Alkannin
(Synonyms: 左旋紫草素) 目录号 : GC35288
A naphthoquinone with diverse biological activities
Cas No.:517-88-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Alkannin is a naphthoquinone and enantiomer of shikonin that has been found in A. tinctoria and has diverse biological activities.1,2,3,4,5 It inhibits tumor-specific pyruvate kinase M2 (PKM2; IC50 = 0.3 μM) with 20- and 10-fold selectivity over PKM1 and pyruvate kinase L (PKL), respectively.1 Alkannin inhibits proliferation of HCT116 and SW480 colorectal cancer cells with IC50 values of 2.38 and 4.53 μM, respectively.2 It halts the cell cycle at the G1 phase and induces apoptosis in HCT116 cells when used at a concentration of 3 μM. Alkannin (1 μM) increases levels of Hsp70 in untreated and UVB-irradiated HaCaT cells as well as inhibits UVB-induced DNA fragmentation and caspase-3 activity in HaCaT cells.3 It is active against methicillin-sensitive and -resistant S. aureus (MICs = 6.25 μg/ml) as well as vancomycin-sensitive and -resistant E. faecalis (MICs = 50 and 25 μg/ml, respectively).4 Alkannin scavenges 2,2-diphenyl-1-picrylhydrazyl radicals in a cell-free assay (EC50 = 22 ppm).5
1.Chen, J., Xie, J., Jiang, Z., et al.Shikonin and its analogs inhibit cancer cell glycolysis by targeting tumor pyruvate kinase-M2Oncogene30(42)4297-4306(2011) 2.Huu Tung, N., Du, G.-J., Wang, C.-Z., et al.Naphthoquinone components from Alkanna tinctoria (L.) Tausch show significant antiproliferative effects on human colorectal cancer cellsPhytother. Res.27(1)66-70(2013) 3.Yoshihisa, Y., Hassan, M.A., Furusawa, Y., et al.Alkannin, HSP70 inducer, protects against UVB-induced apoptosis in human keratinocytesPLoS One7(10)e47903(2012) 4.Shen, C.-C., Syu, W.-J., Li, S.-Y., et al.Antimicrobial activities of naphthazarins from Arnebia euchromaJ. Nat. Prod.65(12)1857-1862(2002) 5.Assimopoulou, A.N., and Papageorgiou, V.P.Radical scavenging activity of Alkanna tinctoria root extracts and their main constituents, hydroxynaphthoquinonesPhytother. Res.19(2)141-147(2005)
| Cas No. | 517-88-4 | SDF | |
| 别名 | 左旋紫草素 | ||
| Canonical SMILES | OC1=C2C(C(C=C([C@H](C/C=C(C)/C)O)C2=O)=O)=C(O)C=C1 | ||
| 分子式 | C16H16O5 | 分子量 | 288.3 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 10 mg/ml,DMSO:PBS (pH 7.2) (1:1): 0.5 mg/ml,Ethanol: 5 mg/ml | 储存条件 | -20°C, protect from light |
| 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 | 3.4686 mL | 17.343 mL | 34.6861 mL |
| 5 mM | 0.6937 mL | 3.4686 mL | 6.9372 mL |
| 10 mM | 0.3469 mL | 1.7343 mL | 3.4686 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。
Pharmacological and analytical aspects of Alkannin/shikonin and their derivatives: An update from 2008 to 2022
Chin Herb Med 2022 Sep 20;14(4):511-527.PMID:36405061DOI:10.1016/j.chmed.2022.08.001.
Alkannin/shikonin (A/S) and their derivatives are naturally occurring naphthoquinones majorly found in Boraginaceae family plants. They are integral constituents of traditional Chinese medicine Zicao (roots of Lithospermum erythrorhizon). In last two decades significant increase in pharmacological investigations on Alkannin/shikonin and their derivatives has been reported that resulted in discovery of their novel mechanisms in various diseases and disorders. This review throws light on recently conducted pharmacological investigations on Alkannin/shikonin and their derivatives and their outputs. Various analytical aspects are also discussed and brief summary of patent applications on inventions containing Alkannin/shikonin and its derivatives is also provided.
Alkannin Inhibits the Development of Ovarian Cancer by Affecting miR-4461
Evid Based Complement Alternat Med 2021 Nov 28;2021:5083302.PMID:34876915DOI:10.1155/2021/5083302.
Background: Previous studies have shown that Alkannin has anticancer, anti-inflammatory, and antibacterial effects. However, the effect of Alkannin in the development of ovarian cancer (OC) remains unknown. Therefore, this study aims to elucidate the function of Alkannin in OC progression. Methods: RT-qPCR and western blot analysis were used to measure mRNA and protein expression. Cell viability and metastasis were detected by the CCK-8 assay, flow cytometry analysis, and transwell assay. Results: Alkannin had no cytotoxicity toward normal ovarian cells, but Alkannin can inhibit cell proliferation and induce apoptosis in OC cells. In addition, Alkannin inhibited cell migration and invasion and blocked EMT in OC. Besides, upregulation of miR-4461 was found in OC tissues and cells, which was regulated by Alkannin. More importantly, miR-4461 can inverse the effects of Alkannin on cell viability and metastasis in OC cells. Conclusion: Alkannin restrains cell viability, metastasis, and EMT in OC by downregulating miR-4461 expression.
Alkannin attenuates amyloid β aggregation and Alzheimer's disease pathology
Mol Pharmacol 2023 Mar 3;MOLPHARM-AR-2021-000468.PMID:36868792DOI:10.1124/molpharm.121.000468.
Alzheimer's disease (AD) is a neurodegenerative disease that is accompanied by memory decline and cognitive dysfunction. Aggregated amyloid β formation and accumulation may be one of the underlying mechanisms of the pathophysiology of AD. Therefore, compounds that can inhibit amyloid β aggregation may be useful for treatment. Based on this hypothesis, we screened plant compounds used in Kampo medicine for chemical chaperone activity and identified that Alkannin had this property. Further analysis indicated that Alkannin could inhibit amyloid β aggregation. Importantly, we also found that Alkannin inhibited amyloid β aggregation after aggregates had already formed. Through the analysis of circular dichroism spectra, Alkannin was found to inhibit β-sheet structure formation, which is an aggregation-prone toxic structure. Furthermore, Alkannin attenuated amyloid β-induced neuronal cell death in PC12 cells, ameliorated amyloid β aggregation in the AD model of Caenorhabditis elegans (C. elegans), and inhibited chemotaxis observed in AD C. elegans, suggesting that Alkannin could potentially inhibit neurodegeneration in vivo Overall, these results suggest that Alkannin may have novel pharmacological properties for inhibiting amyloid β aggregation and neuronal cell death in AD. Significance Statement Aggregated amyloid β formation and accumulation is one of the underlying mechanisms of the pathophysiology of Alzheimer's disease. We found that Alkannin had chemical chaperone activity, which can inhibit β-sheet structure formation of amyloid β and its aggregation, neuronal cell death, and Alzheimer's disease phenotype in C. elegans. Overall, Alkannin may have novel pharmacological properties for inhibiting amyloid β aggregation and neuronal cell death in Alzheimer's disease.
Advance in Anti-tumor Mechanisms of Shikonin, Alkannin and their Derivatives
Mini Rev Med Chem 2018;18(2):164-172.PMID:28245783DOI:10.2174/1389557517666170228114809.
Shikonin, Alkannin and their derivatives, the main ingredient of Lithospermum erythrorhizon and Arnebia euchroma (Royle) Johnst native to Inner Mongolian and Northwest of China respectively, hold promising potentials for antitumor effects via multiple-target mechanisms. This review will emphasize the importance of their antitumor activity in apoptosis, necroptosis and immunogenic cell death, and expound the relationship of their antitumor activity and naphthoquinone scaffold that could generate ROS and alkylating agent. Meanwhile, the antitumor mechanisms of naturally-occurring shikonin, Alkannin and their derivatives, which were divided into the direct interaction involved in alkylating agent, covalently binding the DNA and protein, as well as the indirect interaction mediated by ROS, nonspecifically influencing the mitochondria or multiple signal pathways, will be systematically summarized and discussed.
Alkannin-Induced Oxidative DNA Damage Synergizes With PARP Inhibition to Cause Cancer-Specific Cytotoxicity
Front Pharmacol 2020 Dec 22;11:610205.PMID:33519476DOI:10.3389/fphar.2020.610205.
Background: Oncogenic transformation is associated with elevated oxidative stress that promotes tumor progression but also renders cancer cells vulnerable to further oxidative insult. Agents that stimulate ROS generation or suppress antioxidant systems can drive oxidative pressure to toxic levels selectively in tumor cells, resulting in oxidative DNA damage to endanger cancer cell survival. However, DNA damage response signaling protects cancer cells by activating DNA repair and genome maintenance mechanisms. In this study, we investigated the synergistic effects of combining the pro-oxidative natural naphthoquinone Alkannin with inhibition of DNA repair by PARP inhibitors. Methods and Results: The results showed that sublethal doses of Alkannin induced ROS elevation and oxidative DNA damage in colorectal cancer but not normal colon epithelial cells. Blocking DNA repair with the PARP inhibitor olaparib markedly synergized with Alkannin to yield synergistic cytotoxicity in colorectal cancer cells at nontoxic doses of both drugs. Synergy between Alkannin and olaparib resulted from interrupted repair of alkannin-induced oxidative DNA damage and PARP-trapping, as it was significantly attenuated by NAC or by OGG1 inhibition and the non-trapping PARP inhibitor veliparib did not yield synergism. Mechanistically, the combination of Alkannin and olaparib caused intense replication stress and DNA strand breaks in colorectal cancer cells, leading to apoptotic cancer cell death after G2 arrest. Consequently, coadministration of Alkannin and olaparib induced significant regression of tumor xenografts in vivo, while each agent alone had no effect. Conclusion: These studies clearly show that combining Alkannin and olaparib can result in synergistic cancer cell lethality at nontoxic doses of the drugs. The combination exploits a cancer vulnerability driven by the intrinsic oxidative pressure in most cancer cells and hence provides a promising strategy to develop broad-spectrum anticancer therapeutics.