^
    Contact us  to learn more about
    our Premium Content:  News alerts, weekly reports and conference planners
    DRUG CLASS:

    KRAS G12V inhibitor

    Related drugs:
    4ms
    Phase I Study of Autologous CD8+ and CD4+ Engineered T Cell Receptor T Cells in Subjects With Advanced or Metastatic Solid Tumor (clinicaltrials.gov)
    P1/2, N=100, Recruiting, Affini-T Therapeutics, Inc. | Not yet recruiting --> Recruiting
    Enrollment open
    |
    KRAS (KRAS proto-oncogene GTPase)
    |
    KRAS mutation • KRAS G12V • KRAS G12 • HLA-A*11
    |
    AFNT-211
    7ms
    Phase I Study of Autologous CD8+ and CD4+ Engineered T Cell Receptor T Cells in Subjects With Advanced or Metastatic Solid Tumor (clinicaltrials.gov)
    P1/2, N=100, Not yet recruiting, Affini-T Therapeutics, Inc.
    New P1/2 trial • Metastases
    |
    KRAS (KRAS proto-oncogene GTPase)
    |
    KRAS mutation • KRAS G12V • KRAS G12 • HLA-A*11
    |
    AFNT-211
    7ms
    Pan-RAS Inhibitor YL-17231 in Patients With Advanced Solid Tumors Harboring Mutations in KRAS, HRAS, or NRAS (clinicaltrials.gov)
    P1, N=60, Not yet recruiting, Shanghai YingLi Pharmaceutical Co. Ltd.
    New P1 trial • Metastases
    |
    PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • HRAS (Harvey rat sarcoma viral oncogene homolog)
    |
    KRAS mutation • NRAS mutation • HRAS mutation
    |
    YL-17231
    7ms
    A Study of YL-17231 in Patients With Advanced Solid Tumors (clinicaltrials.gov)
    P1, N=80, Recruiting, Shanghai YingLi Pharmaceutical Co. Ltd.
    New P1 trial • Metastases
    |
    PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • MSI (Microsatellite instability)
    |
    MSI-H/dMMR • KRAS wild-type • RAS wild-type
    |
    YL-17231
    10ms
    Mitigation of tumor microenvironment-mediated immunosuppression using a PD1-41BB switch protein with optimal affinity tcrs for first-in-class, 3rd generation TCR-T therapies (ESMO 2023)
    Methods Two first-in-class, 3rd generation TCR-T therapies, MDG1015 and MDG2011, were developed using optimal affinity TCRs specific for a cancer-testis antigen, NY-ESO-1/LAGE-1a, and a neoantigen, mutated KRAS G12V, respectively. Conclusions The combination of optimal affinity TCRs combined with the PD1-41BB CSP provides strong protection of TCR-T cells against two variable mechanisms of TME immunosuppression based on the demonstration of CSP-enhanced poly-cytokine secretion, proliferation and mitigation against exhaustion in vitro. This observation warrants application in the clinic for this novel approach to potentially overcome the major challenges in solid tumor TMEs.
    PD(L)-1 Biomarker • IO biomarker
    |
    KRAS (KRAS proto-oncogene GTPase) • PD-1 (Programmed cell death 1) • CTAG1B (Cancer/testis antigen 1B) • TNFRSF9 (TNF Receptor Superfamily Member 9) • CTAG2 (Cancer/testis antigen 2)
    |
    PD-L1 expression • KRAS mutation • PD-L1 overexpression • KRAS G12V • PD-1 expression • KRAS G12
    11ms
    Mutant KRAS G12V-specific TCR Transduced T Cell Therapy for Advanced Solid Tumor (clinicaltrials.gov)
    P1, N=11, Not yet recruiting, Peking University
    New P1 trial • Metastases
    |
    KRAS (KRAS proto-oncogene GTPase)
    |
    KRAS G12V • KRAS G12
    |
    cyclophosphamide • oxaliplatin • YK0901