gsc cells

Atracurium besylate (51W89) is a non-depolarizing neuromuscular blocking agent with short duration of action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents.

MCI-INI-3 is a selective competitive inhibitor of human ALDH1A3, with a Ki value of 0.55 μM for ALDH1A3 and 78.2 μM for ALDH1A1. It inhibits retinoic acid biosynthesis and can reduce the viability of glioblastoma cells GSC-83 and GSC-326.

PROTACMAGLdegrader-1 is an orally active PROTAC agent that simultaneously targets both monoacylglycerol lipase (MAGL) and the E3 ubiquitin ligase MDM2. It functions by degrading MAGL and inhibiting the interaction between MDM2 and p53. Additionally, PROTACMAGLdegrader-1 has partial blood-brain barrier (BBB) penetration and can induce apoptosis in glioblastoma stem cells (GSC).

SHP1705 is a potent and selective Cryptochrome 2 (CRY2) activator with circadian rhythm-modulating activity. It inhibits BMAL1-CLOCK transcriptional activity and prolongs survival in glioblastoma (GBM) mice established from glioblastoma stem cells (GSCs).

MXC-017 is an apoptosis inducer capable of crossing the blood-brain barrier, specifically targeting glioma stem cells (GSCs). It effectively prevents the formation of radiation-induced GSCs while promoting G0/G1 cell cycle arrest and apoptosis. With minimal off-target effects, MXC-017 exhibits no significant cytotoxicity even at concentrations up to 10 µM. Additionally, it significantly extends the median survival in patient-derived orthotopic xenograft (PDOX) glioblastoma (GBM) mouse models when used in conjunction with radiation therapy.

2-Fluoropalmitic acid (2-Fluorohexadecanoic acid), a fatty acid containing fluorine atoms, serves as a potential therapeutic agent for glioblastoma (GBM) by inhibiting the viability, proliferation, and stem-like phenotype of glioma stem cells (GSCs), suppressing the expression of phosphorylated erk, CD133, and SOX-2, and leading to decreased MMP-2 activity and increased methylation of the MGMT promoter.