Gambogenic acid
(Synonyms: 新藤黄酸) 目录号 : GC38062
Gambogenic acid是藤黄的主要活性成分，能抑制Aurora A激酶，IC50值为1.425μM。
Cas No.:173932-75-7
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
Gambogenic acid, the main active component of gamboge, inhibits Aurora A kinase, with an IC50 value of 1.425μM[1]. Gambogenic acid triggers endoplasmic reticulum (ER) stress-mediated apoptosis through the reactive oxygen species/IRE1α/c-Jun N-terminal kinase signalling pathway[2]. Gambogenic acid has been widely used as an anticancer agent to inhibit the growth of different cancer cells[3].
In vitro, Gambogenic acid treatment for 72h significantly inhibited the proliferation of HCC827, H1650, and HCC827 erlotinib-resistant (HCC827ER) cells with IC50 values of 1.510, 1.328, and 0.909μM, respectively[4]. Treatment of HepG2 cells with 3μM Gambogenic acid for 24h promoted apoptosis, accompanied by a decrease in Bcl-2 levels and an increase in Bax expression levels[5]. Treatment with 1μM Gambogenic acid for 48h inhibited the invasion and migration of A375 cells and induced ferroptosis in A375 cells treated with TGF-β1 (5ng/ml; 48h)[6].
In vivo, Gambogenic acid treatment via intraperitoneally injection at a dose of 2mg/kg/day for 21 days significantly reduced tumor volume and weight in HCT116 cell-xenograft mice, without affecting body weight[7]. Intraperitoneal injection of Gambogenic acid (10mg/kg/day) for 7 consecutive days in male Sprague-Dawley rats can prevent liver oxidative damage caused by acetaminophen (APAP) and alleviate liver histopathological changes caused by APAP[8].
References:
[1] Liu C, Xu J, Guo C, et al. Gambogenic acid induces endoplasmic reticulum stress in colorectal cancer via the aurora a pathway[J]. Frontiers in Cell and Developmental Biology, 2021, 9: 736350.
[2] Zhao Q, Zhong J, Bi Y, et al. Gambogenic acid induces Noxa-mediated apoptosis in colorectal cancer through ROS-dependent activation of IRE1α/JNK[J]. Phytomedicine, 2020, 78: 153306.
[3] Mi L, Xing Z, Zhang Y, et al. Unveiling gambogenic acid as a promising antitumor compound: a review[J]. Planta Medica, 2024, 90(05): 353-367.
[4] Xu L, Meng X, Xu N, et al. Gambogenic acid inhibits fibroblast growth factor receptor signaling pathway in erlotinib-resistant non-small-cell lung cancer and suppresses patient-derived xenograft growth[J]. Cell death & disease, 2018, 9(3): 262.
[5] Yan F, Wang M, Li J, et al. Gambogenic acid induced mitochondrial-dependent apoptosis and referred to phospho-Erk1/2 and phospho-p38 MAPK in human hepatoma HepG2 cells[J]. Environmental toxicology and pharmacology, 2012, 33(2): 181-190.
[6] Wang M, Li S, Wang Y, et al. Gambogenic acid induces ferroptosis in melanoma cells undergoing epithelial-to-mesenchymal transition[J]. Toxicology and applied pharmacology, 2020, 401: 115110.
[7] Zhao Q, Zhong J, Bi Y, et al. Gambogenic acid induces Noxa-mediated apoptosis in colorectal cancer through ROS-dependent activation of IRE1α/JNK[J]. Phytomedicine, 2020, 78: 153306.
[8] Ding Z, Li Y, Tang Z, et al. Role of gambogenic acid in regulating PI3K/Akt/NF-kβ signaling pathways in rat model of acute hepatotoxicity[J]. Bioscience, Biotechnology, and Biochemistry, 2021, 85(3): 520-527.
Gambogenic acid是藤黄的主要活性成分，能抑制Aurora A激酶，IC50值为1.425μM[1]。Gambogenic acid通过活性氧/IRE1α/c-Jun氨基末端激酶信号通路，引发内质网应激介导的细胞凋亡[2]。Gambogenic acid已被广泛用于抗癌剂抑制不同癌细胞生长[3]。
在体外，Gambogenic acid处理72小时能显著抑制HCC827、H1650及HCC827厄洛替尼耐药细胞（HCC827ER）的增殖，IC50值分别为1.510μM、1.328μM和0.909μM[4]。使用3μM的Gambogenic acid处理HepG2细胞24小时可促进细胞凋亡，同时伴随Bcl-2水平下降和Bax表达水平升高[5]。用1μM的Gambogenic acid处理48小时能抑制A375细胞的侵袭和迁移，并在TGF-β1处理的A375细胞中诱导铁死亡[6]。
在体内，通过每日腹腔注射2mg/kg剂量的Gambogenic acid，连续21天治疗，能显著降低HCT116细胞移植瘤小鼠的肿瘤体积和重量，且不影响小鼠体重[7]。在雄性Sprague-Dawley大鼠中连续7天腹腔注射Gambogenic acid，可预防acetaminophen (APAP)引起的肝脏氧化损伤，并减轻APAP导致的肝脏组织病理学变化[8]。
| Cell experiment [1]: | |
Cell lines | HepG2 cells |
Preparation Method | HepG2 cells were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum, 100units /ml penicillin, and 100μg/ml streptomycin. Cells were cultured at 37°C in a humidified atmosphere with 5% CO2. Subsequently, HepG2 cells in the logarithmic growth phase were collected and seeded in 96-well culture plates overnight at a density of approximately 6×104 cells/ml. Cells were incubated with different concentrations of Gambogenic acid (0, 0.75, 1.5, 3, 6, and 12μM). At various time points of 24, 48, or 72h, 5.0mg/ml MTT was added, and cells were then incubated at 37°C for 4h and measured at a wavelength of 570nm. |
Reaction Conditions | 0, 0.75, 1.5, 3, 6, and 12μM; 24, 48, and 72h |
Applications | Gambogenic acid treatment reduced the percentage of viable HepG2 cells in a concentration- and time-dependent manner. |
| Animal experiment [2]: | |
Animal models | Female BALB/c-nu mice |
Preparation Method | Female BALB/c-nu mice (4 weeks of age) were maintained under specific pathogen free (SPF) conditions and provided with sterile food and water. HCT116 cells (1×106 cells per mouse) were injected subcutaneously into the right abdomen of each mouse. When the tumor volume was approximately 100mm3, mice were randomly divided into a vehicle group, a 2mg/kg Gambogenic acid group, and a positive control 15mg/kg paclitaxel (PTX) group (n=6 mice in each group). Mice were intraperitoneally injected with Gambogenic acid daily and PTX three times a week. Tumor size was measured and calculated using the standard formula: 0.5×length×width2. The body weight of mice was measured at the same time. After 21 days, all mice were euthanized, and tumors were collected for analysis. |
Dosage form | 2mg/kg/day for 21 days; i.p. |
Applications | Gambogenic acid treatment significantly reduced tumor volume and weight in mice without affecting body weight. |
References: | |
| Cas No. | 173932-75-7 | SDF | |
| 别名 | 新藤黄酸 | ||
| Canonical SMILES | O=C(O)/C(C)=C\C[C@@]1(C2=O)OC(C)(C)[C@]([C@]31OC4=C5C(O)=C(C/C=C(C)/CC/C=C(C)\C)C(O)=C4C/C=C(C)\C)([H])C[C@@]2([H])C=C3C5=O | ||
| 分子式 | C38H46O8 | 分子量 | 630.77 |
| 溶解度 | DMSO: 250 mg/mL (396.34 mM) | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.5854 mL | 7.9268 mL | 15.8536 mL |
| 5 mM | 317.1 μL | 1.5854 mL | 3.1707 mL |
| 10 mM | 158.5 μL | 792.7 μL | 1.5854 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。
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet