P1, N=18, Recruiting, Pamela Munster | Trial completion date: Feb 2027 --> Jan 2028 | Trial primary completion date: Jan 2026 --> Jan 2028

RASD1 is frequently silenced in MM through promoter hypermethylation. This epigenetic inactivation is associated with adverse clinical features and enhanced cell survival, supporting a tumor suppressor role for RASD1 in MM pathogenesis.

P1/2, N=72, Active, not recruiting, Otsuka Beijing Research Institute | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Dec 2025 --> May 2026

P=N/A, N=10, Not yet recruiting, The Second Medical Center of Chinese PLA General Hospital​; The Second Medical Center of Chinese PLA General Hospital?

P2, N=20, Not yet recruiting, The FIrst Affiliated Hospital, College of Medicine, Zhejiang University; The FIrst Affiliated Hospital, College of Medicine, Zhejiang University

P2, N=28, Not yet recruiting, The FIrst Affiliated Hospital, College of Medicine, Zhejiang University; The FIrst Affiliated Hospital, College of Medicine, Zhejiang University

P2, N=32, Not yet recruiting, The FIrst Affiliated Hospital, College of Medicine, Zhejiang University; The FIrst Affiliated Hospital, College of Medicine, Zhejiang University

P2, N=54, Not yet recruiting, The First Affiliated Hospital of Zhejiang University, School of Medicine,; The First Affiliated Hospital of Zhejiang University, School of Medicine,

On the other hand, the expression of BCL-XL and MCL1 in leukemia cells could be easily semi-quantified by immunostaining, with these results correlating with those obtained by qPCR. These results indicate that immunostaining for BCL-XL and MCL1 upon bone marrow examination at diagnosis not only can predict susceptibility to VEN + AZA therapy, but may also be useful for patient stratification for VEN + AZA treatment in the future.

P1, N=26, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: May 2026 --> Dec 2025

P1/2, N=33, Active, not recruiting, University of Southern California | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

Interestingly, this synergistic lethality was not observed with azacitidine or treatment with GSK3685032, a potent DNMT1 inhibitor, both of which produce a comparable level of global hypomethylation to decitabine. Treatment with decitabine and ATR inhibitor reduces leukemia burden and prolongs survival in in vivo mouse models of TP53-mutated AML. Collectively, these show that TP53 loss generates a selective vulnerability to decitabine-induced replication stress, with the combination of ATR inhibition and decitabine showing promise as a new therapeutic approach for TP53-MN.