Harmine hydrochloride
(Synonyms: 哈尔碱盐酸盐(水合),Telepathine hydrochloride) 目录号 : GC38413
A unique regulator of PPARγ expression
Cas No.:343-27-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Peroxisome proliferator-
1.Hauner, H.The mode of action of thiazolidinedionesDiabetes Metab. Res. Rev.18(Suppl. 2)S10-S15(2002) 2.Waki, H., Park, K.W., Mitro, N., et al.The small molecule harmine is an antidiabetic cell-type-specific regulator of PPARγ expressionCell Metab.5(5)357-370(2007)
| Cas No. | 343-27-1 | SDF | |
| 别名 | 哈尔碱盐酸盐(水合),Telepathine hydrochloride | ||
| Canonical SMILES | CC1=NC=CC2=C1NC3=C2C=CC(OC)=C3.Cl | ||
| 分子式 | C13H13ClN2O | 分子量 | 248.71 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.0207 mL | 20.1037 mL | 40.2075 mL |
| 5 mM | 0.8041 mL | 4.0207 mL | 8.0415 mL |
| 10 mM | 0.4021 mL | 2.0104 mL | 4.0207 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Harmine hydrochloride Triggers G2/M Cell Cycle Arrest and Apoptosis in HCT116 Cells through ERK and PI3K/AKT/mTOR Signaling Pathways
Prev Nutr Food Sci 2021 Dec 31;26(4):445-452.PMID:35047441DOI:10.3746/pnf.2021.26.4.445.
Colorectal carcinoma (CRC) is one of the most common and aggressive malignant carcinomas. There is a pressing need to develop naturally derived novel drugs with minimal side effects for treatment of CRC. In this study, we aimed to investigate the anticancer effects of Harmine hydrochloride (HMH), a hydrophilic and stable substance that is easily absorbed by tissues and similar to harmine, and the underlying mechanism of action in human CRC HCT116 cells. HMH inhibited the growth, colony formation, and migration ability of HCT116 cells. Additionally, HMH induced G2 cell cycle arrest by reducing expression of p-cdc2, cdc2, and cyclin B1, proteins that regulate the G2/M phase, and expression of Rb, a protein that regulates cell proliferation, in a dose-dependent manner. HMH mediated apoptosis by downregulating expression of apoptotic proteins (such as caspase-3, caspase-9, and PARP) and the anti-apoptotic protein Bcl-2 and by inducing expression of Bax, a pro-apoptotic protein. Furthermore, HMH reduced the levels of p-ERK, p-PI3K, p-AKT, and p-mTOR in HCT116 cells, and significantly inhibited p-ERK and p-AKT expression in cells treated with of HMH and PD98059, an ERK inhibitor, or LY294002, an AKT inhibitor (P<0.05 and P<0.01). These results demonstrate the inhibi-tory effect of HMH on cell proliferation and migration through inducing apoptosis by inhibiting ERK and PI3K/AKT/mTOR signaling pathways, indicating its potential therapeutic applications in CRC.
Harmine hydrochloride Mediates the Induction of G2/M Cell Cycle Arrest in Breast Cancer Cells by Regulating the MAPKs and AKT/FOXO3a Signaling Pathways
Molecules 2021 Nov 5;26(21):6714.PMID:34771123DOI:10.3390/molecules26216714.
Breast cancer (BC) is one of the most common causes of death among women worldwide. Recently, interest in novel approaches for BC has increased by developing new drugs derived from natural products with reduced side effects. This study aimed to treat BC cells with Harmine hydrochloride (HMH) to identify its anticancer effects and mechanisms. HMH treatment suppressed cell growth, migration, invasion, and colony formation in MCF-7 and MDA-MB-231 cells, regardless of the hormone signaling. It also reduced the phosphorylation of PI3K, AKT, and mTOR and increased FOXO3a expression. Additionally, HMH treatment increased p38 phosphorylation in MCF-7 cells and activated c-Jun N-terminal kinase (JNK) phosphorylation in MDA-MB-231 cells in a dose-dependent manner, where activated p38 and JNK increased FOXO3a expression. Activated FOXO3a increased the expression of p53, p21, and their downstream proteins, including p-cdc25, p-cdc2, and cyclin B1, to induce G2/M cell cycle arrest. Furthermore, HMH inhibited the PI3K/AKT/mTOR pathway by significantly reducing p-AKT expression in combination with LY294002, an AKT inhibitor. These results indicate that mitogen-activated protein kinases (MAPKs) and AKT/FOXO3a signaling pathways mediate the induction of cell cycle arrest following HMH treatment. Therefore, HMH could be a potential active compound for anticancer bioactivity in BC cells.
Experimental study of antiparkinsonian action of the Harmine hydrochloride original compound
Pharmacol Rep 2019 Dec;71(6):1050-1058.PMID:31605892DOI:10.1016/j.pharep.2019.06.002.
Background: The effects of chemical products on the nervous system have been studied by various scientists. In this work, the antiparkinsonian action of a water-soluble form of Harmine hydrochloride was studied. The present studies aim to research antiparkinsonian action of the Harmine hydrochloride original compound. Methods: To achieve the objective of the study, the authors used haloperidol-induced catalepsy and a method of Parkinson's syndrome (PS) induced by the MPTP (the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) neurotoxin. The experiments were performed on rats and mice which were divided into groups of 10 animals. Results: It was established that Harmine hydrochloride (HH), at a certain dose, eliminated haloperidol-induced catalepsy in rats and reduced oligokinesia and rigidity in the parkinsonism test in mice. Seven days after the experiment, the authors found the presence of rigidity in animals which had received the neurotoxin. It manifested itself in a shortened stride length compared to this parameter in intact controls. Conclusions: During the study the efficacy of Harmine hydrochloride was equivalent to the effects of levodopa at a certain dose, which suggested that Harmine hydrochloride compensated dopamine deficiency in the brain.
The impact of Harmine hydrochloride on growth, apoptosis and migration, invasion of gastric cancer cells
Pathol Res Pract 2020 Aug;216(8):152995.PMID:32402536DOI:10.1016/j.prp.2020.152995.
It has been reported that Harmine hydrochloride (HH) has an inhibitory effect on tumor cells, but the effect and mechanism of HH on gastric cancer cells remains unclear. The aim of this study was to investigate the effect and mechanism of HH on human gastric cancer cell line. In present study, results showed that HH could inhibit AGS, SGC7901 and HGC-27 cells in a time-dose-dependent manner (P < 0.01). Furthermore, this study demonstrated that more cells were arrested in G0/G1 phase, and apoptosis rate of AGS cells was significantly increased after HH treatment (P < 0.01). In addition, the study results showed that the mRNA and proteins of CyclinE, CyclinD1, PCNA declined dramatically, while p27, p21 increased significantly (P < 0.01). The results in this research also showed that the mRNA and proteins of Survivin and Bcl-2 decreased, while the expression of Bax, caspase-3, Bad increased significantly (P < 0.01). Also, the results of this study showed that invasion and migration of AGS cells decreased significantly after HH treatment (P < 0.01), with the expression of MMP-2, HIF-1 α and PRDX1 decreasing on observation after HH treatment (P < 0.01). In conclusion, HH has the property to inhibit GC cells via regulating GC cells' proliferation, apoptosis, invasion and migration.
Harmine hydrochloride inhibits Akt phosphorylation and depletes the pool of cancer stem-like cells of glioblastoma
J Neurooncol 2013 Mar;112(1):39-48.PMID:23392846DOI:10.1007/s11060-012-1034-x.
Harmine hydrochloride (Har-hc), a derivative from Harmine which is a natural extractive from plants, has been considered for treatment of kinds of cancers and cerebral diseases. In this study, we found that Har-hc clearly decreased cell viability, induced apoptosis and inhibited Akt phosphorylation in glioblastoma cell lines. Moreover, Har-hc had the ability to inhibit self-renewal and promote differentiation of glioblastoma stem like cells (GSLCs) accompanied by inhibition of Akt phosphorylation. Especially, we demonstrated that Har-hc inhibited neurosphere formation of human primary GSLCs. In vivo test also confirmed Har-hc decreased the tumorigenicity of GSLCs. Thus we conclude that Har-hc has potent anti-cancer effects in glioblastoma cells, which is at least partially via inhibition of Akt phosphorylation. Administration of Har-hc may act as a new approach to glioblastoma treatment.