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mouse bone marrow osteoclast precursor cells

" in MedChemExpress (MCE) Product Catalog:
製品番号 製品名 Target 研究分野 構造式
  • HY-102065

    Prostaglandin Receptor RANKL/RANK Metabolic Disease
    SC-19220 is a prostaglandin E2 receptor EP1 antagonist. SC-19220 blocks functional EP1 receptor activation, and RANK/RANKL signaling pathway. SC-19220 inhibits osteoclast formation and bone resorption by pre-existing osteoclasts. SC-19220 can be used for the research of osteoporotic disorders, inflammatory bone resorption .
    SC-19220
  • HY-121282B

    Pecazine acetate

    Apoptosis MALT1 Others
    Mepazine acetate (Pecazine acetate) is a drug that has the activity to inhibit the protease activity of MALT1. Mepazine acetate is often used to study the role of MALT1 in biology. Treatment of mouse bone marrow precursor cells with mepazine acetate strongly inhibited RANK ligand (RANKL)-induced osteoclast formation. Mepazine acetate also inhibited the expression of multiple osteoclast markers such as TRAP, feline hepsin K, and calcitonin. The protective effect of mepazine acetate was not affected by MALT1 deficiency. The mechanism of action of mepazine acetate may involve MALT1-independent mechanisms, and this aspect needs to be considered in future studies .
    Mepazine acetate
  • HY-102065R

    Reference Standards Prostaglandin Receptor RANKL/RANK Metabolic Disease
    SC-19220 (Standard) is the analytical standard of SC-19220 (HY-102065). This product is intended for research and analytical applications. SC-19220 is a prostaglandin E2 receptor EP1 antagonist. SC-19220 blocks functional EP1 receptor activation, and RANK/RANKL signaling pathway. SC-19220 inhibits osteoclast formation and bone resorption by pre-existing osteoclasts. SC-19220 can be used for the research of osteoporotic disorders, inflammatory bone resorption .
    SC-19220 (Standard)
  • HY-182757

    RANKL/RANK Nuclear Factor of activated T Cells (NFAT) Cathepsin Metabolic Disease Inflammation/Immunology
    Y1693 is an orally active RANKL inhibitor with a Kd of 5.03 μM for hRANKL. Y1693 inhibits the activation of the downstream c-fos/NFATc1 signaling pathway by blocking its interaction with RANK. Y1693 significantly inhibits RANKL-induced osteoclast differentiation, F-actin ring formation and bone resorptive activity, while downregulating the mRNA and protein expressions of TRAP, cathepsin K, c-fos and NFATc1. Y1693 shows no obvious cytotoxicity to bone marrow-derived macrophages and osteoclast precursor cells, and exhibits favorable ADME properties. Y1693 improves ovariectomy-induced osteoporosis in mice and reverses ligation-induced periodontal alveolar bone loss. Y1693 is applicable to research related to osteoporosis and periodontal diseases .
    Y1693

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