OTX-008

We conclude that LGALS1 possesses significant prognostic value for predicting ICI response in HNSCC. LGALS1 may represent a multimodal therapeutic target to sensitize tumors to immunotherapy, as its blockade simultaneously modulates tumor cells, myeloid cells, and CD8 T cells to overcome multi-layered resistance and promote robust anti-tumor immunity.

The mRNA expression levels of the transcription factors T-bet (TBX21), RORC2, and Foxp3 were analyzed in peripheral blood mononuclear cells (PBMCs) from colorectal cancer patients and healthy donors following co-culture with COLO 201 cells in the presence of galectin-1 inhibitor OTX 008, galectin-3 inhibitor GB1107, or both...Conversely, in healthy donor cells, galectin-3 blockade suppressed RORC2 and induced FOXP3 expression. Notably, the most pronounced downregulation of FOXP3 was achieved by simultaneously inhibiting both galectins.

Approaches such as OTX008, anti-Gal1 monoclonal antibodies, and Gal1-targeted vaccines have demonstrated the ability to downregulate tumour progression by inhibiting Gal1 activity. These findings highlight the therapeutic promise of Gal1 not only as a novel target for cancer therapy but also as a potential prognostic biomarker, offering opportunities for the development of more effective and less toxic treatment strategies.

Treatment with OTX008, an LGALS1 inhibitor, markedly diminished the viability of primary malignant bone marrow cells from AML patients. Notably, LGALS1 expression was significantly reduced exclusively in AML-M5 patients after treatment, which may be due to its higher expression in AML-M5 subtype compared to other FAB subtypes. In summary, our findings indicate that LGALS1 could serve as an independent prognostic risk factor and a promising therapeutic target in AML, providing novel insights into AML pathogenesis and laying the foundation for the development of new therapeutic strategies.

Combining OTX008 with clinical taxane formulations effectively reversed paclitaxel resistance in vitro and in vivo. Elevated galectin-1 levels thus serve as an indicator of response to paclitaxel therapy in ESCC, offering a therapeutic intervention strategy to overcome drug resistance.

in this study, high levels of Gal-1 and PLR were associated with poorer OS in SCLC patients, supporting their utility as clinical prognostic biomarkers. Moreover, the in vivo model suggests the inhibition of Gal-1 as a novel potential therapy for this disease with very poor prognosis.

Our findings reveal a regulatory axis for programmed death ligand 1 (PD-L1) expression in NPC cells, and targeting one component in this axis, Lgals1, is effective in boosting the immunogenicity of NPCs, providing a therapeutic avenue for treating NPC in clinic.

OTX008 decreased the viability of OSCC and NOK cells in a dose-dependent manner. The significant regulation of FOS suggests OTX008 causes early induction of the MAPK pathway via the immediate response gene FOS as a subunit of the AP-1 complex.