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DRUG CLASS:

KRAS G12V inhibitor

18d
New P1 trial
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12
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Erbitux (cetuximab)
2ms
Autologous CD8+ and CD4+ Transgenic T Cells Expressing High Affinity KRASG12V Mutation-Specific T Cell Receptors (FH-A11KRASG12V-TCR) in Treating Patients With Metastatic Solid Tumor Cancers With KRAS G12V Mutations (clinicaltrials.gov)
P1, N=24, Recruiting, Fred Hutchinson Cancer Center | Suspended --> Recruiting | Trial completion date: Feb 2026 --> Jan 2028 | Trial primary completion date: Feb 2026 --> Jan 2028
Enrollment open • Trial completion date • Trial primary completion date • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • NTRK (Neurotrophic receptor tyrosine kinase)
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KRAS mutation • TMB-H • BRAF mutation • HER-2 amplification • ROS1 fusion • KRAS G12 • NTRK fusion
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cyclophosphamide • bendamustine • fludarabine IV
3ms
Trial suspension • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • NTRK (Neurotrophic receptor tyrosine kinase)
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KRAS mutation • TMB-H • BRAF mutation • HER-2 amplification • ROS1 fusion • KRAS G12 • NTRK fusion
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cyclophosphamide • bendamustine • fludarabine IV
6ms
Enrollment closed
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12
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AFNT-211
8ms
A first-in-class EGFR-directed KRAS G12V selective inhibitor. (PubMed, Cancer Cell)
Using a targeted RNAi delivery platform, we achieve effective tumor silencing of KRASG12V and significant anti-tumor activity across several cancer models. Our findings represent a technological advance in oncogene targeting using RNAi and provide new biologic insights in KRAS targeting with potential implications for safety and efficacy.
Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation
8ms
Enrollment open
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cyclophosphamide • fludarabine IV
9ms
NW-301 TCR-T in Patients With Advanced Solid Tumor (clinicaltrials.gov)
P1, N=44, Not yet recruiting, Peking University
New P1 trial
9ms
Identification and characterization of oncogenic KRAS G12V inhibitory peptides by phage display, molecular docking and molecular dynamic simulation. (PubMed, Comput Biol Med)
Both peptides demonstrated significant inhibition of KRAS G12V-carrying cancer cell lines (NCI-H2444 and SW620), reducing cell viability by 70-75 % at 400 μM after 48 h while showing minimal effects (20-30 % reduction) on wild-type KRAS-carrying Caco-2 cells, which is equal to DMSO diluent control. These findings provide new insights into peptide-based targeting of KRAS G12V and demonstrate the potential of using subtractive phage display for developing selective inhibitors against oncogenic mutations.
Journal
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KRAS (KRAS proto-oncogene GTPase)
|
KRAS mutation • KRAS wild-type • RAS wild-type
10ms
New P1 trial
|
cyclophosphamide • fludarabine IV
12ms
Enrollment closed • Enrollment change • IO biomarker
|
HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • NTRK (Neurotrophic receptor tyrosine kinase)
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KRAS mutation • TMB-H • BRAF mutation • HER-2 amplification • ROS1 fusion • KRAS G12 • NTRK fusion
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cyclophosphamide • bendamustine • fludarabine IV
1year
QTX3544-201: QTX3544 in Patients With Advanced Solid Tumors With KRAS G12V Mutations (clinicaltrials.gov)
P1, N=237, Recruiting, Quanta Therapeutics | Not yet recruiting --> Recruiting
Enrollment open
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Erbitux (cetuximab)