decitabine / Generic mfg. - LARVOL DELTA

Synergistic induction of apoptosis by the epigenetic modulator decitabine and metformin in gastric cancer cells highlights the potential for combination therapy. (PubMed, Sci Rep) - No abstract available

Journal • Gastric Cancer • Oncology • Solid Tumor

Genotype-guided Targeted Agents Plus EZH2i for Primary Refractory PTCL (clinicaltrials.gov) - P1/2 | N=86 | Not yet recruiting | Sponsor: Ruijin Hospital

New P1/2 trial • Hematological Malignancies • Lymphoma • Non-Hodgkin’s Lymphoma • Oncology • Peripheral T-cell Lymphoma • T Cell Non-Hodgkin Lymphoma

Bortezomib, Sorafenib Tosylate, and Decitabine in Treating Patients With Acute Myeloid Leukemia (clinicaltrials.gov) - P1 | N=15 | Active, not recruiting | Sponsor: National Cancer Institute (NCI) | Trial completion date: Mar 2026 ➔ Mar 2027

Trial completion date • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology

Composite nanovesicles for enhanced chemodynamic cancer therapy via decitabine-mediated epigenetic reactivation. (PubMed, J Control Release) - "Furthermore, Dac epigenetically restores the expression of STING and GSDME via DNA demethylation, markedly augmenting cGAS-STING activation and pyroptosis. As a result, PLMD treatment enhances dendritic cell maturation and T-cell priming, ultimately achieving pronounced tumor growth inhibition and robust antitumor immune responses in a 4T1 tumor model."

Journal • Oncology • Solid Tumor • CASP3 • GSDME • NQO1

The combined inhibitory effect of butaselen and decitabine against lung cancer cells. (PubMed, Sci Rep) - "The combined treatment was associated with downregulation of DNMT1, a reduced Bcl‑2/Bax ratio, and upregulation of HOXA9, p21, and E‑cadherin. These preclinical findings suggest that the combination of BS and DAC represents a mechanistically rationalized and promising therapeutic strategy for lung cancer that warrants further evaluation in in vivo models and early‑phase clinical trials."

Journal • Hematological Disorders • Hematological Malignancies • Lung Cancer • Oncology • Solid Tumor • ANXA5 • BAX • BCL2 • CDH1 • CDKN1A • DNMT1 • HOXA9

Venetoclax and Decitabine vs Intensive Chemotherapy as Induction for Young Patients with Newly Diagnosed AML. (PubMed, Blood) - P3 | "Patients aged 18-59 years eligible for intensive chemotherapy were randomized 1:1 to receive VEN-DEC or IA-12 (idarubicin and cytarabine). In conclusion, VEN-DEC demonstrated non-inferior response rates with superior safety over IA-12 in young AML patients. The trial was registered at ClinicalTrials.gov as #NCT05177731."

Journal • Acute Myelogenous Leukemia • Hematological Disorders • Hematological Malignancies • Infectious Disease • Leukemia • Oncology • Thrombocytopenia • RUNX1 • RUNX1T1

Enhanced Remission and Survival Outcomes with Decitabine Plus Venetoclax in Additional Sex Comb Like 1 Mutated Acute Myeloid Leukemia. (PubMed, J Vis Exp) - "The use of DEC for 5 or 10 days as the hypomethylating agents combination with VEN did not affect the CR/Cri rate. In conclusion, DEC plus VEN was associated with improved clinical responses and survival signals in ASXL1-mutated AML, warranting prospective confirmation."

Journal • Review • Acute Myelogenous Leukemia • Hematological Disorders • Hematological Malignancies • Leukemia • Oncology • ASXL1

Dosing decitabine and venetoclax for terminal differentiation to improve outcomes in TP53 mutant MDS and AML. (ASCO 2025) - P2 | "Venetoclax (Ven) added to the hypomethylating agents (HMA) of Decitabine or Azacitidine is the current standard of care for elderly patients with AML and is frequently used in high-risk MDS (HR-MDS). In this cohort, of elderly patients with poor risk TP53 mutated MDS and AML the use of a non-cytotoxic dosing schedule of Decitabine and Ven resulted in over half the patients achieving a CR and transfusion independence. The median OS of 11.3 months compares favorably to currently approved cytotoxic dosing of HMA/Ven."

Acute Myelogenous Leukemia • Myelodysplastic Syndrome • TP53

Prospera (ABNL-MARRO 002): A randomized phase 2 study of pacritinib vs. hydroxyurea in patients with advanced proliferative chronic myelomonocytic leukemia (CMML) (ASH 2025) - P2 | "In the phase 3 DACOTA trial (Itzykson et al., JCO 2022),decitabine modestly delayed leukemic transformation compared to HU but did not improve event-free oroverall survival and was associated with increased early mortality. The primary endpoint is CBR at Week 24, defined by modified IWG MDS/MPNcriteria incorporating hematologic improvement, spleen volume reduction, and symptom response.Secondary endpoints include CBR at any time, duration of response, event-free survival, leukemia-freesurvival, and overall survival.Correlative studies will assess treatment-related changes in clonal dynamics, cytokine signaling, andhematopoietic composition using longitudinal peripheral blood and bone marrow sampling. Single-celltranscriptomic and immunophenotypic profiling will be employed to characterize pacritinib's impact onboth the malignant clone and the surrounding immune microenvironment."

Clinical • Metastases • P2 data • Chronic Myelomonocytic Leukemia • Hematological Malignancies • Leukemia • Myelofibrosis • Myeloproliferative Neoplasm • Thrombocytopenia • IRAK1

A CASE REPORT OF MULTI- DRUG COMBINATION THERAPY FOR RELAPSED/REFRACTORY ANGIOIMMUNOBLASTIC T-CELL LYMPHOMA (EBMT 2026) - "The standard first-line treatment for AITL typically involves the CHOP regimen(cyclophosphamide,doxorubicin, vincristine,and prednisone) or CHOP-like protocols... We conducted a single-case retrospective analysis of a 54-year-old male patient with R/R AITL who had progressed following prior treatment with first-line CHOPE (CHOP plus etoposide) and second-line GDP (gemcitabine, doxorubicin liposome and corticosteroid) regimens. After one cycle of chidamide, mitoxantrone, azacitidine and corticosteroid therapy at our linstitution, the original lesions showed significant shrinkage with partial resolution; however, a new lesion emerged, indicating disease progression...The treatment regimen was subsequently modified to a multi-agent combination: chidamide (20 mg twice weekly), decitabine (10 mg d1-5), mitoxantrone liposome (20 mg d2), bevacizumab (600mg day 1), bortezomib (2mg d1, 4, 8) and dexamethasone (20mg d1-4 ), repeated every 21days... Chidamide, a histone deacetylase..."

Case report • Clinical • Combination therapy • IO biomarker • Bone Marrow Transplantation • Immune Modulation • Immunology • Infectious Disease • Lymphoma • Non-Hodgkin’s Lymphoma • Peripheral T-cell Lymphoma • T Cell Non-Hodgkin Lymphoma • Thrombocytopenia • CD7

Venetoclax with Decitabine as Frontline Treatment for Younger Adults with Newly Diagnosed ELN Adverse-Risk AML. (PubMed, Blood) - No abstract available

Journal • Acute Myelogenous Leukemia

Decitabine, venetoclax, and ponatinib for advanced phase chronic myeloid leukaemia and Philadelphia chromosome-positive acute myeloid leukaemia: a single-arm, single-centre phase 2 trial. (PubMed, Lancet Haematol) - P2 | "The combination of decitabine, venetoclax, and ponatinib is safe and shows promising activity in patients with advanced phase chronic myeloid leukaemia, including those with multiple previous therapies or high-risk disease features. Further studies evaluating chemotherapy and venetoclax-based combination strategies using newer-generation BCR::ABL1 tyrosine kinase inhibitors are warranted."

Journal • Metastases • P2 data • Acute Myelogenous Leukemia • Cardiovascular • Chronic Myeloid Leukemia • Febrile Neutropenia • Hematological Malignancies • Infectious Disease • Neutropenia • Oncology • ABL1

A PHASE 1B STUDY OF NAVTEMADLIN IN COMBINATION WITH DECITABINE AND VENETOCLAX IN ACUTE MYELOID LEUKEMIA (EHA 2025) - P1 | "NAV in combination with DAC and DAC/VEN is well tolerated and associated with promising responses in R/R AML. MCL-1/BIM heterodimer expression may help predict patients who are most likely to respond."

Combination therapy • IO biomarker • P1 data • Acute Myelogenous Leukemia • Hematological Disorders • Hematological Malignancies • Leukemia • Neutropenia • Oncology • BCL2 • BCL2L1 • GDF15 • MCL1

Results of the Phase 1B study of pegargiminase (ADI-PEG 20) in combination with AZA-VEN in newly diagnosed high-risk AML patients not candidates for intensive chemotherapy (ASH 2025) - P1 | "Pegargiminase (ADI-PEG 20), ametabolism-targeting therapeutic consisting of the arginine-degrading enzyme arginine deiminasecombined with polyethylene glycol, demonstrated high synergy with VEN-decitabine in pre-clinicalmodels and anti-leukemic activity as monotherapy and with cytarabine in clinical trials...We conducted a phase 1A/B trial evaluating triplet therapy with ADI-PEG 20+ azacitidine and venetoclax (AZA-VEN) in relapsed/refractory (R/R) and newly diagnosed (ND) AML(NCT05001828).MethodsThe phase 1A dose escalation cohort in R/R AML (n=13) was previously reported...Rates of CRc and MRD-negativity were high, with durableresponses observed. OS was better than expected, in this very-high risk AML population."

Clinical • Combination therapy • P1 data • Acute Myelogenous Leukemia • Infectious Disease • Pneumonia • Respiratory Diseases • ASS1 • FLT3 • KMT2A • NF1 • NRAS • PTPN11

Maintenance Therapy of Hypomethylating Agent (HMA) in Favorable Risk Acute Myeloid Leukemia (AML) Patients (clinicaltrials.gov) - P2 | N=77 | Recruiting | Sponsor: The First Affiliated Hospital of Soochow University | Trial primary completion date: Dec 2025 ➔ Dec 2026

Trial primary completion date • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • CEBPA • NPM1

Combinatorial drug screen identifies therapeutic vulnerabilities of pancreatic cancer subtypes (ESMO-TAT 2026) - "decitabine, oxidative stress inducer elesclomol, and mitogen-activated protein kinase kinase (MEK) inh...rabusertib and AZD7762 ranked among the top combinations with AZD3965...adavosertib also sparked interest, as CHK1 and WEE1 inh... This systematic approach identifies candidate drug pairs for further preclinical testing and highlights translational starting points for developing personalized combination therapies to overcome resistance."

Colon Cancer • Colorectal Cancer • Oncology • Pancreatic Cancer • Pancreatic Ductal Adenocarcinoma • Solid Tumor • CHEK1 • SLC16A1

Pembrolizumab and Decitabine With or Without Venetoclax in Treating Patients With Acute Myeloid Leukemia or Myelodysplastic Syndrome That Is Newly-Diagnosed, Recurrent, or Refractory (clinicaltrials.gov) - P1 | N=54 | Recruiting | Sponsor: City of Hope Medical Center | Trial completion date: Feb 2026 ➔ Jul 2027 | Trial primary completion date: Feb 2026 ➔ Jul 2027

Trial completion date • Trial primary completion date • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Myelodysplastic Syndrome • Oncology

LS1781: Ascorbic Acid and Chemotherapy for the Treatment of Relapsed or Refractory Lymphoma, CCUS, and Chronic Myelomonocytic Leukemia (clinicaltrials.gov) - P2 | N=80 | Recruiting | Sponsor: Mayo Clinic | Trial completion date: Mar 2027 ➔ Nov 2033 | Trial primary completion date: Mar 2027 ➔ Feb 2031

Trial completion date • Trial primary completion date • B Cell Lymphoma • Chronic Myelomonocytic Leukemia • Diffuse Large B Cell Lymphoma • Hematological Disorders • Hematological Malignancies • High-grade B-cell lymphoma • Hodgkin Lymphoma • Leukemia • Lymphoma • Non-Hodgkin’s Lymphoma • Oncology • BCL2 • CD4 • DNMT3A • IDH1 • IDH2 • SF3B1 • SRSF2 • TET2 • U2AF1 • ZRSR2

Cuproptosis induction in TP53-mutated acute myeloid leukemia (AACR 2026) - "In contrast, cytarabine, idarubicin, and venetoclax activity was substantially diminished in TP53-deficient cells, consistent with the known resistance of TP53-mutated AML to these standard therapies. Notably, combining low-dose elesclomol with the hypomethylating agent decitabine, which has established clinical efficacy in TP53-mutated AML, produced a synergistic increase in apoptosis in TP53-deficient AML cells.Together, these findings demonstrate that copper ionophores can bypass TP53-associated resistance to AML cell death by activating cuproptosis rather than relying on p53-dependent apoptotic pathways. The robust activity of copper ionophores across diverse TP53-deficient AML models, coupled with the enhanced efficacy observed in combination with decitabine, underscores cuproptosis induction as a promising therapeutic approach for TP53-deficient AML."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • TP53

HMA-induced oncogene reactivation as a driver of disease progression in MDS (AACR 2026) - "Hypomethylating agents (HMAs), including azacitidine and decitabine, are widely used for high-risk myelodysplastic syndromes (MDS) and selected AML, yet most patients eventually relapse, and survival after HMA failure remains dismal. They support a new mechanistic framework in which treatment-induced epigenetic reawakening promotes malignant fitness, and they identify SALL4 and CGAGs as high-value biomarkers and therapeutic targets. This work motivates development of companion diagnostic strategies and combination regimens pairing HMAs with targeted degraders to prevent therapy-induced disease acceleration and improve patient outcomes."

Acute Myelogenous Leukemia • Hematological Malignancies • Myelodysplastic Syndrome • Oncology • DDX43 • HORMAD1 • SALL4

Profiling histone modifications in single cells to gain insight into the effects of epigenetic drug treatment on tumor cells (AACR 2026) - "To assess drug induced changes in acetylation, we profiled H3K27ac patterns in thousands of single cells from a lung cancer cell line (A549 WT and A549 p53 KO) before and after epigenetic treatment (decitabine + panabinistat vs DMSO control).We observed global cell-type-specific acetylation in response to epigenetic therapy in both A549 WT and A549 p53 KO cells...In summary, the validated scCUT&Tag method provides a high-throughput, automated approach to identify genes regulated in response to epigenetic drug treatment of tumor cells at the single-cell level. Integrating this single-cell expression data provides deeper insight into cellular regulation, particularly in the context of drug responses in tumor cells."

Epigenetic controller • Tumor cell • Lung Cancer • Oncology • Solid Tumor

G3BP1 knockdown sensitizes the acute myeloid leukemia cell line HL60 to venetoclax by inducing apoptosis (AACR 2026) - "HL60/shG3BP1 cells exhibited reduced sensitivity to Ara-C compared to control cells (IC50 value: 7 µM, 0.5 µM, respectively), while conversely demonstrating increased sensitivity to venetoclax (IC50 value: 4nM, 900nM, respectively). Sensitivity to other tested agents, including daunorubicin, etoposide, and Decitabine, remained unchanged. Knockdown of G3BP1 in HL60 cells resulted in enhanced sensitivity to venetoclax. This enhanced sensitivity might be explained by the impairment of G3BP1-mediated SG formation."

IO biomarker • Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • BCL2 • CASP3 • G3BP1 • WT1

Targeting mitochondrial and glutathione metabolism sensitizes leukemia cells to DNA-hypomethylating agents and venetoclax combination therapy (AACR 2026) - "Acute myeloid leukemia (AML) is the most common acute leukemia diagnosed in adults. In human AML xenograft models, inhibition of this enzyme significantly restored sensitivity to HMA (decitabine or azacytidine)-VEN combination therapy in resistant or poorly responsive AML cells. Together, our findings identify glutathione-based metabolic adaption as a potential mechanism of HMA resistance and highlight targeting mitochondrial and glutathione metabolism as a promising therapeutic strategy to enhance the efficacy of HMA-containing combination regimens."

Combination therapy • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Myelodysplastic Syndrome • Oncology • FLT3 • IDH1 • IDH2

Combining DNA methylation inhibition and STING agonist in the treatment of metastatic triple-negative breast cancer (AACR 2026) - "Altogether, this work suggests that the DNA methylation inhibition with decitabine and the stimulation of the IFNβ pathway with STINGa represent a new approach to efficiently target the metastatic TNBC that currently lacks effective targeted therapies and immunotherapies. This study also brought new evidences that decitabine/STINGa combination therapy is dependent on the TBK1/IFNβ pathway and NK cells in targeting metastatic TNBC in vivo."

Epigenetic controller • IO biomarker • Metastases • Breast Cancer • Oncology • Solid Tumor • Triple Negative Breast Cancer • IFNB1

Enhancement of antigen presentation restores immune recognition in rhabdomyosarcoma (AACR 2026) - "RMS cell lines (n=9) were treated with IFN-γ and clinically relevant drugs, decitabine (DAC), mocetinostat, and tazemetostat. Pediatric tumors show distinct patterns of antigen presentation, such as high MHC-I in alveolar soft part sarcoma and low expression in RMS, though individual tumor subtypes exhibit internal variability. IFN-γ and epigenetic agents restore antigen presentation, including increased NLRC5 expression. Pharmacological treatment and NLRC5 restoration enhanced antigen presentation and sensitized RMS PDX to TCR mediated T-cell cytotoxicity."

IO biomarker • Alveolar Soft Tissue Sarcoma • Oncology • Rhabdomyosarcoma • Sarcoma • Solid Tumor • HLA-A • HLA-B • HLA-C • IFNG • NLRC5 • PRAME