Gambogic Acid
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Cat.No：IG0050 Solarbio
CAS：2752-65-0
Storage：Powder:2-8℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year
Purity：HPLC≥98%
Appearance：Solid
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> Small Molecule Compounds > Inhibitors & Antagonists & Agonists > Apoptosis > Gambogic Acid
Product Information
| CAS | 2752-65-0 |
| Name | Gambogic Acid |
| Molecular Formula | C38H44O8 |
| Molecular Weight | 628.75 |
| Solubility | Soluble in DMSO |
| Purity | HPLC≥98% |
| Appearance | Solid |
| Storage | Powder:2-8℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year |
| MDL | MFCD16878985 |
| SMILES | O=C(O)/C(C)=C\C[C@@]1(C2=O)OC(C)(C)[C@@](C[C@@]2([H])C=C34)([H])[C@]31OC5=C(C(O)=C(C=C[C@](CC/C=C(C)/C)(C)O6)C6=C5C/C=C(C)\C)C4=O |
| InChIKey | GEZHEQNLKAOMCA-RRZNCOCZSA-N |
| InChI | InChI=1S/C38H44O8/c1-20(2)10-9-15-36(8)16-14-24-29(39)28-30(40)26-18-23-19-27-35(6,7)46-37(33(23)41,17-13-22(5)34(42)43)38(26,27)45-32(28)25(31(24)44-36)12-11-21(3)4/h10-11,13-14,16,18,23,27,39H,9,12,15,17,19H2,1-8H3,(H,42,43)/b22-13-/t23-,27+,36-,37+,38-/m1/s1 |
| PubChem CID | 9852185 |
| Target Point | Bcl-2 Family |
| Passage | Apoptosis |
| Background | It has been reported to inhibit Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1. |
| Biological Activity | Gambogic acid 来自 Garcinia hanburyi 树的藤黄树脂。Gambogic acid 抑制 Bcl-XL，Bcl-2，Bcl-W，Bcl-B，Bfl-1 和 Mcl-1，IC50 分别为 1.47 μM，1.21 μM，2.02 μM，0.66 μM，1.06 μM 和 0.79 μM。[1-2] |
| IC50 | Bcl-B:0.66μM;mcl-1:0.79μM;Bfl-1:1.06μM;Bcl-2:1.21μM;Bcl-xL:1.47μM;Bcl-W:2.02μM [1-2] |
| In Vitro | 藤黄酸(Gambogic Acid)是一种药用化合物，来自树木的藤黄树(Garcinia hanburyi)。藤黄酸已经记录了培养中针对肿瘤细胞系的细胞毒活性，其中杀死50％细胞所需的浓度(LD50为~1μM)。使用FPA对抗藤黄酸对6种人抗凋亡Bcl-2家族蛋白的活性。藤黄酸取代不同程度的FITC-BH3肽与所有6种蛋白结合，Bcl-XL的IC50为1.47μM，Bcl-2为1.21μM，Bcl-W为2.02μM，Bcl-B为0.66μM，1.06μM为Bfl-1，Mcl-1为[0.79μM] [1]。在暴露48小时后通过MTT测定评估藤黄酸(GA)或顺铂(CDDP)对A549，NCI-H460和NCI-H1299细胞的生长抑制作用。用Gambogic Acid和CDDP观察到细胞生长的浓度依赖性抑制，A549细胞的IC50为3.56±0.36和21.88±3.21μM，NCI-H460细胞的IC50为4.05±0.51和25.76±4.03μM，和1.12±0.31μM NCI-H1299细胞为25.21±4.38μM[2]。 |
| In Vivo | 为了进一步研究藤黄酸是否协同CDDP对抗体内肿瘤生长，将A549肿瘤植入SCID小鼠中。当用CDDP联合藤黄酸处理小鼠时，肿瘤抑制率为69.3％，而单独用CDDP和GA处理的小鼠的肿瘤抑制率分别为57.2％和29.0％[2]。 |
| Cell Experiment | 通过MTT测定确定藤黄酸，单独的CDDP或组合处理的体外细胞活力效应。将细胞(2×10 4个细胞/ mL)接种到96孔培养板中。孵育过夜后，用藤黄酸(0.44，0.88，1.75，3.5，7，10.5和14μM)处理A549细胞;用藤黄酸(0.5，1，2，4，8，12和16μM)处理NCI-H460细胞;用藤黄酸(0.125，0.25，0.5，1，2和4μM)处理NCI-H1299细胞。对于在NSCLC细胞中的组合治疗，测试三种序列：(a)将藤黄酸随后将CDDP细胞暴露于藤黄酸48小时，然后在冲洗出藤黄酸后，用CDDP处理细胞另外48小时;(b)将CDDP接着将藤黄酸细胞暴露于CDDP 48小时，然后在冲洗掉CDDP后，将细胞用藤黄酸处理另外48小时;(c)同时处理细胞暴露于藤黄酸和ADM两小时48小时。通过使用组合指数(CI)[2]分析药物相互作用的性质。 |
| Animal Experiment | 小鼠[2]为了确定藤黄酸与CDDP结合的体内抗肿瘤活性，将活A549细胞(每只小鼠5×106 /100μLPBS)皮下注射到7-8周龄雄性SCID的右侧腹部。老鼠。当平均肿瘤体积达到100 mm3时，将小鼠随机分为4个治疗组，包括对照组(仅生理盐水，n = 5)，藤黄酸(每2天3.0 mg/kg，静脉注射; n = 6)，CDDP(每周4mg/kg，静脉内; n = 6)，和顺序组合(在藤黄酸处理前一天进行CDDP处理，n = 6)。 CDDP(4mg/kg，每周)通常以小于最大耐受剂量的剂量施用，以试图允许更容易检测与铂基试剂和藤黄酸的组合治疗的任何累加效应。用calipre每2天测量一次肿瘤大小。每2天记录一次体重。 14天后，杀死小鼠并切除肿瘤并储存在-80℃直至进一步分析。 |
| Data Literature Source | [1]. Zhai D，et al. Gambogic acid is an antagonist of antiapoptotic Bcl-2 family proteins. Mol Cancer Ther. 2008 Jun;7(6):1639-46. [2]. Wang LH，et al. Gambogic acid synergistically potentiates cisplatin-induced apoptosis in non-small-cell lung cancer through suppressing NF-κB and MAPK/HO-1 signalling. Br J Cancer. 2014 Jan 21;110(2):341-52 |
| Unit | Bottle |
| Specification | 5mg 10mg 20mg |
据报道，可以抑制 Bcl-XL，Bcl-2，Bcl-W，Bcl-B，Bfl-1 和 Mcl-1。
Remark：These protocols are for reference only. Solarbio does not independently validate these methods.
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2. For your safety and health, please wear laboratory clothes, disposable gloves and masks.
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