Lapachol
(Synonyms: 拉帕醇) 目录号 : GC39123
A naphthoquinone with diverse biological activities
Cas No.:84-79-7
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
Lapachol is a naphthoquinone originally isolated from T. impetiginosa and has diverse biological activities.1,2,3,4,5 It is larvicidal against T. canis when used at a concentration of 2 mg/ml.1 Lapachol (10 and 100 ?M) inhibits topoisomerase I and topoisomerase II activities, as well as induces apoptosis and DNA damage in C6 rat glioma cells.2 It reduces B. atrox venom phospholipase A2 (PLA2) activity in a turbidimetric assay when used at a concentration of 10 ?g/ml.3 Lapachol (3 and 10 mg/kg) reduces synovial leukocyte infiltration and joint destruction in a mouse model of collagen-induced arthritis.4 It also reduces carrageenan-induced paw edema and abscess formation in rats.5
1.Mata-Santos, T., Pinto, N.F., Mata-Santos, H.A., et al.Anthelmintic activity of lapachol, β-lapachone and its derivatives against Toxocara canis larvaeRev. Inst. Med. Trop. Sao Paulo57(3)197-204(2015) 2.Xu, H., Chen, Q., Wang, H., et al.Inhibitory effects of lapachol on rat C6 glioma in vitro and in vivo by targeting DNA topoisomerase I and topoisomerase IIJ. Exp. Clin. Cancer Res.35(1)178(2016) 3.Strauch, M.A., Tomaz, M.A., Monteiro-Machado, M., et al.Lapachol and synthetic derivatives: In vitro and in vivo activities against Bothrops snake venomsPLoS One14(1)(2019) 4.Peres, R.S., Santos, G.B., Cecilio, N.T., et al.Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritisArthritis Res. Ther.19(1)47(2017) 5.de Almeida, E.R., da Silva Filho, A.A., do Santos, E.R., et al.Antiinflammatory action of lapacholJ. Ethnopharmacol.29(2)239-241(1990)
| Cas No. | 84-79-7 | SDF | |
| 别名 | 拉帕醇 | ||
| Canonical SMILES | O=C(C(CC=C(C)C)=C1O)C2=CC=CC=C2C1=O | ||
| 分子式 | C15H14O3 | 分子量 | 242.27 |
| 溶解度 | DMSO: ≥ 100 mg/mL (412.76 mM) | 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 | 4.1276 mL | 20.6381 mL | 41.2763 mL |
| 5 mM | 0.8255 mL | 4.1276 mL | 8.2553 mL |
| 10 mM | 0.4128 mL | 2.0638 mL | 4.1276 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。
Lapachol and lapachone analogs: a journey of two decades of patent research(1997-2016)
Expert Opin Ther Pat 2017 Oct;27(10):1111-1121.PMID:28586252DOI:10.1080/13543776.2017.1339792.
Lapachol (1), β-lapachone (2) and α-lapachone (3) are three well-studied natural products isolated from Tabebuia impetiginosa having most interesting chemodiversity and demonstrating diverse biological effects. Areas covered: The current review summarizes the recent and past discovery of chemotherapeutic agents based on the compounds 1-3. This review presents an overview of patents filed over the past two decades (1997 to 2016) mostly relating to the anticancer effects of these Lapachol and lapachone analogues. Expert opinion: The large number of interesting patents published on the therapeutic potential of quinones 1-3 and their synthetic derivatives lends credence to the importance of these molecules. Moreover, these quinones demonstrated potent anticancer effects towards various cancer cell lines and chemical modification of these quinones have led to products displaying enhanced anticancer effects. It is noteworthy that the majority of patents published are on the anticancer effects of quinones 1-3 and their synthetic derivatives along with a limited number of additional biological effects. It is our opinion that in order to get lead compounds, there needs to be a greater focus on the elucidation of the precise mechanism of action of these compounds including SAR and in vivo studies.
Lapachol acetylglycosylation enhances its cytotoxic and pro-apoptotic activities in HL60 cells
Toxicol In Vitro 2020 Jun;65:104772.PMID:31935485DOI:10.1016/j.tiv.2020.104772.
Lapachol is a plant-derived naphthoquinone that kills several types of cancer cells. Derivatives of this molecule may therefore prove to be useful chemotherapeutic agents. In this study, we explored whether glycosylation increases the cytotoxic potency of Lapachol towards HL-60 human leukemia cells. Two beta-glycosides were synthesized and characterized: LA4A (lapachol-β-glucoside) and LA4C (lapachol-N-acetylglucosamine-β-glucoside). The sugar moieties of both novel molecules were per-acetylated to facilitate cellular uptake. The IC50 values (in μM) for LA4A (5.7) and LA4C (5.3) were lower than those for Lapachol (25). LA4A and LA4C triggered typical signs of apoptosis, such as the exposure of phosphatidylserine on the outside of cells, chromatin condensation, DNA fragmentation and a decrease of the mitochondrial transmembrane potential (ΔΨm) prior to cell lysis. Moreover, DNA fragmentation triggered by the lapachol-glycosides was reduced by pre-treatment with the caspase inhibitor, z-VAD-fmk. While LA4A and LA4C activated caspases-3, -8 and -9, Lapachol failed to activate these apoptotic proteases, even when used at high concentrations. Finally, the toxicity of Lapachol and its derivatives was also tested on non-tumor cells. We used human peripheral neurons (PeriTox test) to evaluate the side effect potential of these compounds. LA4C was clearly less toxic than LA4A. We conclude that LA4C had the most favorable profile as drug candidate (high tumor cell toxicity, reduced neurotoxicity). In general, this study shows that the cytotoxicity of Lapachol towards HL-60 can be enhanced by glycosylation, and that the therapeutic ratio may be modified by the type of sugar added.
Novel Ru(II)-bipyridine/phenanthroline-lapachol complexes as potential anti-cancer agents
J Inorg Biochem 2022 Dec;237:112005.PMID:36155170DOI:10.1016/j.jinorgbio.2022.112005.
For the first time, we herein report on the syntheses of two new Ru(II)/bipyridine/phenanthroline complexes containing Lapachol as ligand: complex (1), [Ru (bipy)2(Lap)]PF6 and complex (2), [Ru(Lap)(phen)2]PF6, where bipy = 2,2'-bipyridine and ph en = 1,10-phenanthroline; Lap = Lapachol (2-hydroxy-3-(3-methylbut-2-en-1- yl)naphthalene-1,4-dione). The complexes were synthesized and characterized by elemental analyses, molar conductivity, mass spectrometry, ultraviolet-visible and infrared spectroscopies, nuclear magnetic resonance (1H, 13C), and single crystal X-ray diffraction, for complex (2). In addition, in vitro cytotoxicity was tested against six cancer cells: A549 (lung carcinoma); DU-145 (human prostate carcinoma); HepG2 (human hepatocellular carcinoma), PC-3 (human prostate adenocarcinoma); MDA-MB-231 (human breast adenocarcinoma); Caco-2 (human colorectal adenocarcinoma), and against two non-cancer cells, FGH (human gingival normal fibroblasts) and PNT-2 (prostate epithelial cells). Complex (1) was slightly more toxic and selective than complex (2) for all cell lines, except against the A549 cells, where (2) was more potent than complex (1). The complexes induced an increase in the reactive oxygen species, and the co-treatment with N-acetyl-L-cysteine remarkably suppressed the ROS generation and prevented the reduction of cell viability, suggesting that the cytotoxicity of the complexes is related to the ROS-mediated pathway. Further studies indicated that the complexes may bind to DNA via minor groove interaction. Our studies also revealed that free Lap induces gene mutations in Salmonella Typhimurium, nevertheless, the complexes demonstrated the absence of genotoxicity by the Ames test. The present study provides a relevant contribution to understanding the anti-cancer potential and genetic toxicological events of new ruthenium complexes containing the Lapachol molecule as a ligand.
Lapachol-Induced Upregulation of Sirt1/Sirt3 is linked with Improved Skin Wound Healing in Alloxan-induced Diabetic Mice
Iran J Pharm Res 2021 Summer;20(3):419-430.PMID:34903998DOI:10.22037/ijpr.2021.112722.13914.
Timely repair of damaged skin is very important to maintain the integrity and homeostasis of skin, but the wound healing process is compromised in diabetic patients due to several extrinsic and intrinsic factors thus lead to leg amputation and death eventually. Sirtuins, a family of seven conserved proteins are known to be associated with pathophysiological processes of the skin. The most important among them are sirt1and sirt3 involved in cell regeneration and cell survival. Naphthoquinone derivatives have a wide range of therapeutic properties, but the potential diabetic wound healing activity of Lapachol has not been identified yet. The present study thus aimed to investigate the wound healing effects of Lapachol in a diabetic mouse model. Diabetic wounded mice were divided into 3 groups; vehicle, Lapachol 0.05%, and Lapachol 0.1%. Skin samples collected from diabetic wounded mice on different time points after treatment for 10 consecutive days were subjected to downstream analysis by western blot, ELISA and histology. Lapachol treatment was found to enhance the expression of sirt1/sirt3 and other proteins involved in cell migration and blood vessel formation. The tissue development rate was increased by Lapachol treatment with better collagen deposition. Interestingly, Lapachol treatment also gave rise to a high concentration of growth factors resulting in speedy and timely recovery of injured skin. In summary, our findings suggest that Lapachol promotes efficient wound healing in a diabetic mouse model by increasing the expression of sirt1 and sirt3 and other proteins related to wound repair and skin regeneration including α-PAK, RAC1/CDC42, VEGF and growth factors viz PDGF and VEGF. This research work finds a novel potential activator of sirtuins in the form of Lapachol and depicts the role of activated sirtuins in diabetic wound healing.
Effect of Lapachol on the Inhibition of Matrix Metalloproteinase Related to the Invasion of Human Fibrosarcoma Cells
Curr Mol Pharmacol 2021 Oct 25;14(4):620-626.PMID:33019942DOI:10.2174/1874467213666201005122230.
Background: Anti-cancer effect of Lapachol contained in Tabebuia avellandae has been poorly understood until now. Objective: The aim of this study was to investigate the inhibitory effect of Lapachol on MMPs related to cell invasion. Its action mechanism was elucidated by analyzing the activity and the expression of MMPs and the proteins involved in the signaling pathway of cell invasion. Methods: The cytotoxicity of Lapachol was evaluated by MTT assay in HT1080 cells. The effects of Lapachol on the expression and the activation of MMPs were analyzed by western blot, immunofluorescence staining, and gelatin zymography assays. Their gene expression was analyzed by RT-PCR, and metastasis was evaluated by cell invasion assay. Results: Lapachol below 2 μM showed no cytotoxicity. It was observed that Lapachol above 0.5 μM inhibited the activation of MMP-2 and MMP-9 stimulated by PMA. In particular, the protein and gene expression levels of MMP-2 stimulated by PMA were remarkably decreased in the presence of Lapachol at 1 μM compared with the PMA treatment group. In addition, Lapachol increased the expression level of TIMP-1 compared with the PMA treatment group. Moreover, Lapachol decreased the expression level of p-p38 among MAPKs compared with the PMA treatment group. It was also found that the expression level of p65, a part of NF-kB, in nuclei was reduced in the presence of Lapachol above 0.5 μM compared with the PMA treatment group. In addition, Lapachol inhibited the invasion of human fibrosarcoma cells stimulated with VEGF. Conclusion: Above results suggest that Lapachol could play an important role in the modulation of MMPs related to cell invasion via the increase in TIMP-1 expression as well as the inactivation of p38 through NF-kB transcription factor.