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Pathways Recommended: Stem Cell/Wnt Cell Cycle/DNA Damage
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glioblastoma cancer stem cells

" in MedChemExpress (MCE) Product Catalog:
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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-16397
    Phenformin
    Maximum Cited Publications
    10 Publications Verification

    Phenethylbiguanide

    		 Mitochondrial Metabolism AMPK Apoptosis Autophagy mTOR Neurological Disease Metabolic Disease Cancer
    Phenformin (Phenethylbiguanide) is an orally active biguanide hypoglycemic agent. Phenformin inhibits mitochondrial respiratory chain complex I, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin inhibits cancer stem cells (CSCs) and possesses potent antitumor potential .
    Phenformin
  • HY-10996A
    KHS101 hydrochloride
    1 Publications Verification

    		 Autophagy HSP Apoptosis Aurora Kinase Microtubule/Tubulin Polo-like Kinase (PLK) Neurological Disease Cancer
    KHS101 is a blood-brain barrier-penetrant anticancer agent that primarily functions by inhibiting HSPD1 (IC50 = 14.4 μM) and TACC3 across different cellular backgrounds. KHS101 promotes the aggregation of HSPD1 with client proteins, destabilizes TACC3, and reduces the levels of TACC3, Aurora A and PLK1. KHS101 induces autophagy, apoptosis, cell cycle exit and neuronal differentiation; it suppresses cancer cell growth, motility, EMT and stemness; it also impairs mitochondrial bioenergetics and glycolysis in glioblastoma cells. KHS101 can be used in research related to glioblastoma multiforme and breast cancer .
    KHS101 hydrochloride
  • HY-115630
    cRIPGBM chloride

    		RIP kinase Caspase Apoptosis Cancer
    cRIPGBM chloride, an orally active, proapoptotic derivative. cRIPGBM can be generated from glioblastoma multiforme (GBM) cancer stem cells (CSCs). cRIPGBM(chloride) targets to receptor-interacting protein kinase 2 (RIPK2) to induce caspase 1-dependent apoptosis. cRIPGBM(chloride) suppresses the formation of RIPK2/TAK1 (prosurvival complex), and increases the formation of RIPK2/caspase 1 (proapoptotic complex). cRIPGBM(chloride) exerts potent anti-tumor activity in vivo in animal models .
    cRIPGBM chloride
  • HY-167851
    CCX662

    		CXCR Neurological Disease Cancer
    CCX662 is a selective CXCR7 inhibitor with human IC50 values of 9 nM (buffer) and 18 nM (100% human serum), and rat IC50 of 14 nM (100% rat serum). CCX662 blocks CXCL12 binding to CXCR7, inhibits CXCR4-directed trans-endothelial migration of CXCR4 +/CXCR7 + cells. CCX662 can be used for the research of glioblastoma multiforme .
    CCX662
  • HY-17663
    KMR-206

    		PARP STAT STING IFNAR Cancer
    KMR-206 is a PARP7 inhibitor with an IC50 of 13.7 nM. KMR-206 relieves AHR-mediated transcriptional repression and enhances CYP1A1 expression in the presence of TCDD. KMR-206 induces the STING-dependent IFN-β signaling pathway and increases the levels of STAT1, pSTAT1 and nuclear PARP7 in cancer cells. KMR-206 reduces the viability of lung adenocarcinoma cells, enhances radiation-induced immunogenic signals, and induces the production of immunogenic signals in glioblastoma cancer stem cells. KMR-206 destabilizes FRA1 to increase IRF1 levels and promotes the IRF3-CBP/p300 interaction. KMR-206 can be used in studies related to lung adenocarcinoma and glioblastoma .
    KMR-206
  • HY-122910
    RIPGBM

    		Apoptosis Cancer
    RIPGBM is a selective inducer of apoptosis in glioblastoma multiforme (GBM) cancer stem cells (CSCs) with an EC50 of ≤500 nM .
    RIPGBM
  • HY-152203
    Mitochondrial respiration-IN-2

    		Drug Derivative Cancer
    Mitochondrial respiration-IN-2 is the fluorine derivative of Virginiamycin M1 (HY-N6686). Mitochondrial respiration-IN-2 can inhibit mitochondrial translation of glioblastoma stem cells .
    Mitochondrial respiration-IN-2
  • HY-10996
    KHS101

    		HSP Microtubule/Tubulin Aurora Kinase Polo-like Kinase (PLK) Autophagy Apoptosis Neurological Disease Cancer
    KHS101 is a blood-brain barrier-penetrant anticancer agent that primarily functions by inhibiting HSPD1 (IC50 = 14.4 μM) and TACC3 across different cellular backgrounds. KHS101 promotes the aggregation of HSPD1 with client proteins, destabilizes TACC3, and reduces the levels of TACC3, Aurora A and PLK1. KHS101 induces autophagy, apoptosis, cell cycle exit and neuronal differentiation; it suppresses cancer cell growth, motility, EMT and stemness; it also impairs mitochondrial bioenergetics and glycolysis in glioblastoma cells. KHS101 can be used in research related to glioblastoma multiforme and breast cancer .
    KHS101
  • HY-175754
    C3TD078

    		WDR5 Cancer
    C3TD078 is a WDR5 WIN site inhibitor with a Ki of 0.03  nM. C3TD078 has potent antiproliferative activity and reduces the stem-cell frequency of cancer stem cells (CSCs). C3TD078 can be used for glioblastoma (GBM) research .
    C3TD078
  • HY-152202
    Mitochondrial respiration-IN-3

    		Mitochondrial Metabolism Cancer
    Mitochondrial respiration-IN-3 is the fluorine derivative of Dalfopristin (HY-A0241). Mitochondrial respiration-IN-3 has cell membrane-permeable. Mitochondrial respiration-IN-3 can inhibit mitochondrial translation of glioblastoma stem cells. Mitochondrial respiration-IN-3 can be used in research of cancer .
    Mitochondrial respiration-IN-3
  • HY-161946
    GBM CSCs-IN-1

    		DNA/RNA Synthesis Apoptosis Cancer
    GBM CSCs-IN-1 (Compound (−)-20), a derivative of rocaglate, is a potent inhibitor of glioblastoma stem cells (GBM CSCs) with an EC50 of 45 nM, functioning by targeting the RNA helicase DDX3. Furthermore, GBM CSCs-IN-1 is also capable of inducing apoptosis .
    GBM CSCs-IN-1
  • HY-123933
    TTGM 5826

    		Glutaminase Neurological Disease Cancer
    TTGM 5826 is a tissue transglutaminase (tTG) inhibitor with an EC50 of 20 μM. TTGM 5826 stabilizes the open conformation of tTG that exhibits protein cross-linking activity, and acts as a competitive inhibitor of tTG-mediated cross-linking activity. TTGM 5826 inhibits the transformed phenotypes of breast cancer cells, brain cancer cells and glioma stem cells. TTGM 5826 can be used in the research of breast cancer, glioblastoma, pancreatic cancer and glioma stem cell-related tumors .
    TTGM 5826
  • HY-181074
    Tubulin polymerization-IN-88

    		Microtubule/Tubulin Apoptosis Bcl-2 Family Neurological Disease Cancer
    Tubulin polymerization-IN-88 is a tubulin inhibitor that blocks tubulin polymerization, leading to microtubule destabilization and disruption of the mitotic spindle. Tubulin polymerization-IN-88 induces G2/M phase arrest and apoptosis in cancer cells, and inhibits cancer cell migration and self-renewal of cancer stem cells. It exhibits in vitro anti-proliferative activity against cancer cells with selectivity over normal cells. Tubulin polymerization-IN-88 also demonstrates in vivo anti-cancer activity without significant toxicity. Tubulin polymerization-IN-88 is applicable for research on glioblastoma, lung cancer, endometrial cancer, ovarian cancer, and leukemia .
    Tubulin polymerization-IN-88
  • HY-138195
    NEO212

    		DNA/RNA Synthesis Apoptosis FAK Src MMP Autophagy Cancer
    NEO212 is an orally active, blood-brain barrier permeable conjugate of Temozolomide (TMZ) (HY-17364) and Perillyl Alcohol (POH) (HY-N7000), with potent anticancer activity. NEO212 overcomes classical TMZ resistance and DNA alkylation by depleting MGMT. By inhibiting the FAK/Src signaling pathway, NEO212 reduces the production of MMP2 and MMP9, induces mesenchymal-epithelial transition, and inhibits the migration, invasion and tumor progression of glioma stem cells. NEO212 disrupts autophagy flux to enhance mitochondrial apoptosis; it induces differentiation of acute myeloid leukemia (AML) cells into macrophages and proliferation arrest .
    NEO212

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