicin, daunorubicin), vincristine, glucocorticoids (prednisone, dexamethasone), L-asparaginase, methotrexate, alkylating agents (cyclophosphamide, ifosfamide), 6-mercaptopurine, cytarabine, and etoposide. At present, only a few genes, TPMT and NUDT15, have well-established clinical utility, whereas the clinical relevance of pharmacogenetic markers for other drugs used in pediatric ALL therapy remains under investigation. The review also highlights the main knowledge gaps in current research and outlines promising directions for future studies aimed at integrating pharmacogenetic testing into clinical practice for personalized treatment of ALL.

P1, N=24, Recruiting, City of Hope Medical Center | Trial completion date: Feb 2026 --> May 2026 | Trial primary completion date: Feb 2026 --> May 2026

P2, N=53, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jan 2027

P3, N=310, Suspended, Alliance for Clinical Trials in Oncology | Trial completion date: Aug 2026 --> Aug 2027 | Trial primary completion date: Mar 2026 --> Mar 2027

Allopurinol co-treatment reduces toxicity while maintaining therapeutic efficacy at lower 6-MP doses. The proposed model warrants prospective evaluation for clinical relevance confirmation.

P=N/A, N=120, Recruiting, West China Second University Hospital

P2/3, N=765, Not yet recruiting, Charite Universitaetsmedizin Berlin KR

P3, N=5951, Recruiting, Children's Oncology Group | Trial completion date: Mar 2030 --> Mar 2032 | Trial primary completion date: Mar 2030 --> Mar 2032

Notably, low-dose 6-mercaptopurine disrupted SAICAR-driven immunosuppression and synergized with anti-PD-1 treatment without inducing systemic immune toxicity. Together, these findings establish SAICAR as an immunometabolic regulator that links purine metabolism to immune evasion and highlight a therapeutically actionable pathway to overcome metabolite-driven resistance to immune checkpoint blockade.

Approximately 28% of patients carried TPMT and/or NUDT15 variants associated with non-wild-type enzymatic activity, increasing the risk of mercaptopurine-induced myelotoxicity. Preemptive genotyping is essential to reduce toxicity, optimize treatment, and advance precision medicine in this population. Additionally, the two TPMT variants p.G126A and p.D137Y, currently not classified within Clinical Pharmacogenetics Implementation Consortium-defined star alleles, highlight the need for functional validation and potential clinical classification to improve pharmacogenetic interpretation in diverse populations.

Propolis serves as a prospective chemotherapeutic adjuvant that enhances the anticancer efficacy of 6-MP and 5-FU, allowing dose reduction, minimizing toxicity, and potentially overcoming drug resistance in breast cancer treatment. However, the therapeutic use of this synergistic technique requires confirmation via pharmacokinetic profiling, extensive vivo research, and considered clinical trials.

These studies shows how these drugs can be loaded and off-loaded using the CTF-2 carrier. This study demonstrates the potential of CTF-2, which is an innovative and promising drug delivery carrier in the treatment of various diseases.