Licarin A
(Synonyms: 利卡灵A,(+)-Licarin A) 目录号 : GC60225
LicarinA((+)-LicarinA)，可从多种植物中分离得到，显着降低二硝基苯肼-人血清白蛋白(DNP-HSA)刺激的RBL-2H3细胞。具有抗过敏作用。LicarinA降低TNF-α和PGD2产生，和COX-2表达。
Cas No.:51020-86-1
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
Licarin A ((+)-Licarin A), a neolignan isolated from various plants, significantly and dose-dependently reduces TNF-α production (IC50=12.6±0.3 μM) in dinitrophenyl-human serum albumin (DNP-HSA)-stimulated RBL-2H3 cells. Anti-allergic effects. Licarin A reduces TNF-α and PGD2 production, and COX-2 expression[1]。
Licarin A is found in plants such as Aristolochia taliscana, Machilus thunbergii and Myristica fragrans, which are used as spices and in folk medicines for nervous and digestive disorders. Licarin A also exhibits anti-inflammatory effects[1]. Licarin A (5-20 μM) reduces TNF-α and prostaglandin D2 (PGD2) secretion via the inhibition of PKCα/βII and p38 MAPK pathways. Licarin A treatment tends to reduce phosphorylated PKCα/βII and p38 MAPK protein levels[1].
[1]. Takuya Matsui, et al. Licarin A Is a Candidate Compound for the Treatment of Immediate Hypersensitivity via Inhibition of Rat Mast Cell Line RBL-2H3 Cells. J Pharm Pharmacol. 2015 Dec;67(12):1723-32.
| Cas No. | 51020-86-1 | SDF | |
| 别名 | 利卡灵A,(+)-Licarin A | ||
| Canonical SMILES | OC1=CC=C([C@@H]2OC3=C(OC)C=C(/C=C/C)C=C3[C@H]2C)C=C1OC | ||
| 分子式 | C20H22O4 | 分子量 | 326.39 |
| 溶解度 | DMSO : ≥ 50 mg/mL (153.19 mM); H2O : < 0.1 mg/mL (insoluble) | 储存条件 | 4°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 | 3.0638 mL | 15.3191 mL | 30.6382 mL |
| 5 mM | 0.6128 mL | 3.0638 mL | 6.1276 mL |
| 10 mM | 0.3064 mL | 1.5319 mL | 3.0638 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。
Licarin A as a Novel Drug for Inflammatory Eye Diseases
J Ocul Pharmacol Ther 2021 Jun;37(5):290-300.PMID:33761287DOI:10.1089/jop.2020.0129.
Purpose: This study investigated the safety and therapeutic efficacy of Licarin A (LCA) in the treatment of intraocular inflammation. Methods:In vitro safety of LCA in retinal pigmented epithelial cells (ARPE-19) and human embryonic stem cell derived-retinal pigmented epithelial cells (hES-RPE) was evaluated using CellTiter-Blue® kit. The chorioallantoic membrane (CAM) assay was used to investigate LCA safety and antiangiogenic activity. In vivo safety of intravitreal LCA was accomplished by clinical examination (including assessment of intraocular pressure), electroretinography (ERG), and histopathology. Uveitis was induced in rats by subcutaneous and intravitreal injection of bacillus Calmette-Guérin (BCG) antigen of Mycobacterium bovis. Intraocular inflammation was graded by slit-lamp and fundus examination, ERG, and histopathology. Results: LCA was safe to cells and to the CAM at concentration below 12.0 μM. LCA significantly reduced the percentage of blood vessels in the CAM. Retinal safety and anti-inflammatory efficacy of intravitreal injection of LCA 6.0 μM were confirmed through clinical, functional, and histopathological evaluation. Significant reduction of inflammatory cytokines (tumor necrosis factor-α and interleukin-6) was also found, when compared to untreated animals. Conclusion: The results suggest that LCA is a potential new drug for the treatment of inflammatory eye disease.
Licarin A, a neolignan isolated from Nectandra oppositifolia Nees & Mart. (Lauraceae), exhibited moderate preclinical efficacy against Schistosoma mansoni infection
Phytother Res 2021 Sep;35(9):5154-5162.PMID:34089558DOI:10.1002/ptr.7184.
Schistosomiasis is a widespread human parasitic disease currently affecting over 200 million people, particularly in poor communities. Chemotherapy for schistosomiasis relies exclusively on praziquantel (PZQ). Previous studies have shown that Licarin A (LIC-A), a dihydrobenzofuran neolignan, exhibited in vitro antiparasitic activity against Schistosoma mansoni adult worms. This study aimed to investigate the potential of LIC-A, isolated as main metabolite from leaves of Nectandra oppositifolia Nees & Mart. (Lauraceae), as an antischistosomal agent orally active in schistosomiasis animal model. PZQ was used as a reference compound. As result, LIC-A showed, at a single dose of 400 mg/kg, to be able to partially cure infected mice (worm burden reductions of ~50%). Parasite eggs, that are responsible for a variety of pathologies and transmission of schistosomiasis, were also moderately inhibited by LIC-A (egg burden reductions of ~50%-60%). Furthermore, it was observed that LIC-A achieved a slight reduction of hepatomegaly and splenomegaly. Collectively, although LIC-A was partially active when administered orally, these results give support for the antiparasitic potential LIC-A as lead compound for novel antischistosomal agent.
Licarin A is a candidate compound for the treatment of immediate hypersensitivity via inhibition of rat mast cell line RBL-2H3 cells
J Pharm Pharmacol 2015 Dec;67(12):1723-32.PMID:26376734DOI:10.1111/jphp.12475.
Objectives: We previously demonstrated that some phenylpropanoids are capable of inhibiting activated mast cells. This study evaluated the anti-allergic effects of Licarin A, a neolignan isolated from various plants, on antigen-stimulated rat mast cell line. Methods: The inhibitory effects of Licarin A on histamine release, tumour necrosis factor-α (TNF-α) and prostaglandin D2 (PGD2) production, and cyclooxygenase-2 (COX-2) expression in dinitrophenyl-human serum albumin (DNP-HSA) rat basophilic leukemia cells (DNP-HSA-stimulated RBL-2H3 cells), were investigated by spectrofluorometry, ELISA and immunoblotting. Key findings: Licarin A significantly and dose-dependently reduced TNF-α production (IC50 12.6 ± 0.3 μm) in DNP-HSA-stimulated RBL-2H3 cells. Furthermore, the levels of PGD2 secretion in DNP-HSA-stimulated cells pretreated with Licarin A were lower than those stimulated with DNP-HSA alone (positive control). Treatment with Licarin A at 20 μm produced slight suppression of DNP-HSA-induced increases in COX-2 mRNA and protein levels. We identified several signalling pathways that mediated these pharmacological effects. Licarin A treatment tended to reduce phosphorylated protein kinase C alpha/beta II (PKCα/βII) and p38 mitogen-activated protein kinase (MAPK) protein levels. Conclusions: Our results demonstrate that Licarin A reduces TNF-α and PGD2 secretion via the inhibition of PKCα/βII and p38 MAPK pathways; this compound may be useful for attenuating immediate hypersensitivity.
Neolignan Licarin A presents effect against Leishmania (Leishmania) major associated with immunomodulation in vitro
Exp Parasitol 2013 Oct;135(2):307-13.PMID:23891943DOI:10.1016/j.exppara.2013.07.007.
Leishmaniasis' treatment is based mostly on pentavalent antimonials or amphotericin B long-term administration, expensive drugs associated with severe side effects. Considering these aforementioned, the search for alternative effective and safe leishmaniasis treatments is a necessity. This work evaluated a neolignan, Licarin A anti-leishmanial activity chemically synthesized by our study group. It was observed that Licarin A effectively inhibited Leishmania (Leishmania) major promastigotes (IC₅₀ of 9.59 ± 0.94 μg/mL) growth, by inducing in these parasites genomic DNA fragmentation in a typical death pattern by apoptosis. Additionally, the neolignan proved to be even more active against intracellular amastigotes of the parasite (EC₅₀ of 4.71 ± 0.29 μg/mL), and significantly more effective than meglumine antimoniate (EC₅₀ of 216.2 ± 76.7 μg/mL) used as reference drug. The antiamastigote activity is associated with an immunomodulatory activity, since treatment with Licarin A of the infected macrophages induced a decrease in the interleukin (IL)-6 and IL-10 production. This study demonstrates for the first time the antileishmanial activity of Licarin A and suggests that the compound may be a promising in the development of a new leishmanicidal agent.
Lethal action of Licarin A derivatives in Leishmania (L.) infantum: Imbalance of calcium and bioenergetic metabolism
Biochimie 2022 Dec 29;S0300-9084(22)00343-1.PMID:36586562DOI:10.1016/j.biochi.2022.12.018.
Natural metabolites present an extraordinary chemo-diversity and have been used as the inspiration for new drugs. Considering the need for new treatments against the neglected parasitic disease leishmaniasis, three semi-synthetic derivatives of natural neolignane Licarin A were prepared: O-acetyl (1a), O-allyl (1b), and 5-allyl (1c). Using an ex vivo assay, compounds 1a, 1b, and 1c showed activity against the intracellular amastigotes of Leishmania (L.) infantum, with IC50 values of 9, 13, and 10 μM, respectively. Despite no induction of hemolytic activity, only compound 1b resulted in mammalian cytotoxicity (CC50 = 64 μM). The most potent compounds (1a and 1c) resulted in selectivity indexes >18. The mechanism of action of compound 1c was evaluated by fluorescent/luminescent based techniques and MALDI-TOF/MS. After a short incubation period, increased levels of the cytosolic calcium were observed in the parasites, with alkalinization of the acidocalcisomes. Compound 1c also induced mitochondrial hyperpolarization, resulting in decreased levels of ATP without altering the reactive oxygen species (ROS). Neither plasma membrane damages nor DNA fragmentation were observed after the treatment, but a reduction in the cellular proliferation was detected. Using MALDI-TOF/MS, mass spectral alterations of promastigote proteins were observed when compared to untreated and miltefosine-treated groups. This chemically modified neolignan induced lethal alterations of the bioenergetic and protein metabolism of Leishmania. Future PKPD and animal efficacy studies are needed to optimize this promising natural-derived compound.