M4205 (IDRX-42) Is a Highly Selective and Potent Inhibitor of Relevant Oncogenic Driver and Resistance Variants of KIT in Cancer

Primary activating mutations in KIT (exon 9/11) are key driver alterations in about 80% of gastrointestinal stromal tumors (GIST). Imatinib, a small-molecule tyrosine kinase inhibitor, is used successfully as first-line therapy for patients with unresectable metastatic or recurrent GIST, but secondary resistance mutations in the KIT kinase domains frequently occur. Currently approved later-line therapies target these mutations incompletely with limited clinical benefit. M4205, a kinome-selective KIT inhibitor, was designed to address this high unmet medical need by inhibiting all relevant KIT driver and resistance mutations. Compared with imatinib, M4205 shows stronger antitumor activity in preclinical GIST models driven by oncogenic KIT driver mutations. M4205 demonstrates clinically relevant efficacy in a range of preclinical GIST models expressing different secondary KIT resistance mutations. The kinase selectivity profile of M4205 is superior to the registered standard of care and investigational agents. M4205, now IDRX-42, is currently being investigated in a phase I first-in-human study in participants with GIST.

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Publication Details

Journal
Molecular Cancer Therapeutics
Published
2025-02-28
DOI
https://doi.org/10.1158/1535-7163.mct-24-0699
Citations
1
Primary Topic
Gastrointestinal Tumor Research and Treatment
Type
article
Field-Weighted Citation Impact
1.81
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article

M4205 (IDRX-42) Is a Highly Selective and Potent Inhibitor of Relevant Oncogenic Driver and Resistance Variants of KIT in Cancer

Nina Linde, Christine Drechsler, Dieter Dorsch, Christina Esdar et al.
1 citations
Molecular Cancer Therapeutics
Gastrointestinal Tumor Research and Treatment
1.81
article

M4205 (IDRX-42) Is a Highly Selective and Potent Inhibitor of Relevant Oncogenic Driver and Resistance Variants of KIT in Cancer

Nina Linde, Christine Drechsler, Dieter Dorsch, Christina Esdar, Andreas Blum, Edith Ross, Eva Sherbetjian, Ulrich Grädler, Andree Blaukat, Birgitta Leuthner, Carl Petersson, Hanno Schieferstein
article en
1 citations

Abstract

Primary activating mutations in KIT (exon 9/11) are key driver alterations in about 80% of gastrointestinal stromal tumors (GIST). Imatinib, a small-molecule tyrosine kinase inhibitor, is used successfully as first-line therapy for patients with unresectable metastatic or recurrent GIST, but secondary resistance mutations in the KIT kinase domains frequently occur. Currently approved later-line therapies target these mutations incompletely with limited clinical benefit. M4205, a kinome-selective KIT inhibitor, was designed to address this high unmet medical need by inhibiting all relevant KIT driver and resistance mutations. Compared with imatinib, M4205 shows stronger antitumor activity in preclinical GIST models driven by oncogenic KIT driver mutations. M4205 demonstrates clinically relevant efficacy in a range of preclinical GIST models expressing different secondary KIT resistance mutations. The kinase selectivity profile of M4205 is superior to the registered standard of care and investigational agents. M4205, now IDRX-42, is currently being investigated in a phase I first-in-human study in participants with GIST.

Molecular Cancer TherapeuticsVol. 24(7)
Merck KGaA, Darmstadt (Germany) (DE)
Good health and well-being
Openalex Percentile: Top 20%
Gastrointestinal Tumor Research and Treatment
1.81
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