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    DRUG:

    KT-413

    i
    Other names: KT-413, KTX-120, IRAKIMiD
    Company:
    Kymera Therap
    Drug class:
    IKZF1 degrader, IKZF3 degrader, IRAK-4 degrader
    Related drugs:
    4ms
    Safety, PK/PD, and Clinical Activity of KT-413 in Adult Patients With Relapsed or Refractory B-cell NHL (clinicaltrials.gov)
    P1, N=80, Suspended, Kymera Therapeutics, Inc.
    Trial completion date • Trial primary completion date
    |
    KT-413
    6ms
    Safety, PK/PD, and Clinical Activity of KT-413 in Adult Patients With Relapsed or Refractory B-cell NHL (clinicaltrials.gov)
    P1, N=80, Suspended, Kymera Therapeutics, Inc. | Recruiting --> Suspended
    Trial suspension
    |
    KT-413
    1year
    PHASE 1 TRIAL OF KT-413, A DEGRADER OF IRAK4 AND IMID SUBSTRATES, IN ADULT PATIENTS WITH RELAPSED OR REFRACTORY B-CELL NON-HODGKIN’S LYMPHOMAS (ICML 2023)
    Initial clinical data with KT-413 demonstrate degradation of IRAK4 and Ikaros/Aiolos in PBMC and tumor. It is anticipated that higher doses will achieve the predicted degradation profile in tumors that may confer clinical benefit in MYD88-mutant patients. Dose escalation is ongoing, and analyses from additional patients will be presented at the meeting.
    Clinical • P1 data
    |
    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • IKZF1 (IKAROS Family Zinc Finger 1) • IRF4 (Interferon regulatory factor 4) • IRAK4 (Interleukin 1 Receptor Associated Kinase 4)
    |
    MYD88 mutation • MYD88 wild-type
    |
    KT-413
    over1year
    Phase 1 Study of KT-413, a Targeted Protein Degrader of IRAK4 and IMiD Substrates, in Adult Patients with Relapsed or Refractory B-Cell Non-Hodgkin Lymphoma (ASH 2022)
    Furthermore, based on new genetic classifications, co-mutations in MYD88 and CD79 (C5 and MCD subgroups) are associated with an inferior survival after standard R-CHOP. Enrollment in the Phase 1a portion of the KT413-DL-101 study is ongoing. NCT05233033.
    Clinical • P1 data • IO biomarker
    |
    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • IKZF1 (IKAROS Family Zinc Finger 1) • IRF4 (Interferon regulatory factor 4) • IL1R1 (Interleukin 1 receptor, type I) • IRAK4 (Interleukin 1 Receptor Associated Kinase 4)
    |
    MYD88 mutation • MYD88 mutation + CD79B mutation • MYD88 wild-type
    |
    Rituxan (rituximab) • KT-413
    over1year
    Precision Targeting of MYD88 Mutant DLBCL Using the Novel Combination of Irakimids and BCL2 Inhibition (ASH 2022)
    Background: Based on new genetic classifications, co-mutations in MYD88 and CD79B (C5 and MCD subgroups) are associated with an inferior survival after standard R-CHOP. Preclinical studies highlight the potential of IRAKIMiDs as a therapeutic approach for the treatment of MYD88MT DLBCL. KTX-582 demonstrates preferential activity in MYD88MT ABC-DLBCL. Single agent venetoclax demonstrated varying potency in ABC-DLBCL cell lines, irrespective of MYD88 mutational status.
    IO biomarker
    |
    BCL2 (B-cell CLL/lymphoma 2) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • IKZF1 (IKAROS Family Zinc Finger 1) • CD79B (CD79b Molecule) • IRAK4 (Interleukin 1 Receptor Associated Kinase 4)
    |
    MYD88 mutation • BCL2 expression • CD79B mutation • MYD88 mutation + CD79B mutation • MYD88 wild-type
    |
    Venclexta (venetoclax) • Rituxan (rituximab) • KT-413 • KTX-582