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| Product Name: | C75 | | Synonyms: | TETRAHYDRO-4-METHYLENE-2-OCTYL-5-OXO-3-FURANCARBOXYLIC ACID;C75;(2S,3R)-4-methylene-2-octyl-5-oxotetrahydrofuran-3-carboxylic acid;(2R,3S)-4-METHYLIDENE-5-OXO-2-N-OCTYL-OXOLANE-3-CARBOXYLIC ACID;(2R*,3S*)-Tetrahydro-4-methylene-2-octyl-5-oxo-3-furancarboxylicacid;(2R,3S)-rel-Tetrahydro-4-Methylene-2-octyl-5-oxo-3-furancarboxylic Acid;trans-Tetrahydro-4-Methylene-2-octyl-5-oxo-3-furancarboxylic Acid;trans-4-Methylene-2-octyl-5-oxotetrahydrofuran-3-carboxylic acid | | CAS: | 191282-48-1 | | MF: | C14H22O4 | | MW: | 254.32 | | EINECS: | | | Product Categories: | pharmacetical | | Mol File: | 191282-48-1.mol |  |
| Melting point | 88-89 °C | | Boiling point | 432.1±45.0 °C(Predicted) | | density | 1.08±0.1 g/cm3(Predicted) | | storage temp. | 2-8°C | | solubility | DMSO: 18 mg/mL | | form | solid | | pka | 3.08±0.40(Predicted) | | color | off-white |
| Uses | trans-Tetrahydro-4-methylene-2-octyl-5-oxo-3-furancarboxylic Acid is a well-known fatty acid synthase (FAS) inhibitor. Studies show that trans-Tetrahydro-4-methylene-2-octyl-5-oxo-3-furancarboxylic Acid is a cell cycle arrest inducer in hepatocellular carcinoma (HCC) cell lines. It has also been shown to blocks resistin-induced increases in lipid accumulation by human macrophages. | | Definition | ChEBI: (2R,3S)-C75 is a 4-methylidene-2-octyl-5-oxotetrahydrofuran-3-carboxylic acid that has 2R,3S-configuration. It is an enantiomer of a (2S,3R)-C75. | | Biological Activity | c 75 is an inhibitor of fatty acid synthase [1].fatty acid synthase (fas) is a multi-enzyme protein that catalyzes fatty acid synthesis. its main function is to catalyze the synthesis of palmitate from acetyl-coa and malonyl-coa. fas is a target for anticancer drug [1].in human breast cancer cells, c 75 reacted preferentially with fas and inhibited fas. the antitumor activity of c 75 is likely mediated by its inhibition of fas [1]. in primary cortical neurons, c 75 inhibited fas activity and increased the activity of carnitine palmitoyltransferase-1 (cpt-1) and fatty acid oxidation, which suggested that c 75 might influence cellular energy balance through regulation of these metabolic pathways. also, c 75 altered neuronal atp levels in a biphasic manner (decreasing initially, followed by a prolonged increase above control levels). the amp-activated protein kinase (ampk) activity was also influenced by c 75 [2]. in human melanoma a-375 cells, c 75 inhibited cell growth through activation of caspase-dependent apoptosis [3].in diet induced obese (dio) mice, chronic c 75 treatment reduced food intake and increased energy expenditure due to increased fatty acid oxidation. c 75 significantly reduced adipose tissue. the reduced food intake was accompanied by an increase in amphetamine and cocaine-related transcript expression [4]. | | in vivo | C75 blocks fasting-induced c-Fos expression in the arcuate nucleus (Arc), lateral hypothalamic area (LHA), and paraventricular nucleus (PVN) 10–24 h after i.p. injection. Intraperitoneal administration of C75 at 30 mg/kg body weight inhibits food intake of mice by ≥95% within 2 h after i.p. injection[3].
C75-treated DIO mice has a 50% greater weight loss, and a 32.9% increased production of energy because of fatty acid oxidation. C75 treatment of rodent adipocytes and hepatocytes and human breast cancer cells increases fatty acid oxidation and ATP levels by increasing CPT-1 activity, even in the presence of elevated concentrations of malonyl-CoA[4]. | | storage | Store at +4°C | | references | [1]. kuhajda fp, pizer es, li jn, et al. synthesis and antitumor activity of an inhibitor of fatty acid synthase. proc natl acad sci u s a, 2000, 97(7): 3450-3454.
[2]. landree le, hanlon al, strong dw, et al. c75, a fatty acid synthase inhibitor, modulates amp-activated protein kinase to alter neuronal energy metabolism. j biol chem, 2004, 279(5): 3817-3827.
[3]. ho ts, ho yp, wong wy, et al. fatty acid synthase inhibitors cerulenin and c75 retard growth and induce caspase-dependent apoptosis in human melanoma a-375 cells. biomed pharmacother, 2007, 61(9): 578-587.
[4]. thupari jn, kim ek, moran th, et al. chronic c75 treatment of diet-induced obese mice increases fat oxidation and reduces food intake to reduce adipose mass. am j physiol endocrinol metab, 2004, 287(1): e97-e104. |
| | C75 Preparation Products And Raw materials |
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