Harmalol
(Synonyms: 去甲骆驼蓬碱,骆驼蓬酚) 目录号 : GC49841
An Analytical Reference Standard
Cas No.:525-57-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Harmalol is an analytical reference standard categorized as a β-carboline alkaloid.1 Harmalol is an active metabolite of harmaline .2 It is a minor component of ayahuasca, a botanical mixture that has hallucinogenic properties.3 This product is intended for research and forensic applications.
1.Tarpley, M., Oladapo, H.O., Strepay, D., et al.Identification of harmine and β-carboline analogs from a high-throughput screen of an approved drug collection; profiling as differential inhibitors of DYRK1A and monoamine oxidase A and for in vitro and in vivo anti-cancer studiesEur. J. Pharm. Sci.162105821(2021) 2.Brierley, D.I., and Davidson, C.Developments in harmine pharmacology - implications for ayahuasca use and drug-dependence treatmentProg. Neuropsychopharmacol. Biol. Psychiatry39(2)263-272(2012) 3.Navickiene, S., Santos, L.F.S., Santos, M.C., et al.Use of coconut charcoal and menthone-thiosemicarbazone polymer as solid phase materials for the determination of N,N-dimethyltryptamine, harmine, harmaline, harmalol, and tetrahydroharmine in Ayahuasca beverage by liquid chromatography-tandem mass spectrometryJ. Braz. Chem. Soc.30(1)180-187(2019)
| Cas No. | 525-57-5 | SDF | Download SDF |
| 别名 | 去甲骆驼蓬碱,骆驼蓬酚 | ||
| Canonical SMILES | OC1=CC=C2C(NC3=C2CCN=C3C)=C1 | ||
| 分子式 | C12H12N2O | 分子量 | 200.2 |
| 溶解度 | DMSO: Slightly soluble,PBS (pH 7.2): 3 mg/mL | 储存条件 | -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 | 4.995 mL | 24.975 mL | 49.95 mL |
| 5 mM | 0.999 mL | 4.995 mL | 9.99 mL |
| 10 mM | 0.4995 mL | 2.4975 mL | 4.995 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。
Therapeutic Role of Harmalol Targeting Nucleic Acids: Biophysical Perspective and in vitro Cytotoxicity
Mini Rev Med Chem 2018;18(19):1624-1639.PMID:29231137DOI:10.2174/1389557518666171211164830.
Background: Harmalol, a beta carboline alkaloid, shows remarkable importance in the contemporary biomedical research and drug discovery programs. With time, there is emerging interest in search for better anti-cancer drugs of plant origin with high activity and lower toxicity. Most of the chemotherapeutic agents due to their non-specific target and toxicity on active healthy cells, use is often restricted, necessitating search for newer drugs having greater potentiality. Objective: The review highlighted the interaction of Harmalol with nucleic acids of different motifs as sole target biomolecules and in vitro cytotoxicity of the alkaloid in human cancer cell lines with special emphasis on its apoptotic induction ability. Methods: Binding study and in vitro cytotoxicity was performed using several biophysical techniques and biochemical assays, respectively. Results: Data from competition dialysis, UV and fluorescence spectroscopic analysis, circular dichroism, viscometry and isothermal calorimetry shows binding and interaction of Harmalol with several natural and synthetic nucleic acids, both DNA and RNA, of different motifs. Furthermore, apoptotic hallmarks like internucleosomal DNA fragmentation, membrane blebbing, cell shrinkage, chromatin condensation, change of mitochondrial membrane potential, comet tail formation and ROS (reactive oxygen species) dependent cytotoxicity being analyzed in the Harmalol treated cancer cells. Conclusion: These results stating the therapeutic role of Harmalol, will lead to the interesting knowledge on the cytotoxicity, mode, mechanism, specificity of binding and correlation between structural aspects and energetics enabling a complete set of guidelines for design of new drugs.
Harmaline and Harmalol inhibit the carcinogen-activating enzyme CYP1A1 via transcriptional and posttranslational mechanisms
Food Chem Toxicol 2012 Feb;50(2):353-62.PMID:22037238DOI:10.1016/j.fct.2011.10.052.
Dioxins are known to cause several human cancers through activation of the aryl hydrocarbon receptor (AhR). Harmaline and Harmalol are dihydro-β-carboline compounds present in several medicinal plants such as Peganum harmala. We have previously demonstrated the ability of P. harmala extract to inhibit TCDD-mediated induction of Cyp1a1 in murine hepatoma Hepa 1c1c7 cells. Therefore, the aim of this study is to examine the effect of harmaline and its main metabolite, Harmalol, on dioxin-mediated induction of CYP1A1 in human hepatoma HepG2 cells. Our results showed that harmaline and Harmalol at concentrations of (0.5-12.5μM) significantly inhibited the dioxin-induced CYP1A1 at mRNA, protein and activity levels in a concentration-dependent manner. The role of AhR was determined by the inhibition of the TCDD-mediated induction of AhR-dependent luciferase activity and the AhR/ARNT/XRE formation by both harmaline and Harmalol. In addition, harmaline significantly displaced [(3)H]TCDD in the competitive ligand binding assay. At posttranslational level, both harmaline and Harmalol decreased the protein stability of CYP1A1, suggesting that posttranslational modifications are involved. Moreover, the posttranslational modifications of harmaline and Harmalol involve ubiquitin-proteasomal pathway and direct inhibitory effects of both compounds on CYP1A1 enzyme. These data suggest that harmaline and Harmalol are promising agents for preventing dioxin-mediated effects.
DNA binding and apoptotic induction ability of Harmalol in HepG2: Biophysical and biochemical approaches
Chem Biol Interact 2016 Oct 25;258:142-52.PMID:27590872DOI:10.1016/j.cbi.2016.08.024.
Harmalol administration caused remarkable reduction in proliferation of HepG2 cells with GI50 of 14.2 μM, without showing much cytotoxicity in embryonic liver cell line, WRL-68. Data from circular dichroism (CD) and differential scanning calorimetric (DSC) analysis of harmalol-CT DNA complex shows conformational changes with prominent CD perturbation and stabilization of CT DNA by 8 °C. Binding constant and stoichiometry was calculated using the above biophysical techniques. The Scatchard plot constructed from CD data showed cooperative binding, from which the cooperative binding affinity (K'ω) of 4.65 ± 0.7 × 10(5) M(-1), and n value of 4.16 were deduced. The binding parameter obtained from DSC melting data was in good agreement with the above CD data. Furthermore, dose dependent apoptotic induction ability of Harmalol was studied in HepG2 cells using different biochemical assays. Generation of ROS, DNA damage, changes in cellular external and ultramorphology, alteration of membrane, formation of comet tail, decreased mitochondrial membrane potential and a significant increase in Sub Go/G1 population made the cancer cell, HepG2, prone to apoptosis. Up regulation of p53 and caspase 3 further indicated the apoptotic role of Harmalol.
Beta-carboline alkaloids harmaline and Harmalol induce melanogenesis through p38 mitogen-activated protein kinase in B16F10 mouse melanoma cells
BMB Rep 2010 Dec;43(12):824-9.PMID:21189160DOI:10.5483/BMBRep.2010.43.12.824.
Melanin synthesis is regulated by melanocyte specific enzymes and related transcription factors. β-carboline alkaloids including harmaline and Harmalol are widely distributed in the environment including several plant families and alcoholic beverages. Presently, melanin content and tyrosinase activity were increased in melanoma cells by harmaline and Harmalol in concentration- and time-dependent manners. Increased protein levels of tyrosinase, tyrosinase-related protein-1 (TRP-1), and TRP-2 were also evident. In addition, immunofluorescence and Western blot analyses revealed harmaline and Harmalol increased cAMP response element binding protein phosphorylation and microphthalmia-associated transcription factor expression. In addition to studying the signaling that leads to melanogenesis, roles of the p38 MAPK pathways by the harmaline and Harmalol were investigated. Harmaline and Harmalol induced time-dependent phosphorylation of p38 MAPK. Harmaline and Harmalol stimulated melanin synthesis and tyrosinase activity, as well as expression of tyrosinase and TRP-1 and TRP-2 indicating that these harmaline and Harmalol induce melanogenesis through p38 MAPK signaling.
Glucuronidation of 3-O-methylnoradrenaline, Harmalol and some related compounds
Biochem J 1968 Nov;110(1):99-104.PMID:5722695DOI:10.1042/bj1100099.
1. The following compounds were glucuronidated in the presence of UDP-glucuronic acid and a microsomal preparation made from guinea-pig liver: (14)C-labelled 3-O-methyladrenaline, 3-O-methylnoradrenaline, 3-methoxytyramine and 4-hydroxy-3-methoxyphenethanol, as well as unlabelled Harmalol and harmol. 2. [(14)C]Homovanillic (4-hydroxy-3-methoxyphenylacetic) acid was not a substrate for the microsomal glucuronyltransferase. 3. The K(m) values for Harmalol and harmol were 0.69x10(-4)m and 0.50x10(-4)m respectively. 4. The K(m) values for UDP-glucuronic acid, in the presence of (14)C-labelled 3-O-methylnoradrenaline, Harmalol and harmol as aglycones, were 0.57x10(-4)m, 0.44x10(-4)m and 2.20x10(-4)m respectively. 5. Mg(2+) added at 2.5-10mm activated glucuronyltransferase, with Harmalol as substrate. Concentrations above 10mm inhibited the enzymic activity. 6. The overall, or net, transglucuronidating activity of microsomal preparations of the liver, with Harmalol as substrate, was greatest for guinea pig, and very much lower for rabbit, mouse and rat.