Cinchonine ((8R,9S)-Cinchonine)
(Synonyms: 辛可宁; (8R,9S)-Cinchonine; LA40221) 目录号 : GC32997
Cinchonine (LA40221) is an alkaloid and a stereoisomer and pseudo-enantiomer of cinchonidine.
Cas No.:118-10-5
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
Cinchonine (LA40221) is an alkaloid and a stereoisomer and pseudo-enantiomer of cinchonidine.
| Cas No. | 118-10-5 | SDF | |
| 别名 | 辛可宁; (8R,9S)-Cinchonine; LA40221 | ||
| Canonical SMILES | O[C@@H](C1=CC=NC2=CC=CC=C12)[C@]3([H])[N@@]4C[C@H](C=C)[C@@H](CC4)C3 | ||
| 分子式 | C19H22N2O | 分子量 | 294.39 |
| 溶解度 | DMSO : 4.76 mg/mL (16.17 mM) | 储存条件 | 4°C, protect from light, stored under nitrogen |
| 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 | 3.3969 mL | 16.9843 mL | 33.9685 mL |
| 5 mM | 0.6794 mL | 3.3969 mL | 6.7937 mL |
| 10 mM | 0.3397 mL | 1.6984 mL | 3.3969 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。
Cinchonine and thiourea
Chem Commun (Camb) 2013 Oct 7;49(77):8583-5.PMID:23948716DOI:10.1039/c3cc40825f.
In this viewpoint, we discuss the seminal work contributed by Dixon, who reported the first use of a bifunctional cinchona-derived thiourea organocatalyst for the enantioselective conjugate addition of malonate esters to nitroalkenes. Since then, this class of catalysts has been extensively utilized in a variety of fundamental transformations. We also highlight here some of the representative studies performed since the publication of this milestone work in 2005.
Cinchonine activates endoplasmic reticulum stress-induced apoptosis in human liver cancer cells
Exp Ther Med 2018 Jun;15(6):5046-5050.PMID:29805529DOI:10.3892/etm.2018.6005.
Cinchonine is a natural compound present in Cinchona bark. It exerts multidrug resistance reversal activity and synergistic apoptotic effect with paclitaxel in uterine sarcoma cells. Whether Cinchonine is effective against human liver cancer, however, remains elusive. A total of five liver cancer cell lines including Bel-7402, MHCC97H, HepG2, Hep3B and SMCC7721 were used. The anti-proliferative effects of Cinchonine on these liver cancer cell lines were assessed by MTT assay. The apoptotic effects of Cinchonine on liver cancer cell lines were assessed by flow cytometry with Annexin V/propidium iodide assay. Caspase-3 activation, poly (ADP-Ribose) polymerase (PARP) cleavage as well as the endoplasmic-reticulum (ER) stress response was detected by western blotting. Balb/c-nude mice bearing HepG2 xenograft tumors were used to evaluate the in vivo antitumor effect of Cinchonine. It was demonstrated that Cinchonine inhibited cell proliferation and promoteed apoptosis in liver cancer cells in a dose-dependent manner. Cinchonine promoted caspase-3 activation and PARP1 cleavage in liver cancer cells. Furthermore, Cinchonine activated the ER stress response by upregulating GRP78 and promoting PERK and Eukaryotic Translation Initiation Factor 2 α phosphorylation. The Balb/c-nude mice experiment revealed that Cinchonine suppressed HepG2 xenograft tumor growth in mice. The findings indicated that Cinchonine promoted ER stress-induced apoptosis in liver cancer cells and suggested that Cinchonine may have a potential beneficial effect for liver cancer treatment.
Cinchonine-induced cell death in pancreatic cancer cells by downregulating RRP15
Cell Biol Int 2023 May;47(5):907-919.PMID:36682038DOI:10.1002/cbin.11987.
Pancreatic cancer is characterized by poor prognosis and high mortality, while its treatment remains unsatisfactory. Cinchonine, a natural compound present in cinchona bark, is a potential anticancer drug. Whether Cinchonine is of relevance to pancreatic cancer therapeutics is unclear. This research showed that the ribosomal RNA-processing 15 homolog (RRP15) expression is decreased in the pancreatic cancer, and RRP15 knockdown inhibited autophagy, and caused apoptosis in pancreatic cancer cells. Cinchonine treatment inhibits the expression of RRP15 and autophagy, and caused apoptosis by leading to the activation of Nrf2 axis in pancreatic cancer cells. Taken together, the above results indicate that Cinchonine treatment inhibited autophagy and induced apoptosis through activating Nrf2 axis by downregulating RRP15 in pancreatic cancer cells.
Inhibition of Porcine Epidemic Diarrhea Virus by Cinchonine via Inducing Cellular Autophagy
Front Cell Infect Microbiol 2022 Jun 14;12:856711.PMID:35774410DOI:10.3389/fcimb.2022.856711.
Porcine epidemic diarrhea virus (PEDV) could cause lethal diarrhea and dehydration in suckling piglets, which can adversely affect the development of the global swine industry. The lack of effective therapeutical and prophylactic treatment especially for PEDV variant strains underlines the importance of effective antiviral strategies, such as identification of novel antiviral agents. In the present study, the antiviral activity of Cinchonine against PEDV was investigated in Vero CCL81 and LLC-PK1 cells at a non-cytotoxic concentration determined by Cell Counting Kit-8 assay in vitro. We found that Cinchonine exhibited a significant suppression effect against PEDV infection and its inhibitory action was primarily focused on the early stage of PEDV replication. Moreover, we also observed that Cinchonine could significantly induce autophagy by detecting the conversion of LC3-I to LC3-II by using western blot analysis. Cinchonine treatment could inhibit PEDV replication in a dose-dependent manner in Vero CCL81 cells, while this phenomenon disappeared when autophagy was attenuated by pre-treatment with autophagy inhibitor 3MA. Consequently, this study indicated that Cinchonine can inhibit PEDV replication via inducing cellular autophagy and thus from the basis for successful antiviral strategies which potentially suggest the possibility of exploiting Cinchonine as a novel antiviral agent.
Cinchonine induces apoptosis of HeLa and A549 cells through targeting TRAF6
J Exp Clin Cancer Res 2017 Feb 23;36(1):35.PMID:28231796DOI:10.1186/s13046-017-0502-8.
Background: Cancer cells are known to over-express TRAF6 that is critical for both AKT and TAK1 activations. The Really Interesting New Gene (RING) domain of TRAF6 is believed to be responsible for the E3 ligase activity, ZINC fingers of TRAF6 provide critical support for the activity of the RING domain which is critical for both AKT and TAK1 activations. Methods: We employed computational docking program to identify small molecules that could effectively and competitively bind with the RING domain of TRAF6, which is believed to be responsible for its E3 ligase activity. MTT assay and flow cytometry were employed to analyze apoptosis of cancer cells. Signaling pathways were detected using immunoprecipitation and western blotting, and immunofluorescence was pursued to assess the nature of binding of Cinchonine to TRAF6. We also performed animal experiments to test effect of Cinchonine in vivo. Results: Cinchonine, a naturally occurring Cinchona alkaloid identified from the docking study, could bind to TRAF6 in HeLa and A549 cells and induce apoptosis of these cancer cells. We found that AKT ubiquitination and phosphorylation as well as phosphorylation of TAK1 were decreased. These activities would lead to subsequent suppression anti-apoptotic protein Bcl-2, while elevating pro-apoptotic protein Bax. Immunofluorescence staining unambiguously demonstrated the binding of Cinchonine specifically at the RING domain of TRAF6 in cells, thereby validating the computational modeling. Animal experiments showed that Cinchonine could suppress tumor growth in mice without showing significant acute toxicity. Conclusion: These investigations suggest that through competitive binding with the RING domain of TRAF6, Cinchonine could induce apoptosis via inhibiting AKT and TAK1 signaling pathways.