BSJ-05-037 is an ITK PROTAC degrader that effectively targets and degrades ITK in T-cell lymphoma cell lines. BSJ-05-037 blocks the activation of the NF-κB / GATA-3 signaling pathway, inhibits PLCγ1 phosphorylation, and reduces the proliferative capacity of T-cell lymphoma cells. BSJ-05-037 enhances the sensitivity of T-cell lymphoma cells to chemotherapy. In mouse models of T-cell lymphoma, BSJ-05-037 induces ITK degradation, reduces GATA-3 expression, decreases tumor volume, and reverses chemotherapy resistance. BSJ-05-037 is applicable to research related to T-cell lymphoma [1] [2] [3]. (Pink: Itk ligand; Blue: Cereblon ligand; Black: linker ).
In Vivo, BSJ-05-037 (50 mg/kg; i.p.; every 8 hours; 3 total doses/once every other day; 14 days) induces ITK degradation, reduces GATA-3 expression, inhibits PLCγ1, decreases tumor volume, and reverses chemoresistance in Hut78/H9 cutaneous T-cell lymphoma xenografts in mice[1].
In Vitro, BSJ-05-037 (0.001-10 μM; 2-16 h) potently induces time- and concentration-dependent degradation of ITK in DERL-2 and Hut78 cells, and this degradation is CRBN-dependent[1]. BSJ-05-037 (1 μM; 10 days) potently inhibits the proliferation of DERL-2 and Jurkat T-cell lymphoma cells[1]. BSJ-05-037 (0.025-0.5 μM; 8 h) dose-dependently inhibits the phosphorylation of PLCγ1 in DERL-2 cells[1]. BSJ-05-037 (1 μM; 24 h-3 days) blocks TCR-induced upregulation of GATA-3 and restores the sensitivity of T8ML-1 cells to Vincristine, thereby overcoming drug resistance mediated by the ITK/NF-κB/GATA-3 axis[1]. BSJ-05-037 (1 μM; 24 h-4 days) induces nearly complete ITK degradation and reduces GATA-3 levels by over 90% in Hut78 and H9 cutaneous T-cell lymphoma cells, while also enhancing the sensitivity of these cells to Vincristine during the 4-day treatment[1].
References:
[1]. Jiang B, et al. ITK degradation to block T cell receptor signaling and overcome therapeutic resistance in T cell lymphomas. Cell Chem Biol. 2023;30(4):383-393.e6.
[2]. Tigu AB, et al. Proteolysis targeting chimeric-based technology in myeloma and lymphoma. Mol Cancer Ther. Published online January 2, 2026.
[3]. Miletić N, et al. Workflow for E3 Ligase Ligand Validation for PROTAC Development. ACS Chem Biol. 2025;20(2):507-521.
In Vivo, BSJ-05-037 (50 mg/kg; i.p.; every 8 hours; 3 total doses/once every other day; 14 days) induces ITK degradation, reduces GATA-3 expression, inhibits PLCγ1, decreases tumor volume, and reverses chemoresistance in Hut78/H9 cutaneous T-cell lymphoma xenografts in mice[1].
In Vitro, BSJ-05-037 (0.001-10 μM; 2-16 h) potently induces time- and concentration-dependent degradation of ITK in DERL-2 and Hut78 cells, and this degradation is CRBN-dependent[1]. BSJ-05-037 (1 μM; 10 days) potently inhibits the proliferation of DERL-2 and Jurkat T-cell lymphoma cells[1]. BSJ-05-037 (0.025-0.5 μM; 8 h) dose-dependently inhibits the phosphorylation of PLCγ1 in DERL-2 cells[1]. BSJ-05-037 (1 μM; 24 h-3 days) blocks TCR-induced upregulation of GATA-3 and restores the sensitivity of T8ML-1 cells to Vincristine, thereby overcoming drug resistance mediated by the ITK/NF-κB/GATA-3 axis[1]. BSJ-05-037 (1 μM; 24 h-4 days) induces nearly complete ITK degradation and reduces GATA-3 levels by over 90% in Hut78 and H9 cutaneous T-cell lymphoma cells, while also enhancing the sensitivity of these cells to Vincristine during the 4-day treatment[1].
References:
[1]. Jiang B, et al. ITK degradation to block T cell receptor signaling and overcome therapeutic resistance in T cell lymphomas. Cell Chem Biol. 2023;30(4):383-393.e6.
[2]. Tigu AB, et al. Proteolysis targeting chimeric-based technology in myeloma and lymphoma. Mol Cancer Ther. Published online January 2, 2026.
[3]. Miletić N, et al. Workflow for E3 Ligase Ligand Validation for PROTAC Development. ACS Chem Biol. 2025;20(2):507-521.