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BioWorld - Thursday, February 19, 2026
Home » AML

Articles Tagged with ''AML''

Cancer and blood cells
Cancer

Omeros reports Oncotox-AML primate data

Feb. 18, 2026
No Comments
Omeros Corp. has successfully completed its initial study in nonhuman primates evaluating the efficacy and safety of its Oncotox-AML cancer therapeutic platform for acute myeloid leukemia (AML). Oncotox-AML is an engineered biologic designed to selectively kill both AML blasts and relapse-related leukemia stem cells.
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Photomicrograph of bone marrow aspirate showing myeloblasts of acute myeloid leukemia
Cancer

Oncotartis’ OT-82 enhances venetoclax efficacy in AML

Dec. 30, 2025
No Comments
Venetoclax has shown good results for adult acute myeloid leukemia (AML) in combination with azacitidine, but there is increasing evidence of inherent and acquired resistance. High expression of nicotinamide phosphoribosyltransferase (NAMPT) has been associated with cancer aggressiveness and poor prognosis due to increased nicotinamide metabolism.
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3D illustration of acute myeloid leukemia cells
Cancer

Preclinical characterization of Sumitomo’s DSP-5336

Dec. 16, 2025
No Comments
Sumitomo Pharma Co. Ltd. is developing the Menin (MEN1)-myeloid/lymphoid or mixed-lineage leukemia (MLL) interaction inhibitor DSP-5336 (enzomenib) for the treatment of MLL-rearranged acute myeloid leukemia.
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Acute myeloid leukemia illustration
Cancer

Apollo’s APL-4098 shows potent antileukemic effects

Dec. 12, 2025
No Comments
Apollo Therapeutics Ltd. has developed APL-4098, a small-molecule general control nonderepressible 2 (GCN2) inhibitor for the potential treatment of AML.
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Hematologic

GB-3226: a first-in-class dual ENL-YEATS/FLT3 inhibitor for AML

Dec. 10, 2025
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ENL-YEATS is an epigenetic reader that sustains transcriptional programs essential for AML, whereas FLT3 mutations, present in approximately 30% of patients, drive malignant proliferation. Dual inhibition of ENL-YEATS and FLT3 may therefore more effectively disrupt complementary drivers of leukemogenesis than FLT3 targeting alone.
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3D illustration of acute myeloid leukemia cells
Cancer

Study unveils the role of Schlafen 12 in leukemogenesis

Nov. 10, 2025
No Comments
The Schlafen (SLFN) family of interferon-inducible genes, involved in the regulation of immune and antiviral responses, has recently attracted attention for the development of novel anticancer therapies.
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Cancer cells being destroyed by immunotherapy
Immuno-oncology

Leukogene’s LTI-214 designated orphan drug for AML

Nov. 5, 2025
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Leukogene Therapeutics Inc.’s lead product candidate LTI-214 (M2T-CD33) has been awarded orphan drug designation by the FDA for the treatment of acute myeloid leukemia (AML).
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Photomicrograph of bone marrow aspirate showing myeloblasts of acute myeloid leukemia
Cancer

Amphista nominates AMX-883 as development candidate

Oct. 16, 2025
No Comments
Amphista Therapeutics Ltd. has nominated AMX-883, a selective and orally bioavailable degrader of BRD9, as its first clinical development candidate. AMX-883 is being advanced for the treatment of acute myeloid leukemia (AML), with an IND application planned for early next year.
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3D illustration of acute myeloid leukemia cells
Cancer

SLC25A1 emerges as biomarker, target for acute myeloid leukemia

Sep. 15, 2025
No Comments
Acute myeloid leukemia (AML) is an aggressive blood cancer with poor clinical outcomes and high mortality rates, primarily driven by drug resistance and relapse. Increasing evidence has confirmed dysregulated cellular metabolism as a tumor hallmark with crucial roles in tumor growth, progression and drug resistance.
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Female healthcare professional holding dollar sign
Cancer

Series B financing to advance Charm Therapeutics’ menin inhibitor

Sep. 2, 2025
No Comments
Charm Therapeutics Ltd. has closed an oversubscribed series B funding round, raising $80 million to advance its next-generation menin inhibitor into clinical development. Current menin inhibitors show promise in acute myeloid leukemia (AML) treatment but are limited by the rapid emergence of resistance mutations that cause treatment failure.
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