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DRUG:

IMT-009

i
Other names: IMT-009, IMT 009, IMT009
Associations
Company:
Immunitas Therap, Lonza
Drug class:
KLRB1 inhibitor, Lymphocyte modulator, NK cell receptor modulator
Associations
4ms
Study of the Monoclonal Antibody IMT-009 in Patients With Advanced Solid Tumors or Lymphomas (clinicaltrials.gov)
P1/2, N=67, Active, not recruiting, Immunitas Therapeutics | Recruiting --> Active, not recruiting | N=151 --> 67 | Trial completion date: Apr 2025 --> Jan 2026 | Trial primary completion date: Apr 2025 --> Jan 2026
Enrollment closed • Enrollment change • Trial completion date • Trial primary completion date • First-in-human
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • MSI (Microsatellite instability)
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BRAF V600E • KRAS mutation • HR positive • MSI-H/dMMR • HER-2 overexpression • PIK3CA mutation • HER-2 overexpression + HR positive
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Fruzaqla (fruquintinib) • IMT-009
over2years
Anti CD161 Antibody IMT-009 Is a Novel Immunotherapeutic Agent That Effectively Blocks the Inhibitory CLEC2D/CD161 Axis in CLEC2D+ B Cell Hematological Malignancies Reinvigorating T and NK Cell Function Leading to Anti-Tumor Benefit (ASH 2023)
Results showed CD161+ cells infiltrated in Hodgkin Lymphoma, and post-R-CHOP treated DLBCL, highlighting the potential sensitivity of these malignancies to IMT-009 treatment. B cell malignancies tend to respond poorly to anti-PD-1 therapy4,5. This lack of efficacy could be driven by a highly immunosuppressive environment mediated by the CLEC2D/CD161 axis. Our results support evaluation of IMT-009 as a novel cancer immunotherapy to disrupt CLEC2D/CD161 signaling, with strong therapeutic potential in lymphomas.
PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • TNFA (Tumor Necrosis Factor-Alpha) • CD34 (CD34 molecule) • KLRB1 (Killer Cell Lectin Like Receptor B1)
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Rituxan (rituximab) • IMT-009
over3years
Study of the Monoclonal Antibody IMT-009 in Patients With Advanced Solid Tumors or Lymphomas (clinicaltrials.gov)
P1/2, N=119, Recruiting, Immunitas Therapeutics | Not yet recruiting --> Recruiting
Enrollment open • Metastases
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • MSI (Microsatellite instability)
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BRAF V600E • KRAS mutation • HR positive • MSI-H/dMMR • HER-2 overexpression • PIK3CA mutation
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IMT-009
over3years
Anti-CD161 antibody IMT-009 is a novel immunotherapeutic agent that reinvigorates T and NK cell function and anti-tumor efficacy through blocking interaction of CD161 with its ligand CLEC2D (SITC 2022)
Finally, multiplexed immunofluorescence data of over 30 solid tumor types showed the highest density of CLEC2D+ and CD161+ cells in the following indications: NSCLC-squamous cell carcinoma, NSCLC- adenocarcinoma, Head and Neck squamous cell carcinoma (HNSCC), Triple negative breast cancer (TNBC), Cutaneous squamous cell carcinoma and Colorectal carcinoma. Conclusions These results support the development of IMT-009 as a novel cancer immunotherapy for application in several solid tumor indications.
Clinical
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CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • TNFA (Tumor Necrosis Factor-Alpha) • CD4 (CD4 Molecule) • KLRB1 (Killer Cell Lectin Like Receptor B1)
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IMT-009
over3years
New P1/2 trial • Metastases
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • MSI (Microsatellite instability)
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BRAF V600E • KRAS mutation • HR positive • MSI-H/dMMR • HER-2 overexpression • PIK3CA mutation
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IMT-009