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Pathways Recommended: Stem Cell/Wnt Cell Cycle/DNA Damage
Results for "

glioblastoma stem cells

" in MedChemExpress (MCE) Product Catalog:

42

Inhibitors & Agonists

1

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1

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1

Peptides

2

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1

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-16900
    Rolipram
    Maximum Cited Publications
    19 Publications Verification

    (R,S)-Rolipram; (±)-Rolipram; ZK 62711

    		 Bacterial HIV Phosphodiesterase (PDE) Epigenetic Reader Domain Amyloid-β Infection Neurological Disease Cancer
    Rolipram is a PDE4 inhibitor, with blood-brain barrier permeability, that reverses β-amyloid-induced learning and memory impairment in rats. Rolipram elevates intracellular cAMP and clevels and regulates the cAMP/CREB signaling pathway, thereby alleviating neuroinflammation and apoptotic responses. Rolipram promotes neuronal differentiation of human bone marrow mesenchymal stem cells and inhibits Methamphetamine- and morphine-induced hyperlocomotion in mice. Rolipram also reduces the viability of glioblastoma stem-like cells and enhances Bevacizumab (HY-P9906)-induced cell death. Rolipram inhibits the expression of proinflammatory cytokines and enhances central noradrenergic transmission. Rolipram is mainly used in studies related to various central nervous system diseases including Alzheimer's disease, major depressive disorder, glioblastoma multiforme, and multiple sclerosis .
    Rolipram
  • HY-B0106
    Levetiracetam
    2 Publications Verification

    UCB L059

    		 DNA Methyltransferase Neurological Disease Cancer
    Levetiracetam, an antiepileptic agent, binds the synaptic vesicle protein SV2A. Levetiracetam enhances Temozolomide effect on glioblastoma stem cell proliferation and apoptosis. Levetiracetam modulates HDAC levels ultimately silencing MGMT, thus increasing Temozolomide effectiveness. A chemosensitizer agent .
    Levetiracetam
  • HY-16397
    Phenformin
    5+ Cited Publications

    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-103693
    NAZ2329
    3 Publications Verification

    		 Phosphatase Cancer
    NAZ2329, the first cell-permeable inhibitor of R5 subfamily of receptor-type protein tyrosine phosphatases (RPTPs), allosterically and preferentially inhibits PTPRZ (IC50=7.5 µM for hPTPRZ1) and PTPRG (IC50=4.8 µM for hPTPRG) over other PTPs. NAZ2329 binds to the active D1 domain and more potently inhibits PTPRZ-D1 fragment (IC50 of 1.1 µM) than the whole intracellular (D1 + D2) fragment (IC50 of 7.5 µM). NAZ2329 can effectively inhibit tumor growth of the glioblastoma cells and suppress stem cell-like properties .
    NAZ2329
  • HY-W587427
    D-2-Phosphoglyceric acid trisodium

    		Endogenous Metabolite Monocarboxylate Transporter Neurological Disease Cancer
    D-2-Phosphoglyceric acid trisodium is a glycolysis and gluconeogenesis intermediate with altered levels linked to MCT4-modulated glycolytic pathways. D-2-Phosphoglyceric acid trisodium shows reduced intracellular levels in hypoxic glioblastoma stem cells after MCT4 knockdown. D-2-Phosphoglyceric acid trisodium can be used for the research of glioblastoma .
    D-2-Phosphoglyceric acid trisodium
  • 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-160972
    MM0299

    		LXR Neurological Disease Cancer
    MM0299 is a selective lanosterol synthase (LSS) inhibitor with an IC50 value of 2.22 μM. MM0299 depletes intracellular cholesterol and acts as a growth inhibitor for glioma stem-like cells. MM0299 exhibits anti-glioblastoma activity. MM0299 is applicable to research related to glioblastoma .
    MM0299
  • 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-B0106R
    Levetiracetam (Standard)

    UCB L059 (Standard)

    		 Reference Standards DNA Methyltransferase Neurological Disease Cancer
    Levetiracetam (Standard) is the analytical standard of Levetiracetam. This product is intended for research and analytical applications. Levetiracetam, an antiepileptic agent, binds the synaptic vesicle protein SV2A. Levetiracetam enhances Temozolomide effect on glioblastoma stem cell proliferation and apoptosis. Levetiracetam modulates HDAC levels ultimately silencing MGMT, thus increasing Temozolomide effectiveness. A chemosensitizer agent .
    Levetiracetam (Standard)
  • HY-N10631
    Paucimannose

    		Endogenous Metabolite Infection Inflammation/Immunology Cancer
    Paucimannose is a mannosidic N-glycan epitope. It acts as a carcinoembryonic antigen, and a marker for cancer, stem cell properties and inflammation. Paucimannose mainly exists in plants and invertebrates. It consists of oligomannose-type N-glycans that preferentially bind to mannose-binding lectin. Paucimannose localizes on the surface of resting cells and translocates upon cell activation. It can be used in studies related to Pseudomonas aeruginosa infection, cancer and pancreatitis .
    Paucimannose
  • 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-157343
    GD3 Ganglioside

    		Apoptosis Mitochondrial Metabolism Caspase Neurological Disease Cancer
    GD3 Ganglioside is an Apoptosis inducer and a biomarker for mouse neural stem cells. GD3 Ganglioside expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside is applicable to research related to glioblastoma .
    GD3 Ganglioside
  • HY-132865
    FTO-IN-3

    		Fat Mass and Obesity-associated Protein (FTO) Cancer
    FTO-IN-3 is a FTO inhibitor that impair self-renewal in glioblastoma stem cells.
    FTO-IN-3
  • HY-157343A
    GD3 Ganglioside sodium

    		Apoptosis Mitochondrial Metabolism Caspase Neurological Disease Cancer
    GD3 Ganglioside sodium is an Apoptosis inducer and biomarker for mouse neural stem cells. GD3 Ganglioside sodium expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside sodium targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside sodium is applicable to research related to glioblastoma .
    GD3 Ganglioside sodium
  • HY-157343B
    GD3 Ganglioside ammonium

    		Apoptosis Mitochondrial Metabolism Caspase Neurological Disease Cancer
    GD3 Ganglioside ammonium is an Apoptosis inducer and biomarker for mouse neural stem cells. GD3 Ganglioside ammonium expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside ammonium targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside ammonium is applicable to research related to glioblastoma .
    GD3 Ganglioside ammonium
  • HY-B0106S
    Levetiracetam-d6

    UCB L059-d6

    		 Isotope-Labeled Compounds DNA Methyltransferase Neurological Disease Cancer
    Levetiracetam-d6 is the deuterium labeled Levetiracetam. Levetiracetam, an antiepileptic agent, binds the synaptic vesicle protein SV2A. Levetiracetam enhances Temozolomide effect on glioblastoma stem cell proliferation and apoptosis. Levetiracetam modulates HDAC levels ultimately silencing MGMT, thus increasing Temozolomide effectiveness. A chemosensitizer agent .
    Levetiracetam-d6
  • HY-Q66655
    YRDC-IN-1

    		DNA/RNA Synthesis Reactive Oxygen Species (ROS) Neurological Disease Cancer
    YRDC-IN-1 is a blood-brain barrier-permeable YRDC inhibitor. YRDC is a key enzyme that catalyzes the formation of N 6-threonylcarbamoyladenosine at position 37 of tRNA (t 6A37). YRDC-IN-1 selectively inhibits the translation of ANN codon-enriched FABP7, thereby reducing lipid droplet formation, increasing ROS, and reversing the acquired resistance of GBM to Temozolomide (TMZ) (HY-17364). YRDC-IN-1 can be used for the research of glioblastoma .
    YRDC-IN-1
  • HY-P10782
    Pt(IV)-M13

    		Peptide-Drug Conjugates (PDCs) Cancer
    Pt(IV)-M13 is a BBB-penetrable Platinum (IV) prodrug-perfluoroaryl macrocyclic peptide conjugate. Pt(IV)-M13 is cytotoxic to glioma stem cells and increases uptake of platinum in the brain. Pt(IV)-M13 can be used in the study of glioblastoma .
    Pt(IV)-M13
  • HY-129341
    WP1193

    		JAK STAT c-Myc Neurological Disease Cancer
    WP1193 is a novel JAK2/STAT3 pathway inhibitor. WP1193 suppresses phosphorylation of JAK2 and STAT3. WP1193 decreases expression of stem cell markers including CD133 and c-myc. WP1193 can be used in the research of glioblastoma .
    WP1193
  • 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-16900R
    Rolipram (Standard)

    (R,S)-Rolipram (Standard); (±)-Rolipram (Standard); ZK 62711 (Standard)

    		 Reference Standards Bacterial HIV Phosphodiesterase (PDE) Epigenetic Reader Domain Amyloid-β Neurological Disease Cancer
    Rolipram (Standard) is the analytical standard of Rolipram (HY-16900). This product is intended for research and analytical applications. Rolipram is a PDE4 inhibitor, with blood-brain barrier permeability, that reverses β-amyloid-induced learning and memory impairment in rats. Rolipram elevates intracellular cAMP and clevels and regulates the cAMP/CREB signaling pathway, thereby alleviating neuroinflammation and apoptotic responses. Rolipram promotes neuronal differentiation of human bone marrow mesenchymal stem cells and inhibits Methamphetamine- and morphine-induced hyperlocomotion in mice. Rolipram also reduces the viability of glioblastoma stem-like cells and enhances Bevacizumab (HY-P9906)-induced cell death. Rolipram inhibits the expression of proinflammatory cytokines and enhances central noradrenergic transmission. Rolipram is mainly used in studies related to various central nervous system diseases including Alzheimer's disease, major depressive disorder, glioblastoma multiforme, and multiple sclerosis .
    Rolipram (Standard)
  • HY-174212
    MXC-017

    		Apoptosis Cancer
    MXC-017 is a blood-brain barrier (BBB)-penetrant apoptosis inducer that directly targets Vimentin (VIM). MXC-017 prevents radiation-induced glioma stem cell (GSC) formation, while promoting G0/G1 cell cycle arrest and apoptosis. MXC-017 exhibits minimal off-target effects and shows no significant cytotoxicity. MXC-017 significantly prolongs median survival when used in combination with radiation therapy in glioblastoma (GBM) mouse models.
    MXC-017
  • HY-101349
    L 741742

    		Dopamine Receptor Apoptosis Autophagy PDGFR ERK mTOR Neurological Disease Cancer
    L 741742 is a highly selective and brain-penetrant D4 dopamine receptor antagonist, with Ki values of 3.5 nM, 770 nM and >1700 nM for human D4, D3 and D2 receptors, respectively. L 741742 suppresses PDGFRβ, ERK1/2, and mTOR signaling pathways, and impairs autophagic flux while disrupting lysosomal function.L 741742 induces G0/G1 cell-cycle arrest and apoptosis, promotes neuronal differentiation of normal human neural stem cells, selectively inhibits growth and clonogenic potential of glioblastoma neural stem cells and primary glioblastoma tumor cells, exerts synergistic effects with Temozolomide (TMZ) (HY-17364) against glioblastoma neural stem cells in vitro, and inhibits glioblastoma neural stem cell xenograft growth in immunocompromised mice. L 741742 can be used for the research of schizophrenia and glioblastoma .
    L 741742
  • 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-173369
    PROTAC MAGL degrader-1

    		PROTACs MAGL Cancer
    PROTAC MAGL degrader-1 is an orally active PROTAC agent that simultaneously targets monoacylglycerol lipase (MAGL) and E3 ubiquitin ligase MDM2. PROTAC MAGL degrader-1 degrades MAGL and inhibits the binding of MDM2 to p53. PROTAC MAGL degrader-1 can partially penetrate the blood-brain barrier (BBB). PROTAC MAGL degrader-1 induces glioblastoma stem cells (GSCs) apoptosis. (E3 ligase ligand: HY-128837; target protein ligand + linker: HY-173370; target protein inhibitor: HY-15249) .
    PROTAC MAGL degrader-1
  • HY-101349A
    L 741742 hydrochloride

    		Dopamine Receptor Apoptosis Autophagy PDGFR ERK mTOR Neurological Disease Cancer
    L 741742 hydrochloride is a highly selective and brain-penetrant D4 dopamine receptor antagonist, with Ki values of 3.5 nM, 770 nM and >1700 nM for human D4, D3 and D2 receptors, respectively. L 741742 hydrochloride suppresses PDGFRβ, ERK1/2, and mTOR signaling pathways, and impairs autophagic flux while disrupting lysosomal function.L 741742 hydrochloride induces G0/G1 cell-cycle arrest and apoptosis, promotes neuronal differentiation of normal human neural stem cells, selectively inhibits growth and clonogenic potential of glioblastoma neural stem cells and primary glioblastoma tumor cells, exerts synergistic effects with Temozolomide (TMZ) (HY-17364) against glioblastoma neural stem cells in vitro, and inhibits glioblastoma neural stem cell xenograft growth in immunocompromised mice. L 741742 hydrochloride can be used for the research of schizophrenia and glioblastoma .
    L 741742 hydrochloride
  • HY-132863
    FTO-IN-2

    		Fat Mass and Obesity-associated Protein (FTO) Cancer
    FTO-IN-2 is a FTO inhibitor that impairs self-renewal in glioblastoma stem cells.
    FTO-IN-2
  • 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-B0106S1
    Levetiracetam-d3

    UCB L059-d3

    		 DNA Methyltransferase Neurological Disease Cancer
    Levetiracetam-d3 is the deuterium labeled Levetiracetam. Levetiracetam, an antiepileptic agent, binds the synaptic vesicle protein SV2A. Levetiracetam enhances Temozolomide effect on glioblastoma stem cell proliferation and apoptosis. Levetiracetam modulates HDAC levels ultimately silencing MGMT, thus increasing Temozolomide effectiveness. A chemosensitizer agent .
    Levetiracetam-d3
  • HY-12772R
    Hydroxy Itraconazole (Standard)

    Itraconazole metabolite Hydroxy Itraconazole (Standard); R-63373 (Standard)

    		 Reference Standards Fungal Drug Metabolite Others
    Levetiracetam (Standard) is the analytical standard of Levetiracetam. This product is intended for research and analytical applications. Levetiracetam, an antiepileptic agent, binds the synaptic vesicle protein SV2A. Levetiracetam enhances Temozolomide effect on glioblastoma stem cell proliferation and apoptosis. Levetiracetam modulates HDAC levels ultimately silencing MGMT, thus increasing Temozolomide effectiveness. A chemosensitizer agent .
    Hydroxy Itraconazole (Standard)
  • HY-181640
    HDAC1/3-IN-1

    		HDAC Apoptosis Neurological Disease Cancer
    HDAC1/3-IN-1 is a selective HDAC1/3 inhibitor, with IC50 values of 256 nM and 340.3 nM against HDAC1 and HDAC3, respectively. HDAC1/3-IN-1 increases the SubG1 cell population and promotes apoptosis of glioma cells and glioblastoma stem cells. HDAC1/3-IN-1 can be used in studies related to glioblastoma .
    HDAC1/3-IN-1
  • HY-181639
    HDAC6-IN-75

    		HDAC Apoptosis Cancer
    HDAC6-IN-75 is a selective HDAC6 inhibitor with an IC50 of 0.17 nM against HDAC6. HDAC6-IN-75 induces the accumulation of acetylated α-tubulin in glioma cells. HDAC6-IN-75 triggers cell cycle changes, increases the SubG1 cell population, and promotes apoptosis in glioma cells and glioblastoma stem cells. HDAC6-IN-75 is applicable for glioma-related research .
    HDAC6-IN-75
  • 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-16900G
    Rolipram

    		Phosphodiesterase (PDE) Epigenetic Reader Domain Amyloid-β Neurological Disease Inflammation/Immunology Cancer
    Rolipram GMP is Rolipram (HY-16900) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Rolipram is a PDE4 inhibitor, with blood-brain barrier permeability, that reverses β-amyloid-induced learning and memory impairment in rats. Rolipram elevates intracellular cAMP and clevels and regulates the cAMP/CREB signaling pathway, thereby alleviating neuroinflammation and apoptotic responses. Rolipram promotes neuronal differentiation of human bone marrow mesenchymal stem cells and inhibits Methamphetamine- and morphine-induced hyperlocomotion in mice. Rolipram also reduces the viability of glioblastoma stem-like cells and enhances Bevacizumab (HY-P9906)-induced cell death. Rolipram inhibits the expression of proinflammatory cytokines and enhances central noradrenergic transmission. Rolipram is mainly used in studies related to various central nervous system diseases including Alzheimer's disease, major depressive disorder, glioblastoma multiforme, and multiple sclerosis .
    Rolipram
  • 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-183250
    eALM1137

    		mTOR Ribosomal S6 Kinase (RSK) Akt DNA-PK Neurological Disease Cancer
    eALM1137 is a mTOR inhibitor with an IC50 of 4.8 nM. eALM1137 mediates dual inhibition of the mTORC1 and mTORC2 signaling pathways, and inhibits DNA-PK (IC50=77 nM). eALM1137 exhibits antiproliferative and cytostatic activities, and induces G1 cell cycle arrest. eALM1137 is applicable to the research of glioblastoma multiforme .
    eALM1137
  • HY-103693R
    NAZ2329 (Standard)

    		Reference Standards Phosphatase Cancer
    NAZ2329 (Standard) is the analytical standard of NAZ2329 (HY-103693). This product is intended for research and analytical applications. NAZ2329, the first cell-permeable inhibitor of R5 subfamily of receptor-type protein tyrosine phosphatases (RPTPs), allosterically and preferentially inhibits PTPRZ (IC50=7.5 µM for hPTPRZ1) and PTPRG (IC50=4.8 µM for hPTPRG) over other PTPs. NAZ2329 binds to the active D1 domain and more potently inhibits PTPRZ-D1 fragment (IC50 of 1.1 µM) than the whole intracellular (D1 + D2) fragment (IC50 of 7.5 µM). NAZ2329 can effectively inhibit tumor growth of the glioblastoma cells and suppress stem cell-like properties .
    NAZ2329 (Standard)
  • 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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