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cholesterol pathway

" in TargetMol Product Catalog
  • Inhibitors & Agonists
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Geranylgeraniol
Tetraprenol, FT-0626663, FT0626663, CJ-24095, CJ24095, CJ 24095
TN671424034-73-9
Geranylgeraniol (FT0626663) is an isoprenoid found in fruits, vegetables, and grains, including rice. Geranylgeraniol (FT0626663) inhibits growth and induces apoptosis of various tumor cells. Geranylgeraniol (FT0626663) protects monocytes against statin-induced cytotoxicity and suppresses the growth of Mycobacterium.
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Mevalonic acid lithium salt
MVA lithium salt
T194262618458-93-6
Mevalonic acid lithium salt (MVA lithium salt) is a precursor of the mevalonic acid pathway, an initiator of cell growth, a key substance in cholesterol synthesis, and stimulates DNA synthesis, morphology transformation, and cell cycling in human lymphocytes from peripheral blood.
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24(S)-hydroxy Cholesterol
Cerebrosterol, 24S-OHC, 24S-HC
T21562474-73-7
24(S)-hydroxy Cholesterol (24S-OHC) is the terminal product of the cholesterol elimination pathway in neural tissues. It is an LXR agonist and a selective positive allosteric modulator of NMDARs. It can serve as a biomarker for NPD, induce cognitive decline in mice, and is useful for studying neurological diseases.
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    Coptisine
    Coptisin
    T5S00533486-66-6
    1. Coptisine (Coptisin) treatment increases cell viability based on its reversal effect on the enhanced activity of Indoleamine 2, 3-dioxygenase . 2. Coptisine treats myocardial I R likely through suppressing myocardial apoptosis and inflammation by inhibiting the Rho ROCK pathway. 3. Coptisine is a potential anti-osteosarcoma drug candidate, via exerting a strong anti-osteosarcoma effect with very low toxicity . 4. Coptisine with a high dosage could inhibit cholesterol synthesis via suppressing the HMGCR expression and promoting the use and excretion of cholesterol via up-regulating LDLR and CYP7A1 expression. 5. Coptisine suppresses adhesion, migration and invasion of MDA-MB-231 breast cancer cells in vitro, the down-regulation of MMP-9 in combination with the increase of TIMP-1 possibly contributing to the anti-metastatic function for breast cancer.
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