LONDON – 11 November 2026 -- CHARM Therapeutics (“CHARM”, “The Company”), a clinical-stage biotechnology company addressing resistance in acute myeloid leukemia (AML) with a best-in-class menin inhibitor, today announces two posters, showcasing preclinical data for CHM-029 and the design of its ongoing Phase I/II clinical trial, will be presented at the upcoming 68th American Society of Hematology (ASH) Annual Meeting and Exposition, taking place from 12-15 December 2026 in New Orleans, Louisiana. Additionally, CHARM collaborator, Dr. Florian Perner Principal Investigator, Department of Hematology, Hemostaseology, Hannover Medical School, Germany will deliver an oral presentation showcasing preclinical data for CHM-056 that supports a superior resistance profile compared to first generation compounds.
In order to determine a clear differentiation to first-generation menin inhibitors which are limited by the emergence of resistance, the two preclinical studies benchmarked CHM-029, currently in clinical development, and CHM-056, a close analog, in head-to-head comparisons against a panel of first-generation clinical stage menin inhibitors: revumenib, bleximenib, ziftomenib and enzomenib.
Key highlights from the abstracts are:
CHM-029 abstract
- CHM-029 demonstrates significantly greater biochemical potency against wild-type menin protein compared to the panel. Further, while each of these first-generation inhibitors became inactive in the presence of at least one MEN1 resistance mutation, CHM-029 retained activity, with biochemical potency below 20 nM against all mutations.
- This differentiated “pan-menin” profile translated to cellular assays with superior efficacy against other relevant AML cell lines driven by menin dependency, including those carrying MEN1 resistance mutations, while remaining inactive in a menin independent AML cell line with an irrelevant genetic background, confirming selectivity for menin.
- CHM-029 was efficacious in MV-4-11 models in vivo, both MEN1 wild-type or M327I, while revumenib was ineffective in the same MEN1 M327I model.
- In forced resistance studies in vitro, cells remained sensitive to CHM-029 even after 165 days of exposure, with no MEN1 resistance mutation detected, while cells treated with revumenib, bleximenib or enzomenib developed resistance within 20 to 30 days.
CHM-056 abstract
- In cellular assays CHM-056 demonstrated greater potency against wild-type and mutant menin compared to all benchmarked compounds.
- In an unbiased base-editor screen, revumenib drove strong selection of sgRNAs targeting resistance mutations at the M327, T349 and G331 hotspots, whereas CHM-056 did not, consistent with a substantially lower probability of drug-driven resistance evolution.
Phase I/II clinical trial design abstract
- The primary objective is to evaluate the safety and efficacy of CHM-029 in patients with AML and to determine the maximum tolerated dose and/or optimal biological dose. (NCT07751991)
Further details will be presented at the meeting.
Presentation details:
Title: Overcoming clinically relevant menin resistance mutations with CHM-056, a next-generation inhibitor designed by protein-ligand co-folding
Presenter: Dr. Florian Perner
Oral Abstract Session: 802. Chemical Biology and Experimental Therapeutics
Date and Time: Saturday 12 December, 4:00pm-5:00pm CT
Location: MCCNO – 353-355
Abstract Number: 453
Title: CHM-029: a next generation menin inhibitor active against all reported clinical resistance mutations in MEN1
Poster Abstract Session: 604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms
Date and Time: Monday 14 December, 6:00pm – 8:00pm CT
Location: MCCNO – Hall F
Abstract Number: 5022
Title: A first in human study of CHM-029, a next generation menin inhibitor, in patients with relapsed or refractory AML with NPM1 mutations, KMT2A or NUP98 rearrangements (Trial in Progress)
Poster Abstract Session: 616. Acute Myeloid Leukemias: Investigational Drug and Cellular Therapies
Date and Time: Monday 14 December, 6:00pm-8:00pm CT
Location: MCCNO – Hall F
Abstract Number: 5151
ENDS
For further information, please contact:
CHARM Therapeutics
Dr Beverley Carr, Chief Business Officer
ICR Healthcare
Namrata Taak / Lindsey Neville / Evi Useh
Phone: 44 (0)20 3709 5700
About menin inhibitors in AML
A key driver of AML is the protein–protein interaction between menin and KMT2A (also known as MLL, or mixed-lineage leukemia protein). In normal cells, KMT2A helps control transcription and differentiation. However, in certain subtypes of AML, the binding of menin to KMT2A drives the up-regulation of genes which directly contribute to the formation and maintenance of leukemic cells.
Menin inhibitors are an important and clinically-validated therapeutic class in the treatment of AML. By disrupting the binding of the KMT2A protein to menin, these inhibitors restore normal gene regulation, triggering differentiation and apoptosis of malignant cells.
About CHARM Therapeutics
CHARM Therapeutics, founded by Laksh Aithani and David Baker, is developing CHM-029, a next-generation menin inhibitor currently being evaluated in a Phase I/II clinical trial for the treatment of acute myeloid leukemia (AML). Unlike first-generation menin inhibitors that rapidly lose potency due to menin resistance mutations, CHM-029 is specifically designed to maintain potency against all known clinical resistance mutations, potentially delivering the durable responses that patients desperately need.
Based in Cambridge and London, CHARM has raised over $150 million from leading international investors including New Enterprise Associates (NEA), SR One, OrbiMed, and F-Prime. The Company is currently evaluating its menin inhibitor candidate in a Phase I/II clinical trial (NCT07751991).
For more information, please visit: www.charmtx.com
Forward-Looking Statements
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