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PKMYT1 is a Targetable Vulnerability in del(17p) High-Risk Multiple Myeloma.

Anaïs Schavgoulidze1, Jian Cui2, Jessica Encinas3

  • 1Institut Universitaire du Cancer de Toulouse-Oncopole, Toulouse, France.

Blood
|June 4, 2026
PubMed
Summary

Targeting PKMYT1 kinase with RP-6306 shows promise for multiple myeloma (MM) patients with 17p deletion. This approach induces cancer cell death while sparing healthy cells, offering a new therapeutic strategy.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • 17p deletion is a poor prognostic factor in multiple myeloma (MM).
  • Identifying targeted therapies for MM with 17p deletion is crucial.

Purpose of the Study:

  • To identify novel therapeutic targets in MM cells with 17p deletion.
  • To evaluate the efficacy of PKMYT1 inhibition as a targeted therapy.

Main Methods:

  • Integrated RNA-sequencing and genetic dependency data from MM patient cells and cell lines.
  • Utilized the selective PKMYT1 inhibitor RP-6306 in vitro and in vivo models.
  • Assessed DNA damage, cell death, tumor burden, and survival.

Main Results:

  • PKMYT1 was identified as a potential therapeutic target in del(17p) MM.
  • RP-6306 induced DNA damage, mitotic catastrophe, and selective cell death in del(17p) MM cells.
  • RP-6306 reduced tumor burden and improved survival in preclinical models.

Conclusions:

  • PKMYT1 is an actionable therapeutic target for MM with 17p deletion.
  • PKMYT1 inhibition represents a promising biomarker-driven strategy for del(17p)/TP53-deficient MM.