SBN is a plant-derived molecular glue that intercepts PD-L1 glycomaturation co-translationally in the ER. When combined with canonical PD-L1 dimerizers, SBN collapses adaptive PD-L1 expression and renders cancer cells exquisitely susceptible to the cytolytic insults of T cells. Due to its favorable safety profile and oral bioavailability, SBN is a promising "glycotherapeutic" phytochemical for T-cell-based immunotherapy, particularly in IFN-rich tumors with reactive PD-L1 expression programs.
1 month ago
Journal • PD(L)-1 Biomarker • IO biomarker
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IFNG (Interferon, gamma) • STAT3 (Signal Transducer And Activator Of Transcription 3)
In conclusion, we propose the iron-rifampicin complex as a potential candidate for nephroprotection against doxorubicin-induced nephrotoxicity, subject to further validation.
SF@LA-NPs developed in this study significantly enhanced the delivery efficiency and antitumor activity of silibinin in glioblastoma cells. Moreover, a dual-mechanism mode of action was elucidated, involving ROS-induced mitochondrial apoptosis and compensatory protective autophagy. These findings provide a promising nano-platform and a theoretical basis for combination therapies targeting apoptosis-autophagy crosstalk in glioblastoma.
P2, N=9, Active, not recruiting, Cancer Institute and Hospital, Chinese Academy of Medical Sciences | Not yet recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Jun 2027 | Trial primary completion date: Mar 2025 --> Dec 2026
2 months ago
Enrollment closed • Trial completion date • Trial primary completion date
While modulating Bcl-2 pathways can be effective in MS, future research should aim to provide greater clarification and to design precision-based drugs capable of neuroprotective effects.
Among 5 255 randomized patients, 374 (7.1%) had LTBI and received preventive treatment, most commonly isoniazid (82.1%) and rifampicin (11.8%). From Year 1-5 (after ~98% of LTBI+ patients completed preventive treatment), transaminase elevations were generally similar among LTBI+ and LTBI- patients. The absence of observed TB risk in guselkumab-treated patients suggests IL-23 inhibitors may be better treatment options than TNFi in high-risk patients, including those in TB-endemic regions.