The third generation AKR1C3-activated prodrug, ACHM-025, eradicates disease in preclinical models of aggressive T-cell acute lymphoblastic leukemia

Blood Cancer J. 2024 Nov 6;14(1):192. doi: 10.1038/s41408-024-01180-x.

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy that expresses high levels of the enzyme aldo-keto reductase family 1 member C3 (AKR1C3). To exploit this finding, we developed a novel prodrug, ACHM-025, which is selectively activated by AKR1C3 to a nitrogen mustard DNA alkylating agent. We show that ACHM-025 has potent in vivo efficacy against T-ALL patient-derived xenografts (PDXs) and eradicated the disease in 7 PDXs. ACHM-025 was significantly more effective than cyclophosphamide both as a single agent and when used in combination with cytarabine/6-mercaptopurine. Notably, ACHM-025 in combination with nelarabine was curative when used to treat a chemoresistant T-ALL PDX in vivo. The in vivo efficacy of ACHM-025 directly correlated with AKR1C3 expression levels, providing a predictive biomarker for response. Together, our work provides strong preclinical evidence highlighting the potential of ACHM-025 as a targeted and effective therapy for aggressive forms of T-ALL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3-Hydroxysteroid Dehydrogenases / antagonists & inhibitors
  • 3-Hydroxysteroid Dehydrogenases / metabolism
  • Aldo-Keto Reductase Family 1 Member C3* / antagonists & inhibitors
  • Animals
  • Cell Line, Tumor
  • Female
  • Humans
  • Mice
  • Mice, SCID
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma* / drug therapy
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma* / metabolism
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma* / pathology
  • Prodrugs* / pharmacology
  • Prodrugs* / therapeutic use
  • Xenograft Model Antitumor Assays*

Substances

  • Aldo-Keto Reductase Family 1 Member C3
  • Prodrugs
  • AKR1C3 protein, human
  • 3-Hydroxysteroid Dehydrogenases