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(−)-C75
CAS No. : 1234694-22-4
MCE 国际站:(−)-C75
产品活性:(−)-C75 是 C75 (HY-12364) 的一种异构体,这是一种合成的脂肪酸合成酶 (FASN) 抑制剂。C75 抑制前列腺癌细胞 PC3 的 IC50 值为 35 μM。C75 是有效的 CPT1A 激活剂。
研究领域:Metabolic Enzyme/Protease
作用靶点:Fatty Acid Synthase (FASN)
In Vitro: C75 inhibits PC3 cell growht with an IC50 of 35 μM at 24 h. C75 (10-50 μM) also reduces the growth of LNCaP spheroids in a concentration-dependent manner with an IC50 of 50 μM. (-)-C75 inhibits FAS activity and has a cytotoxic effect on tumor cell lines, without affecting food consumption. (+)-C75 inhibits CPT1 and its administration produces anorexia, suggesting that central inhibition of CPT1 is essential for the anorectic effect of C75. The differential activity of C75 enantiomers may lead to the development of potential new specific drugs for cancer and obesity.
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. 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.
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文献和实验Abstract Table of Contents Materials Figures Literature Cited Abstract Members of the G
Nature 三连发:竞争消除,有你没我,论癌细胞的「霸道行为」
克隆如何发挥其与野生型肠道干细胞相比的竞争优势,并最终为靶向治疗结直肠癌奠定了基础。 图片来源: Nature主要研究内容 Apc 突变体具有明显的竞争优势 首先,研究人员建立了 WT 和 Apc−/−的共培养体系,他们发现,WT/WT 共培养物的相对贡献随着时间的推移基本保持不变;而 Apc−/−类器官在与 WT 类器官共培养物中迅速占主导地位。进一步的分析发现,这种现象不仅仅是由不同的 Apc−/−和 WT 的增殖比率造成的,而且与 Apc−/−细胞共培养时
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