Jean-Charles Soria: Eliminating MLLT1/3 to Disrupt Oncogenic Transcriptional Programs in AML
Jean-Charles Soria/gustaveroussy.fr

Jean-Charles Soria: Eliminating MLLT1/3 to Disrupt Oncogenic Transcriptional Programs in AML

Jean-Charles Soria, SVP and Oncology Therapeutic Area Head at Amgen, shared a post on LinkedIn by Amgen, adding:

“Acute myeloid leukemia remains one of the most biologically complex and treatment-refractory hematologic malignancies, with relapse driven by persistent oncogenic transcriptional programs and therapeutic resistance.

Amgen’s acquisition of Dark Blue Therapeutics adds a first-in-class small-molecule targeted protein degrader designed to eliminate MLLT1/3, key epigenetic co-factors driving defined AML subtypes.

  • Event-driven pharmacology: catalytic MLLT1/3 degradation vs occupancy-based inhibition → sustained pathway suppression
  • Target selection matters: non-enzymatic, scaffold proteins (MLLT1/3) inaccessible to classic inhibitors
  • Transcriptional reprogramming: disruption of leukemogenic gene networks → anti-leukemic activity
  • Resistance biology: degradation enables single-agent activity and rational combinations to extend remission durability
  • Platform relevance: expands small-molecule degradation into hematologic malignancies.”

Quoting Amgen’s post:

“Heading into 2026: Amgen bolsters its oncology pipeline.

Amgen will acquire UK-based Dark Blue Therapeutics Ltd., adding an investigational small molecule to treat acute myeloid leukemia (AML).

‘Acute myeloid leukemia remains one of the most difficult cancers to treat, and we see an urgent need for new mechanisms capable of changing the trajectory of this disease,’ said Jay Bradner, M.D., EVP of R&D at Amgen.

Acquisition Details.”

Jean-Charles Soria: Eliminating MLLT1/3 to Disrupt Oncogenic Transcriptional Programs in AML

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