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DRUG CLASS:

DNMT inhibitor

2d
A Study of Lenalidomide and CC-486 With Radiation Therapy in Patients With Plasmacytoma (clinicaltrials.gov)
P2, N=21, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Nov 2025 --> Nov 2026 | Trial primary completion date: Nov 2025 --> Nov 2026
Trial completion date • Trial primary completion date
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lenalidomide • Onureg (azacitidine oral)
3d
Eltanexor (KPT-8602) With Inqovi (Decitabine-Cedazuridine) in High-Risk Myelodysplastic Syndromes (clinicaltrials.gov)
P1/2, N=3, Terminated, National Cancer Institute (NCI) | Completed --> Terminated; Drug company withdrew support.
Trial termination
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Inqovi (decitabine/cedazuridine) • eltanexor (KPT-8602)
4d
Decitabine conditioning improves NK cell maturation and limits CD8+ T cell terminal differentiation post-alloSCT in acute myeloid leukemia patients. (PubMed, Transplant Cell Ther)
Overall, addition of DAC to the conditioning regimen was associated with favorable immunomodulatory effects on NK and T cells post-alloSCT in AML patients. These findings suggest that DAC may enhance donor NK and T cell-mediated graft-versus-tumor responses supporting its further clinical evaluation as an adjuvant prior to alloSCT.
Journal
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CD8 (cluster of differentiation 8) • PD-1 (Programmed cell death 1) • IFNG (Interferon, gamma) • TNFA (Tumor Necrosis Factor-Alpha) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • TIGIT (T Cell Immunoreceptor With Ig And ITIM Domains 2) • CD4 (CD4 Molecule) • CD69 (CD69 Molecule) • IL2 (Interleukin 2) • KLRG1 (Killer Cell Lectin Like Receptor G1) • B3GAT1 (Beta-1,3-Glucuronyltransferase 1)
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decitabine
6d
TMEM91::TAL1 Fusion gene in a middle-aged female with rapid MDS to secondary AML progression: a case report. (PubMed, Hematology)
Despite multiple cycles of azacitidine, within one month, the patient had transitioned into sAML with blasts increased to 55% with heterogeneity in the sample, and TMEM91::TAL1 expression increased to 2.83%...This case illustrates the value of comprehensive molecular profiling, including RNA-seq, in cases of rapidly progressive MDS that cannot be diagnosed through standard molecular diagnostics. The temporal relationship between expression of the fusions and disease progression warrants additional studies of TMEM91::TAL1 in myeloid malignancies.
Journal
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DNMT3A (DNA methyltransferase 1) • TAL1 (TAL BHLH Transcription Factor 1)
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azacitidine
7d
Pediatric T-Lymphoblastic Leukemia With Aberrant B-Cell Marker Expression: A Potential Role for Targeted Therapy. (PubMed, EJHaem)
While the patient failed high-risk T-LBLL induction therapy, blinatumomab followed by decitabine and venetoclax induced a morphologic remission. This case illustrated the importance of integrating MFC analysis with NGS data to provide individualized patient treatment. The authors have confirmed clinical trial registration is not needed for this submission.
Journal
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NUP214 (Nucleoporin 214)
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Venclexta (venetoclax) • Blincyto (blinatumomab) • decitabine
9d
Enrollment change
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Inqovi (decitabine/cedazuridine)
10d
Post-transplant MRD Monitoring by TP53 Duplex Sequencing with APR-246 + Azacitidine Maintenance Predicts Outcomes. (PubMed, Blood Adv)
Specifically, MRD negativity after cycle 12 strongly predicted OS (33.9 vs 20.4 months; P=.005) and EFS (33.9 vs 10.1 months; P=.004) with a trend for RFS (32.6 vs 13.5 months; P=.06). TP53 MRD was strongly predictive of outcomes, supporting incorporation of this assay in future novel strategies.
Journal
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TP53 (Tumor protein P53)
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TP53 mutation
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azacitidine • eprenetapopt (APR-246)
11d
LANTana: Lutathera and ASTX727 in Neuroendocrine Tumours (clinicaltrials.gov)
P1, N=27, Recruiting, Imperial College London | Trial completion date: Dec 2025 --> Feb 2029 | Trial primary completion date: Dec 2025 --> Jun 2026
Trial completion date • Trial primary completion date
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Inqovi (decitabine/cedazuridine) • Lutathera (lutetium Lu 177 dotatate)
11d
Integrated transcriptomic and methylome analysis reveals retinoic acid pathway activation after decitabine treatment in EBV associated gastric cancer. (PubMed, bioRxiv)
Among the pathways disrupted, retinoic acid signaling is of particular interest, as retinoid receptors such as RARα and RARβ are frequently hypermethylated and repressed in EBVaGC. Our findings indicate that DNMT inhibition can partially reverse RA receptor silencing, supporting further investigation of DNMTi-RA combination strategies as a novel therapy for EBV + gastric cancer.
Journal
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RARA (Retinoic Acid Receptor Alpha)
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decitabine
11d
Pitavastatin counteracts venetoclax resistance mechanisms in acute myeloid leukemia by depleting geranylgeranyl pyrophosphate. (PubMed, bioRxiv)
Loss of p53 function is strongly associated with venetoclax resistance, and adding venetoclax to 5-azacitidine provides no overall survival benefit in TP53 -mutant AML. The pro-apoptotic actions of pitavastatin depend on depletion of geranylgeranyl pyrophosphate (GGPP) and can be recapitulated by inhibiting GGPP synthase or geranylgeranyltransferase-1 enzymes. These results provide a mechanistic rationale for adding pitavastatin to AML regimens to prevent or overcome venetoclax resistance.
Journal • IO biomarker
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TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • MCL1 (Myeloid cell leukemia 1)
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TP53 mutation • FLT3 mutation
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Venclexta (venetoclax) • azacitidine • pitavastatin
13d
PD-1 Inhibitor, Azacitidine and Low-dose DLI in AML Relapse After Allo-HSCT (clinicaltrials.gov)
P=N/A, N=43, Recruiting, The First Affiliated Hospital of Soochow University | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Jul 2025 --> Jul 2026
Trial completion date • Trial primary completion date
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AiRuiKa (camrelizumab) • azacitidine
14d
SEPT9 methylation as a diagnostic and predictive biomarker in the progression of ductal carcinoma in situ to invasive breast cancer. (PubMed, Sci Rep)
Additionally, decitabine treatment induced a reduction in SEPT9 methylation levels, which affects microtubule stability, suggesting a potential mechanistic link to tumor invasion. These findings indicate that SEPT9 methylation is a promising biomarker for distinguishing invasive breast cancer from DCIS and for identifying high-risk DCIS lesions with greater potential for progression.
Journal
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SEPTIN9 (Septin 9)
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decitabine