乙莫克舍 124083-20-1

乙莫克舍 124083-20-1 乙莫克舍 124083-20-1
产品名称：乙莫克舍 124083-20-1
产品编号：sl9518
中文别称 乙莫克舍
英文别称 Etomoxir
CAS 124083-20-1
熔点:32-34°C
沸点:405.0±25.0°C(Predicted)
密度:1.163
储存条件:Inertatmosphere,2Chemicalbook-8°C
溶解度:≥32.7mg/mLinDMSO;≥109.6mg/mLinEtOH;≥48.3mg/mLinH2Owithgentlewarming
包装 瓶
规格 10mg
生物活性
Etomoxir((R)-(+)-Etomoxir)是肉碱棕榈酰转移酶1a(CPT-1a)抑制剂，通过抑制CPT-1a可抑制脂肪酸氧化，并抑制人、大鼠和豚鼠中棕榈酸酯的氧化。靶点CPT-1a
体外研究
Etomoxyrbind不可逆地抑制CPT1活性的催化滴度，但也能预氧化酸氧化酶。乙氧基是由位于子宫线粒体膜的半软骨肉毒碱棕榈酰转移酶1（CPT1）的抑制剂产生的。Etomoxyr，在canactasperoximal体内增殖，增加生命生长的DNA合成。因此，在没有CPT1抑制剂的情况下，依托莫西可以被认为是PPARα激动剂。环氧.乙烷羧酸-肉毒碱多酰转移酶抑制剂抑制了Etomoxism，并已被用于治疗儿童早期的治疗剂所保护。急性依托莫司治疗是可逆的，部分活性的肉毒碱棕榈酰转移酶I。结果，脂肪酸输入线粒体和β氧化减少，从而使细胞内的脂肪酸模拟化学书籍和葡萄糖氧化无效。用乙氧基延长培养（24小时）对几种代谢酶的表达产生不同的影响.
体内研究
Etomoxir可抑制游离脂肪酸（FFA）氧化相关的关键酶EPT1。P53与Etomoxil抑制的Bax直接相互作用，进一步证实P53和Bax的直接作用，以及FAO介导的线粒体ROS生成和b/dbmice的溶解。每天用Etomoxir，一种特殊的PT抑制剂，以20mg/kg体重注射8天。Etomoxir治疗后的心脏CPT活性降低了44%。Lew用20mg/kg Etomoxis治疗8天，不改变血糖，这与药物喂养研究相比较。同样，Etomoxirfeeding不会影响一般的生长特征，如体重增加，也不会影响后肢肌肉量。然而，Etomo药物治疗组的心脏和肝脏质量都显著增加了11%。
biological activity

Etomoxir ((R) - (+) - Etomoxir) is an inhibitor of carnitine palmitoyltransferase 1a (CPT-1a), which can inhibit fatty acid oxidation and inhibit the oxidation of palmitic acid esters in humans, rats, and guinea pigs by inhibiting CPT-1a. Target CPT-1a

In vitro research

Etomoxyrbid irreversibly inhibits the catalytic titer of CPT1 activity, but can also pre oxidize acid oxidase. Ethoxy is produced by an inhibitor of semi chondroitine palmitoyltransferase 1 (CPT1) located on the mitochondrial membrane of the uterus. Etomoxyr proliferates in the body of acarasperoximal, increasing DNA synthesis for life growth. Therefore, in the ab.sence of CPT1 inhibitors, etomoxy can be considered PPAR α Excitants. Epoxy ethane carboxylate carnitine polyacyltransferase inhibitors inhibit Etomoxism and have been used as protective agents for early childhood treatment. Acute etoposide treatment is reversible, with partially active carnitine palmitoyltransferase I. As a result, fatty acids enter mitochondria and β Reduced oxidation leads to ineffective simulation of intracellular fatty acids and glucose oxidation. Prolonged cultivation with ethoxy (24 hours) has different effects on the expression of several metabolic enzymes

In vivo research

Etomoxir can inhibit the key enzyme EPT1 related to free fatty acid (FFA) oxidation. The direct interaction between P53 and Etomoxil inhibited Bax further confirms the direct interaction between P53 and Bax, as well as the mitochondrial ROS generation and b/dbmice dissolution mediated by FAO. Etomoxir, a special PT inhibitor, is administered daily at a dose of 20mg/kg body weight for 8 days. The cardiac CPT activity decreased by 44% after Etomoxir treatment. Lew treated with 20mg/kg Etoxicis for 8 days without changing blood sugar, compared to drug feeding studies. Similarly, Etomoxirfeeding does not affect general growth characteristics, such as weight gain, nor does it affect muscle mass in the hind limbs. However, the heart and liver mass in the Etomo drug treatment group significantly increased by 11%.
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