NECA

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

NECA 是腺苷受体激动剂，可增加荧光素和低分子量右旋糖酐的脑外渗，与血脑屏障调节无关。

NECA is an agonist of Adenosine receptor increases cerebral extravasation of fluorescein and low molecular weight dextran independent of blood-brain barrier modulation.

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After the administration of 5'-N-Ethylcarboxamidoadenosine (NECA), the mean number of cocaine infusions obtained per session is decreased significantly in a dose-dependent manner [5'-N-Ethylcarboxamidoadenosine (NECA): F(4,12)=14.9; P<0.001]. The administration of 5'-N-Ethylcarboxamidoadenosine (NECA) [F(4,12)=16.1; P<0.001] results in a significant increase in latencies above values obtained for vehicle treatment. Daily i.p. injection of 5'-N-Ethylcarboxamidoadenosine (NECA) at 0.3 mg/kg/day for two weeks reduces malondialdehyde (MDA) levels in diabetic rats, but does not affect control rats. Daily treatment with NECA (0.3 mg/kg/day, i.p. for two weeks) reduces diabetes-induced gene expression of tumor necrosis factor (TNF)-α and interleukin (IL)-18 in diabetic rats, but does not affect control rats. Daily i.p. injection of 5'-N-Ethylcarboxamidoadenosine (NECA) at 0.3 mg/kg/day for two weeks also blocks the activation of JNK MAPK in diabetic rats, but does not affect control rats.

5'-N-Ethylcarboxamidoadenosine

Endocrinology/Hormones

AChR

Adenosine receptor

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35920-39-9

308.29

C12H16N6O4

>98% (HPLC)

DMSO:150 mg/mL (486.55 mM)

CCNC(=O)[C@H]1O[C@H]([C@H](O)[C@@H]1O)n1cnc2c(N)ncnc12

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(-20℃)

With Ice Pack

≥ 2 years