Licoricidin
(Synonyms: 甘草西定) 目录号 : GC36456
Licoricidin (LCD) 从甘草 Glycyrrhiza uralensis Fisch 中分离，具有抗癌活性。Licoricidin (LCD) 通过诱导周期停滞，诱导细胞凋亡 (apoptosis) 和自噬 (autophagy)，是一种对抗结直肠癌的潜在化学预防或化学治疗剂。Licoricidin (LCD) 通过抑制肿瘤血管生成和淋巴管生成以及肿瘤组织局部微环境的变化抑制肺转移。Licoricidin (LCD) 通过体外和体内 Akt 和 NF-κB 途径的失活，增强吉西他滨诱导的骨肉瘤 (OS) 细胞的细胞毒性。Licoricidin (LCD) 通过 ROS 清除阻断 UVA 诱导的光老化，限制 MMP-1 的活性，被认为是新的局部应用的抗衰老制剂中的活性成分。
Cas No.:30508-27-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
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Licoricidin (LCD) is isolated from Glycyrrhiza uralensis Fisch, possesses anti-cancer activities. Licoricidin (LCD) inhibit SW480 cells (IC50=7.2 μM) by inducing cycle arrest, apoptosis and autophagy, and is a potential chemopreventive or chemotherapeutic agent against colorectal cancer[1]. Licoricidin (LCD) inhibits Lung Metastasis by inhibition of tumor angiogenesis and lymphangiogenesis as well as changes in the local microenvironment of tumor tissues the anticarcinogenic effect[1]. Licoricidin enhanced gemcitabine-induced cytotoxicity in Osteosarcoma (OS) cells by inactivation of the Akt and NF-κB pathways in vitro and in vivo[3]. Licoricidin blocks UVA-induced photoaging via ROS scavenging, limits the activity of MMP-1, it can be considered as an active ingredient in new topically applied anti-ageing formulations[4].
Licoricidin (LCD) (0-20 μM; 24 hours) dose-dependently inhibits the viability of colon cancer cell lines with various pathological and genetic characters, namely SW480, HCT116, SW620 and LoVo cells, with IC50 values of 7.2, 5.4, 4.5 and 5.1 μM, respectively[1].Licoricidin (LCD) (0-20 μM; 0-12 hours) induces cell apoptosis was accompanied with the activation of caspase-3 by cleavage in a time- and dose-dependent manner[1].Licoricidin (LCD) (0-20 μM; 0-12 hours) induces autophagy of SW480 cells, increases the cleavage of LC3-I to LC3-II and the degradation of p62 in a time and dose dependent manner[1].Licoricidin (LCD) (0-5 μg/ml; 18 hours) inhibits cell migration, MMP-9 secretion, and VCAM expression in 4T1 cells[2]. Cell Viability Assay[1] Cell Line: SW480, HCT116, SW620 and LoVo cells
Licoricidin (LCD) (intraperitoneal injection; 5, 10, or 20 mg/kg; once daily; 15 days) significantly inhibited the growth of SW480 xenografts in nude mice with an inhibitory rate of 43.5%[1].Licoricidin (LCD) (intraperitoneal injection; 5, 10, or 20 mg/kg; once daily; 32 days) reduces pulmonary metastasis and the expression of CD45, CD31, HIF-1α, iNOS, COX-2, and VEGF-A in tumor tissues, additionally, decreases protein expression of VEGF-R2, VEGF-C, VEGF-R3, and LYVE-1 in tumor tissues of licoricidin-treated mice[2]. Animal Model: SW480 xenografted tumor growth in nude mice[1]
[1]. Ji S, et al. Licoricidin inhibits the growth of SW480 human colorectal adenocarcinoma cells in vitro and in vivo by inducing cycle arrest, apoptosis and autophagy. Toxicol Appl Pharmacol. 2017 Jul 1;326:25-33. [2]. Park SY, et al. Licoricidin, an Active Compound in the Hexane/Ethanol Extract of Glycyrrhiza uralensis, Inhibits Lung Metastasis of 4T1 Murine Mammary Carcinoma Cells. Int J Mol Sci. 2016 Jun 14;17(6). [3]. Wang Y, et al. Licoricidin enhances gemcitabine-induced cytotoxicity in osteosarcoma cells by suppressing the Akt and NF-κB signal pathways. Chem Biol Interact. 2018 Jun 25;290:44-51. [4]. Kim KJ, et al. Licoricidin, an isoflavonoid isolated from Glycyrrhiza uralensis Fisher, prevents UVA-induced photoaging of human dermal fibroblasts. Int J Cosmet Sci. 2017 Apr;39(2):133-140.
| Cas No. | 30508-27-1 | SDF | |
| 别名 | 甘草西定 | ||
| Canonical SMILES | COC1=C2C(OC[C@@H](C3=C(C(C/C=C(C)/C)=C(O)C=C3)O)C2)=CC(O)=C1C/C=C(C)/C | ||
| 分子式 | C26H32O5 | 分子量 | 424.53 |
| 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 | 2.3555 mL | 11.7777 mL | 23.5555 mL |
| 5 mM | 0.4711 mL | 2.3555 mL | 4.7111 mL |
| 10 mM | 0.2356 mL | 1.1778 mL | 2.3555 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 | ||||||||||
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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。
Licoricidin combats gastric cancer by targeting the ICMT/Ras pathway in vitro and in vivo
Front Pharmacol 2022 Oct 13;13:972825.PMID:36339587DOI:10.3389/fphar.2022.972825.
Licoricidin, a type of isoflavonoid, is extracted from the root of Glycyrrhiza glabra. It has been widely proven that Licoricidin possesses multiple biological activities, including anti-cancer effects and a powerful antimicrobial effect against Helicobacter pylori (H. pylori). However, the exact mechanism of Licoricidin against gastric cancer remains unclear. In this study, we comprehensively explored the effects of Licoricidin on MGC-803 gastric cancer cells in vitro and in vivo and further elucidated its mechanism of action. Our results revealed that Licoricidin exhibited multiple anti-gastric cancer activities, including suppressing proliferation, inducing apoptosis, arresting the cell cycle in G0/G1 phase, and inhibiting the migration and invasion abilities of MGC-803 gastric cancer cells. In addition to this, a total of 5861 proteins were identified by quantitative proteomics research strategy of TMT labeling, of which 19 differential proteins (two upregulated and 17 downregulated) were screened out. Combining bioinformatics analyses and the reported roles in cancer progression of the 19 proteins, we speculated that isoprenyl carboxyl methyltransferase (ICMT) was the most likely target of Licoricidin. Western blot assays and IHC assays subsequently proved that Licoricidin significantly downregulated the expression of ICMT, both in MGC-803 cells and in xenograft tumors. Moreover, Licoricidin effectively reduced the level of active Ras-GTP and blocked the phosphorylation of Raf and Erk, which may be involved in its anti-gastric cancer effects. In summary, we first demonstrated that Licoricidin exerted favorable anti-gastric cancer activities via the ICMT/Ras pathway, which suggests that Licoricidin, as a natural product, could be a novel candidate for the management of gastric cancer.
Licoricidin Abrogates T-Cell Activation by Modulating PTPN1 Activity and Attenuates Atopic Dermatitis In Vivo
J Invest Dermatol 2021 Oct;141(10):2490-2498.e6.PMID:33857487DOI:10.1016/j.jid.2021.02.759.
Licoricidin, the fifth-highest fraction among the isolated 48 molecules from Glycyrrhiza uralensis extracts, has been known as an anti-inflammatory bioactive molecule; however, few studies have shown its inhibitory effect on T-cell activation and atopic dermatitis (AD). This study examined the therapeutic potential of Licoricidin in AD by modulating T-cell activation with molecular mechanisms. Licoricidin attenuated the expression of IL-2 mRNA in stimulated T cells without cytotoxicity. Because tyrosine-protein phosphatase nonreceptor type 1 was predicted to interact physically with Licoricidin in T cells in silico analysis, the results of tyrosine-protein phosphatase nonreceptor type 1 activity assay and phosphorylation study predicted that Licoricidin might abrogate the activity of tyrosine-protein phosphatase nonreceptor type 1 during T-cell activation. Pretreatment with Licoricidin controlled the dephosphorylation of Lck on TCR-mediated stimulation. Moreover, Licoricidin alleviated the symptoms of dinitrochlorobenzene- and/or mite extract-induced AD, including ear thickness and serum IgE level. Microscopic analysis also showed the effects of Licoricidin on the thickness of the dermis and epidermis and infiltration of immune cells. Furthermore, mRNA levels of proinflammatory cytokines were attenuated in the ear lesions of licoricidin-treated AD mice. Therefore, Licoricidin has therapeutic potential for treating AD, and its underlying mechanism involves effective modulation of T-cell activation by controlling tyrosine-protein phosphatase nonreceptor type 1 to maintain Lck phosphorylation.
In vitro investigation of permeability and metabolism of Licoricidin
Life Sci 2019 Oct 1;234:116770.PMID:31421085DOI:10.1016/j.lfs.2019.116770.
Aim Licoricidin has multiple pharmacological activities. The present study was designed to investigate the permeability and pharmacokinetic behavior of Licoricidin using in vitro models. Material and methods: First, human liver microsomes and recombinant human supersomes were used to investigate the interactions between metabolic enzymes and Licoricidin. In addition, rat, minipig, rabbit, dog, monkey, and human liver microsomes were used to determine metabolic differences among species. The parallel artificial membrane permeability assay (PAMPA) was used to explore Licoricidin permeability behavior. Key findings: At 100 μM, Licoricidin strongly inhibited CYP2C9, CYP2C19, CYP3A4, UGT1A3, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT2B4, UGT2B7, UGT2B15, and UGT2B17. Licoricidin metabolism exhibited considerable differences among species; dog, pig, and rat liver microsomes showed higher metabolic capacity than the other species. Seven Licoricidin metabolites were identified by liquid chromatography-tandem mass spectrometry, and hydration and hydroxylation were the major metabolic pathways. The PAMPA permeability of Licoricidin was moderate at both pH 4.0 and 7.4. Significance: The present study will support further pharmacological or toxicological research on Licoricidin.
Licoricidin improves neurological dysfunction after traumatic brain injury in mice via regulating FoxO3/Wnt/β-catenin pathway
J Nat Med 2020 Sep;74(4):767-776.PMID:32656716DOI:10.1007/s11418-020-01434-5.
Traumatic brain injury (TBI) is a major cause of death and disability around the world with no effective treatments currently. The present study was aimed to investigate the neuroprotective effect of Licoricidin, one of the major components of licorice extract, on TBI mice and further explore the underlying mechanism. Male C57BL/6 mice were modeled by a modified weight-drop method to mimic TBI. All animals received treatment 30 min after TBI. The modified Neurological Severity Score (NSS) tests were performed at 2 h and 1-3 days after TBI. The brain edema was analyzed by dry-wet weight method. The malonaldehyde (MDA) levels and the activities of glutathione peroxidase (GSH-PX), superoxide dismutase (SOD) and catalase (CAT) were determined by Elisa. Apoptotic neurons were detected using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) immunofluorescence and the expression of apoptotic proteins were measured by western blot. Activation of the FoxO3/Wnt/β-catenin was evaluated by western blot. The results showed that treatment with Licoricidin could significantly decline the NSS scores and reduce the brain edema, hence promote the recovery of neurological function in TBI mice. It also elevated the phosphorylation of p66shc, brought down the levels of MDA, as well as antagonized the decrement in activities of GSH-PX, SOD and CAT induced by TBI. Moreover, Licoricidin decreased the TUNEL positive neurons, downregulated the expression of Cyt-C, cleaved-Caspase-3, cleaved-Caspase-9 and Bax and upregulated the Bcl-2, attenuated cellular apoptosis. Licoricidin decreased the expression of FoxO3 and increased the Wnt/β-catenin in TBI mice. In conclusion, Licoricidin exerted neuroprotective effect on TBI model and the effect was possibly due to its antioxidative effect and antiapoptotic effect via regulating the FoxO3/Wnt/β-catenin pathway. Licoricidin may be a candidate drug for TBI therapy.
Licoricidin enhances gemcitabine-induced cytotoxicity in osteosarcoma cells by suppressing the Akt and NF-κB signal pathways
Chem Biol Interact 2018 Jun 25;290:44-51.PMID:29782821DOI:10.1016/j.cbi.2018.05.007.
Osteosarcoma (OS) is the most common bone malignancy in children and adolescents. Combined treatments of anti-cancer drugs can remarkably improve chemotherapeutic outcomes. Gemcitabine and Licoricidin both have potential anti-tumor activity in several cancers. However, the combined therapeutic efficiency of gemcitabine and Licoricidin for OS has not been explored. Here, we found that Licoricidin or gemcitabine inhibited OS cell viability in a dose-dependent manner. Cotreatment with Licoricidin and gemcitabine enhanced gemcitabine-induced cytotoxicity in OS cells. Licoricidin suppressed activation of the Akt and nuclear factor-kappa B (NF-κB) pathways. Gemcitabine had no effect on Akt signal, but facilitated the activation of NF-κB signal in OS cells. Moreover, combined treatment of Licoricidin and gemcitabine markedly curbed the activation of Akt and NF-κB pathways in OS cells. Inhibition of the Akt and NF-κB pathways enhanced gemcitabine-induced cytotoxicity in OS cells. In vivo assay further manifested that Licoricidin enhanced gemcitabine-induced cytotoxicity in tumor xenograft models of OS via inactivation of the Akt and NF-κB pathways. In conclusion, Licoricidin enhanced gemcitabine-induced cytotoxicity in OS cells by inactivation of the Akt and NF-κB pathways in vitro and in vivo.