| CAS |
No.442-51-3 |
| 中文名称 |
去氢骆驼蓬碱(10mM in DMSO,无菌） |
| 英文名称 |
Harmine(10mM in DMSO，Sterile） |
| 分子式 |
C13H12N2O |
| 分子量 |
212.25 |
| 溶解性 |
请根据自己的实验要求使用。 |
| 外观(性状) |
无菌溶液 |
| 储存条件 |
Stroe at -20℃，6 months. |
| 靶点 |
5-HT Receptor;DYRK;MAO-A;PPARγ |
| 通路 |
Neuronal Signaling;GPCR & G Protein;Protein Tyrosine Kinase/RTK;;Cell Cycle;DNA Damage/DNA Repair |
| 背景说明 |
是一种具有抗癌和抗炎活性的双特异性酪氨酸磷酸化调节激酶 (DYRK) 抑制剂。对 5-HT2A 血清素受体具有高亲和力。通过抑制 Wnt 信号通路来调节 PPARγ 的表达。 还选择性地结合 MAO-A 并可逆地抑制MAO-A。 |
| 生物活性 |
Harmine is a natural dual-specificity tyrosine phosphorylation-regulated kinase (DYRK) inhibitor with anticancer and anti-inflammatory activities. Harmine has a high affinity of 5-HT2A serotonin receptor， with an Ki of 397 nM.[1-4] |
| In Vitro |
Harmine inhibits tau phosphorylation by DYRK1A by selected DANDYs， with an IC50 of 190 nM[2].Harmine negatively regulates homologous recombination (HR) by interfering Rad51 recruitment， resulting in severe cytotoxicity in hepatoma cells. Furthermore， NHEJ inhibitor Nu7441 markedly sensitizes Hep3B cells to the anti-proliferative effects of Harmine[3]. |
| In Vivo |
It is shown that brain water content is significantly increased in the TBI group. Treatment with Harmine significantly reduces the tissue water content at 1， 3 and 5 days， compared with the TBI group. Harmine treatment significantly reduces the escape latency at 3 and 5 days， compared with the TBI group. Post-TBI administration of Harmine significantly improves the motor function recovery of the rats at 1， 3 and 5 days following TBI， compared with the TBI group without Harmine treatment. The neuronal survival rate in the Harmine-treated group is significantly increased， compared with the TBI group. Administration of Harmine results in marked elevation in the expression of GLT-1， compared with the TBI group. The administration of Harmine significantly reduces the expression of caspase 3， compared with the TBI group[4]. |
| 动物实验 |
Rats[4]A total of 150 male Sprague-Dawley rats (age， 10-12 weeks; weighing， 280-320 g; are used in the present study. The rats are randomly divided into three groups: Sham-operated group (sham; n=15); the TBI group (TBI; n=35) and the TBI + Harmine-treated group (Harmine; n=35). Harmine is administered immediately following TBI (i.p， 30 mg/kg per day) for up to 5 days. The sham and TBI groups receive equal volumes of 0.9% saline solution (i.p.). The rats are grouped as follows for examination of behavioral recovery: Sham， n=3; TBI， n=7; and Harmine， n=7. Following TBI， the NSS is evaluated at 1， 3 and 5 days. Each rat is assessed by an observer who is blinded to the animal treatment[4]. |
| 数据来源文献 |
[1]. Glennon RA， et al. Binding of beta-carbolines and related agents at serotonin (5-HT(2) and 5-HT(1A))， dopamine (D(2)) and benzodiazepine receptors. Drug Alcohol Depend. 2000 Aug 1;60(2):121-32.
[2]. Neumann F， et al. DYRK1A inhibition and cognitive rescue in a Down syndrome mouse model are induced by new fluoro-DANDY derivatives. Sci Rep. 2018 Feb 12;8(1):2859.
[3]. Zhang L， et al. Harmine suppresses homologous recombination repair and inhibits proliferation of hepatoma cells. Cancer Biol Ther. 2015;16(11):1585-92.
[4]. Zhong Z， et al. Treatment with harmine ameliorates functional impairment and neuronal death following traumatic brain injury. Mol Med Rep. 2015 Dec;12(6):7985-91. |
| 规格 |
1ml |
| 单位 |
瓶 |
中文
英语
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