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Results for "

migration ability

" in MedChemExpress (MCE) Product Catalog:

9

Inhibitors & Agonists

2

Natural
Products

1

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-147187
    MNK8

    		STAT Apoptosis Bcl-2 Family Survivin Cancer
    MNK8 is a potent STAT3 (signal transducer and activator of transcription 3) inhibitor. MNK8 inhibits STAT3 activation and reduced its DNA binding ability. MNK8 shows good growth inhibition against hepatocellular carcinoma (HCC) cells. MNK8 induces apoptosis in HCC cells. MNK8 reduces prosurvival proteins expression and migration/invasion of HCC cells .
    MNK8
  • HY-N0060BS
    (E)-Ferulic acid-d3

    (E)-Coniferic acid-d3

    		 β-catenin Bcl-2 Family Ferroptosis Endogenous Metabolite Cancer
    (E)-Ferulic acid-d3 is the deuterium labeled (E)-Ferulic acid. (E)-Ferulic acid is a isomer of Ferulic acid which is an aromatic compound, abundant in plant cell walls. (E)-Ferulic acid causes the phosphorylation of β-catenin, resulting in proteasomal degradation of β-catenin and increases the expression of pro-apoptotic factor Bax and decreases the expression of pro-survival factor survivin. (E)-Ferulic acid shows a potent ability to remove reactive oxygen species (ROS) and inhibits lipid peroxidation. (E)-Ferulic acid exerts both anti-proliferation and anti-migration effects in the human lung cancer cell line H1299[1].
    (E)-Ferulic acid-d3
  • HY-121605
    RL71

    		Others Cancer
    RL71 is a curcuminoid anticancer agent that exhibits potent cytotoxicity against a variety of ER-negative breast cancer cells. RL71 (1 μM) induces cell cycle arrest in the G2/M phase and induces apoptosis in SKBr3 cells. RL7 also decreases HER2/neu phosphorylation and increases p27. RL71 also significantly reduced the phosphorylation of Akt and transiently increased the stress kinases JNK1/2 and p38 MAPK. Furthermore, RL71 exhibited anti-angiogenic potential in vitro, inhibiting the migration of HUVEC cells and the ability of these cells to form tubular networks .
    RL71
  • HY-144099
    Keap1-Nrf2-IN-4

    		E1/E2/E3 Enzyme Apoptosis Cancer
    Keap1-Nrf2-IN-4 is a potent neddylation inhibitor. Keap1-Nrf2-IN-4 exhibits potent anti-proliferation activity against MGC-803 cells (IC50=2.55 µM). Keap1-Nrf2-IN-4 blocks the migration ability and induces apoptosis of gastric cancer cells. Keap1-Nrf2-IN-4 inhibits tumor growth without obvious toxicity .
    Keap1-Nrf2-IN-4
  • HY-146809
    Galectin-3 antagonist 2

    		Galectin Cancer
    Galectin-3 is a β Galactoside specific carbohydrate recognition protein (lectin) has the ability to promote the migration of B cell precursor acute lymphoblastic leukemia (BCP-ALL) cells and withstand drug research.
    Galectin-3 antagonist 2
  • HY-116903
    Pfn1-IN-2

    		Others Cancer
    Pfn1-IN-2 is an inhibitor of Profilin1 (Pfn1) and has the activity to interfere with the interaction between Pfn1 and actin. Pfn1-IN-2 can significantly reduce the overall level of intracellular filamentous (F) actin. Pfn1-IN-2 also slows down the migration and proliferation of endothelial cells (EC). Pfn1-IN-2 can inhibit the angiogenic ability of endothelial cells both in vivo and in vitro .
    Pfn1-IN-2
  • HY-116452
    YLT192

    		VEGFR Cancer
    YLT192 is an orally active and highly bioavailable VEGFR2 inhibitor with potent anti-angiogenic activity and anti-tumor efficacy. YLT192 significantly inhibited the kinase activity of VEGFR2 and inhibited the proliferation, migration, invasion and tube formation of human umbilical cord vascular endothelial cells. YLT192 also inhibited VEGF-induced VEGFR2 phosphorylation and its downstream signaling regulators. YLT192 also showed the ability to inhibit angiogenesis in vivo in zebrafish embryo models and alginate-coated tumor cell experiments. YLT192 can directly inhibit the proliferation of cancer cells and induce their apoptosis .
    YLT192
  • HY-113325R
    NADP (Standard)

    		Endogenous Metabolite Metabolic Disease Inflammation/Immunology Cancer
    NADP (Standard) is the analytical standard of NADP. This product is intended for research and analytical applications. NADP is a coenzyme involved in cellular electron transfer reactions in biological metabolism, which is alternately oxidized (NADP+) and reduced (NADPH), and can maintain cellular redox homeostasis and regulate many biological events, including cellular metabolism. NADPH is a universal electron donor that provides reducing ability for synthetic metabolic reactions and redox balance. NADPH plays a multifunctional role in regulating inflammation, redox homeostasis, and synthetic metabolism processes .
    In Vitro:NADP can impair folate metabolism and nucleotide biosynthesis in HCT116 cells at high concentrations, leading to the cessation of proliferation and prioritizing cell survival .
    NADP forms NAADP through IL-8-driven CD38 to mobilize Ca 2+ and influence cell migration .
    NADP de novo synthesis mediated by NADK upregulation provides power for anabolic reaction and antioxidant system to promote breast cancer metastasis .
    NADP is upregulated in ROS generation mediated by hyperglycemia and IDPc induction, thereby protecting renal cells from oxidative stress .
    NADP (Standard)
  • HY-B2167R
    Docosahexaenoic acid (Standard)

    		Endogenous Metabolite Neurological Disease Cancer
    Docosahexaenoic acid (Standard) is the analytical standard of Docosahexaenoic acid. This product is intended for research and analytical applications. Docosahexaenoic Acid (DHA) is an omega-3 fatty acid abundantly present brain and retina. It can be obtained directly from fish oil and maternal milk. In Vitro: Docosahexaenoic acid (DHA) is essential for the growth and functional development of the brain in infants. DHA is also required for maintenance of normal brain function in adults. The inclusion of plentiful DHA in the diet improves learning ability and memory . DHA is an essential requirement in every step of brain development like neural cell proliferation, migration, differentiation, synaptogenesis. The multiple double bonds and unique structure allow DHA to impart special membrane characteristics for effective cell signaling. Many development disorders like dyslexia, autism spectrum disorder, attention deficit hyperactivity disorder, schizophrenia etc. are causally related to decreased level of DHA . DHA is a potent RXR ligand inducing robust RXR activation already at low micro molar concentrations. The EC50 for RXRα activation by DHA is about 5-10 μM fatty acid . In Vivo: Docosahexaenoic acid administration over 10 weeks significantly reduces the number of reference memory errors, without affecting the number of working memory errors, and significantly increases the docosahexaenoic acid content and the docosahexaenoic acid/arachidonic acid ratio in both the hippocampus and the cerebral cortex . DHA treatment exerts neuroprotective actions on an experimental mouse model of PD. There is a decrease tendency in brain lipid oxidation of MPTP mice but it does not significantly .
    Docosahexaenoic acid (Standard)

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