Neogambogic acid
(Synonyms: 新藤黄酸) 目录号 : GC38969
Neogambogic acid 是藤黄的有效成分，可诱导细胞凋亡并具有抗癌作用。 Neogambogic acid 对耐甲氧西林的金黄色葡萄球菌 (MRSA) 具有明显的抑制活性。
Cas No.:93772-31-7
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
Neogambogic acid, an active ingredient in garcinia, induces apoptosis and has anticancer effect. Neogambogic acid has significant inhibitory activity toward methicillin-resistant Staphylococcus aureus (MRSA)[1][2].
[1]. Wang K, et al. The mechanism of neogambogic acid-induced apoptosis in human MCF-7 cells.Acta Biochim Biophys Sin (Shanghai). 2011 Sep;43(9):698-702.
| Cas No. | 93772-31-7 | SDF | |
| 别名 | 新藤黄酸 | ||
| Canonical SMILES | C/C(C(O)=O)=C/C[C@@]1(OC(C)(C)[C@]2([H])C3)[C@@]2(OC4=C(C(O[C@@](CC/C=C(C)/C)(C)C5)=C6C5O)C/C=C(C)/C)C(C(C4=C6O)=O)=C[C@@]3([H])C1=O | ||
| 分子式 | C38H46O9 | 分子量 | 646.77 |
| 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 | 1.5461 mL | 7.7307 mL | 15.4614 mL |
| 5 mM | 0.3092 mL | 1.5461 mL | 3.0923 mL |
| 10 mM | 0.1546 mL | 0.7731 mL | 1.5461 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。
Neogambogic acid relieves myocardial injury induced by sepsis via p38 MAPK/NF-κB pathway
Korean J Physiol Pharmacol 2022 Nov 1;26(6):511-518.PMID:36302625DOI:10.4196/kjpp.2022.26.6.511.
Sepsis-associated myocardial injury, an invertible myocardial depression, is a common complication of sepsis. Neogambogic acid is an active compound in garcinia and exerts anthelmintic, anti-inflammatory, and detoxification properties. The role of Neogambogic acid in sepsis-associated myocardial injury was assessed. Firstly, mice were pretreated with Neogambogic acid and then subjected to lipopolysaccharide treatment to induce sepsis. Results showed that lipopolysaccharide treatment induced up-regulation of biomarkers involved in cardiac injury, including lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I (cTnI). However, pretreatment with Neogambogic acid reduced levels of LDH, CK-MB, and cTnI, and ameliorated histopathological changes in the heart tissues of septic mice. Secondly, Neogambogic acid also improved cardiac function in septic mice through reduction in left ventricular end-diastolic pressure, and enhancement of ejection fraction, fractional shortening, and left ventricular systolic mean pressure. Moreover, Neogambogic acid suppressed cardiac apoptosis and inflammation in septic mice and reduced cardiac fibrosis. Lastly, protein expression of p-p38, p-JNK, and p-NF-κB in septic mice was decreased by Neogambogic acid. In conclusion, Neogambogic acid exerted anti-apoptotic, anti-fibrotic, and anti-inflammatory effects in septic mice through the inactivation of MAPK/NF-κB pathway.
Anticancer activity and underlying mechanism of Neogambogic acid
Chin J Nat Med 2018 Sep;16(9):641-643.PMID:30269840DOI:10.1016/S1875-5364(18)30103-1.
Garcinia, a kind of dry resin secreted by Garcinia hanburyi Hook. F. G., is a traditional Chinese medicine with various biological functions such as detoxification, anti-inflammatory, and anthelmintic activities. Recent studies suggest that garcinia has potential anticancer activity. Increasing evidences indicate that the main active monomer gambogic acid isolated from garcinia can inhibit the growth of various cancer cells. Neogambogic acid is an isolated compound with a similar chemical structure as gambogic acid. Preliminary studies show that the Neogambogic acid can selectively inhibit the growth of various cancer cells, and has a broader antitumor activity and lower toxicity than gambogic acid. In this review, we summarize the advances made in the investigation of the anti-tumor effect of Neogambogic acid in recent years.
Neogambogic acid suppresses characteristics and growth of colorectal cancer stem cells by inhibition of DLK1 and Wnt/β-catenin pathway
Eur J Pharmacol 2022 Aug 15;929:175112.PMID:35772568DOI:10.1016/j.ejphar.2022.175112.
Purpose: Targeting cancer stem cells (CSCs) may be an efficacious strategy against cancer. We were devoted to exploring the role of Neogambogic acid in characteristics and growth of colorectal CSCs. Methods: SW480 and HCT116 cells were treated with Neogambogic acid at different concentrations and transfected with siDLK1 and pcDNA3.1-DLK1 plasmids. The effect of Neogambogic acid on the viability of SW480 and HCT116 cells was assessed by MTT assay. Spheroid formation assay was adopted to enrich colorectal CSCs from SW480 and HCT116 cells. The effect of Neogambogic acid on colony number, aldehyde dehydrogenase (ALDH) level, apoptosis and cell cycle of SW480 and HCT116 CSCs was detected by colony formation and flow cytometry assays. The expressions of CSC markers, proliferation marker (proliferation nuclear antigen (PCNA)), apoptosis markers (cleaved caspase-3, cleaved caspase-9), Wnt/β-catenin pathway markers (P-GSK3β, GSK3β, β-catenin and Wnt) and DLK1 were determined by qRT-PCR or Western blot. Results: Neogambogic acid suppressed viability, the spheroid formation ability and the levels of CSC markers in colorectal cancer (CRC) cells, accompanied with inhibition of colony-formation and ALDH level, apoptosis induction and G0/G1 phase arrest. Furthermore, Neogambogic acid inhibited expressions of PCNA, P-GSK3β, P-GSK3β/GSK3β, β-catenin and Wnt, but promoted those of cleaved caspase-3, cleaved caspase-9 and GSK3β in colorectal CSCs. DLK1 silencing caused opposite results. DLK1 overexpression abrogated the effects of Neogambogic acid on colorectal CSCs. Conclusion: Neogambogic acid could be an efficacious natural compound targeting colorectal CSCs via inhibition of DLK1 and Wnt/β-catenin pathway. Thus, Neogambogic acid may be an attractive agent against CRC.
Neogambogic acid induces apoptosis of melanoma B16 cells via the PI3K/Akt/mTOR signaling pathway
Acta Biochim Pol 2020 Jun 19;67(2):197-202.PMID:32558531DOI:10.18388/abp.2020_5188.
Background: Neogambogic acid, as one of the main components of gamboge, exhibits high activities against various tumors. Objective: To explore the mechanism by which melanoma B16 cell apoptosis was induced by Neogambogic acid. Methods: Melanoma B16 cells were treated with different concentrations of Neogambogic acid solutions (0, 1.5, 3.0, 6.0 μM). The proliferation inhibition rate was measured by MTT assay. Cell morphology was observed by inverted microscope. Cell migration and invasion were tested by Transwell assay. Flow cytometry was performed to detect the apoptosis rate and cell cycle of B16 cells. The expressions of PI3K/Akt/mTOR signaling pathway-related proteins were detected by Western blot. Results: The proliferation inhibition rate of B16 cells significantly increased with rising Neogambogic acid concentration (P<0.05). The invasive and migration capacities of B16 cells decreased significantly after treatment with Neogambogic acid (P<0.05). The apoptosis rate also increased with rising concentration of Neogambogic acid. After 24 h of treatment, the percentage of G0/G1 phase cells increased gradually as the Neogambogic acid concentration rose, whereas those of S phase and G2/M phase cells decreased. With increasing concentration of Neogambogic acid, the expressions of p-PI3K, p-Akt and p-mTOR proteins reduced in a time-dependent manner, but those of PI3K and Akt proteins remained basically unchanged. Conclusion: Neogambogic acid can inhibit the proliferation, invasion and migration of melanoma B16 cells and induce their apoptosis, which may be regulated via the PI3K/Akt/mTOR signaling pathway.
Preparation of Neogambogic acid Nanoliposomes and its Pharmacokinetics in Rats
J Coll Physicians Surg Pak 2018 Dec;28(12):937-940.PMID:30501831DOI:10.29271/jcpsp.2018.12.937.
Objective: To prepare Neogambogic acid nanoliposomes (GNA-NLC) and study its pharmacokinetics (PK) in rats. Study design: An experimental study. Place and duration of study: Mudanjiang Medical University, Mudanjiang, China, from January 2016 to October 2017. Methodology: GNA-NLC was prepared by emulsion evaporation-low temperature solidification. The entrapment efficiency, average particle size, and zeta potential were investigated. Male Wistar rats were injected with 1 mg/mL gambogic acid and GNA-NLC into the caudal vein respectively, and the plasma concentration was determined by UPLC- MS/MS. The pharmacokinetic parameters of the two agents were compared. Results: GNA-NLC prepared in this study were mostly spherical spheroids with an average particle size of 146.35 ±1.72 nm, polydispersity coefficient of 0.26 ±0.02, zeta potential of -28.24 ±0.13 MV, entrapment efficiency of 84.63%, and drug loading capacity of 4.23%. DSC showed that Neogambogic acid nanoparticles had formed and Neogambogic acid was amorphous in the matrix. The pharmacokinetics results in rats showed that GNA-NLC plasma concentration was significantly higher than that of common preparation of gambogic acid, with a half-life period of 10.14 ±0.03 hours, 4.57 times that of gambogic acid. AUC0 ~ 24h of gambogic acid in GNA-NLC lipidosome was 58.36 ±0.23 μg/h/mL, 4.83 times that of gambogic acid. Conclusion: GNA-NLC can be prepared successfully by emulsion evaporation-low temperature solidification. The method is simple and easy to control. The GNA-NLC has a long cycle, and high blood concentration, sustained release compared with the raw material gambogic acid.