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Gambogic Acid (Guttatic Acid, Guttic Acid)

Alias: ß-Guttiferrin; ß-Guttiferrin; ß-Guttilactone; Cambogic acid; Guttatic acid; 2752-65-0; (-)-Gambogic Acid; R-gambogic acid; B''-Guttiferin; Gambogic-acid; beta-Guttiferin; Guttic acid
Cat No.:V0033 Purity: ≥98%
Gambogic Acid (also called Guttatic Acid, Guttic Acid) is a naturally occurring xanthonoid isolated from the brownish or orange resin from Garcinia hanburyi.
Gambogic Acid (Guttatic Acid, Guttic Acid)
Gambogic Acid (Guttatic Acid, Guttic Acid) Chemical Structure CAS No.: 2752-65-0
Product category: Caspase
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Gambogic Acid (also called Guttatic Acid, Guttic Acid) is a naturally occurring xanthonoid isolated from the brownish or orange resin from Garcinia hanburyi. It is presently undergoing clinical trials in China and may have antitumor properties. Gambogic acid works by competitively inhibiting Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bcl-B, and Mcl-1 with IC50 values of 1.47, 1.21, 2.02, 0.66, 1.06, and 0.79 μM, respectively. Caspases are activated by gambogic acid with an EC50 range of 0.78-1.64 μM. The cytotoxic natural substance GA blocks the ability of several antiapoptotic Bcl-2 family members to suppress the release of apoptogenic proteins from mitochondria by competing for the BH3 peptide binding sites on these proteins. The proliferation of human gastric carcinoma MGC-803 cells was shown to be inhibited by GA in vitro in a dose-dependent manner. The rate of inhibition reached 89.45% after 72 hours of GA 5 mg/ml exposure to the cells.

Biological Activity I Assay Protocols (From Reference)
Targets
Bcl-2 (Ki < 0.01 nM)
ln Vitro
Gambogic Acid, a caged xanthone derived from Garcinia hanburyi, inhibits human Bcl-2 family proteins and activates caspases to effectively induce apoptosis in a variety of cancer cell types. Additionally, gambogic acid inhibits Kir2.1 channels with an EC50 of ≤ 100 nM.[1][2][3] At nM concentrations, gambogic acid significantly reduces the proliferation, migration, invasion, tube formation, and microvessel growth of human umbilical vein endothelial cells (HUVEC).[4]
ln Vivo
Gambogic Acid effectively inhibits tumor angiogenesis and suppressed tumor growth with low side effects using metronomic chemotherapy with Gambogic Acid.[4] Gambogic acid has a variety of useful properties, such as the induction of apoptosis, inhibition of proliferation, and prevention of tumor angiogenesis and cancer metastasis.[5] Gambogic acid effectively inhibits tumor growth in both animal tumor models and human clinical trials with few adverse effects and little toxicity to the immune and hematopoietic systems. It is possible for gambogic acid to cause tumor-specific toxicity and tissue-specific proteasome inhibition.[6] 45 mg/kg (i.p.) is the mice LD50.[7]
Enzyme Assay
Time-Resolved-Fluorescence Resonance Energy Transfer (TR-FRET) Assays[1]
For TR-FRET assays, GST-Bcl-XL and anti-GST-terbium were mixed together with the FITC-Bad BH3 peptide in PBS containing 0.005% tween 20 in 96 well plates in a total volume of 20 μl per well. After incubation at room temperature for 30 min, 2 μl of gambogic acid-containing solutions were added to the reaction mixtures containing 10 nM of Bcl-XL, 10 nM of FITC-Bad BH3 peptide and 2 nM of anti-GST-terbium for 30 min at room temperature. TR-FRET signals were measured with a SpectraMax M5 plate reader using the following settings: excitation at 330nm, emission for FITC signal at 490 nm, and emission for terbium signal at 520 nm.
Mitochondria Purification and Protein Release Assays[1]
HeLa cells were pelleted by centrifugation, and then washed once in HM buffer (10 mM HEPES, pH 7.4, 250 mM mannitol, 10 mM KCl, 5 mM MgCl2, 1 mM EGTA), containing 1 mM PMSF and a mixture of protease inhibitors. The cell pellet was then homogenized in HM buffer by 50 strokes of a dounce homogenizer, using a B-type pestle. The homogenate was centrifuged twice at 600g for 5 min to remove nuclei and debris. The resulting supernatant was centrifuged at 10,000g for 10 min, and the resulting mitochondria-containing pellet was washed twice with the HM buffer.[1]
For mitochondrial protein release assays, 10 μl of mitochondria (50 μg) were added into a final volume of 50 μl HM buffer containing gambogic acid, tBid or tBid pre-incubated with gambogic acid or Bcl-2 family proteins at 30°C for 15 min. The reactions were further incubated at 30°C for 40–60 min, then mitochondria were pelleted by centrifugation and the supernatants were collected, boiled in Laemmli sample buffer, and analyzed by SDS-PAGE/immunoblotting using anti-SMAC antibody.
The natural product gambogic acid (GA) has been reported to have cytotoxic activity against tumor cells in culture and was identified as an active compound in a cell-based high-throughput screening assay for activators of caspases, proteases involved in apoptosis. Using the antiapoptotic Bcl-2 family protein, Bfl-1, as a target for screening of a library of natural products, we identified GA as a competitive inhibitor that displaced BH3 peptides from Bfl-1 in a fluorescence polarization assay. Analysis of competition for BH3 peptide binding revealed that GA inhibits all six human Bcl-2 family proteins to various extents, with Mcl-1 and Bcl-B the most potently inhibited [concentrations required for 50% inhibition (IC(50)), < 1 micromol/L]. Competition for BH3 peptide binding was also confirmed using a time-resolved fluorescence resonance energy transfer assay. GA functionally inhibited the antiapoptotic Bcl-2 family proteins as shown by experiments using isolated mitochondria in which recombinant purified Bcl-2 family proteins suppress SMAC release in vitro, showing that GA neutralizes their suppressive effects on mitochondria in a concentration-dependent manner. GA killed tumor cell lines via an apoptotic mechanism, whereas analogues of GA with greatly reduced potency at BH3 peptide displacement showed little or no cytotoxic activity. However, GA retained cytotoxic activity against bax-/-bak-/- cells in which antiapoptotic Bcl-2 family proteins lack a cytoprotective phenotype, implying that GA also has additional targets that contribute to its cytotoxic mechanism. Altogether, the findings suggest that suppression of antiapoptotic Bcl-2 family proteins may be among the cytotoxic mechanisms by which GA kills tumor cells.[1]
gambogic acid (GA), a xanthone derived from the resin of the Garcinia hanburyi, has been recently demonstrated to bind transferrin receptor and exhibit potential anticancer effects through a signaling mechanism that is not fully understood. Because of the critical role of NF-kappaB signaling pathway, we investigated the effects of GA on NF-kappaB-mediated cellular responses and NF-kappaB-regulated gene products in human leukemia cancer cells. Treatment of cells with GA enhanced apoptosis induced by tumor necrosis factor (TNF) and chemotherapeutic agents, inhibited the expression of gene products involved in antiapoptosis (IAP1 and IAP2, Bcl-2, Bcl-x(L), and TRAF1), proliferation (cyclin D1 and c-Myc), invasion (COX-2 and MMP-9), and angiogenesis (VEGF), all of which are known to be regulated by NF-kappaB. GA suppressed NF-kappaB activation induced by various inflammatory agents and carcinogens and this, accompanied by the inhibition of TAK1/TAB1-mediated IKK activation, inhibited IkappaBalpha phosphorylation and degradation, suppressed p65 phosphorylation and nuclear translocation, and finally abrogated NF-kappaB-dependent reporter gene expression. The NF-kappaB activation induced by TNFR1, TRADD, TRAF2, NIK, TAK1/TAB1, and IKKbeta was also inhibited. The effect of GA mediated through transferrin receptor as down-regulation of the receptor by RNA interference reversed its effects on NF-kappaB and apoptosis. Overall our results demonstrate that GA inhibits NF-kappaB signaling pathway and potentiates apoptosis through its interaction with the transferrin receptor.[3]
Cell Assay
MTT assay is used to assess how treatments such as gambogic acid, CDDP alone, or both together, affect in vitro cell viability. In 96-well culture plates, the cells (2×104 cells per mL) are seeded. Following an overnight incubation, gambogic acid is applied to NCI-H460, A549, and NCI-H1299 cells in the following concentrations: 0.125, 0.25, 0.25, 0.5, 1, 2, and 4 μM, 0.44, 0.88, 1.75, 3.5, 7, 10.5 and 14 μM, and 0.44, 0.88, 1.75, 4, 8, 12, and 16 μM respectively. In NSCLC cells, three sequences are tested for the combined treatment: (a) Gambogic Acid followed by CDDP cells are exposed to Gambogic Acid for 48 h, and then after washout of Gambogic Acid, cells are treated with CDDP for an additional 48 h; (b) CDDP followed by Gambogic Acid cells are exposed to CDDP for 48 h, and then after washout of CDDP, cells are treated with Gambogic Acid for an additional 48 h; and (c) concurrent treatment cells are exposed to both Gambogic Acid and ADM for 48 h. The nature of the drug interaction is analysed by using the combination index (CI)[2].
Animal Protocol
Mice: A549 viable cells (5×106/100 μL PBS per mouse) are subcutaneously injected into the right flank of male SCID mice that are 7 to 8 weeks old in order to assess the in vivo antitumor activity of gambogic acid combined with CDDP. The mice are randomly assigned to one of four treatment groups when the tumor volume reaches 100 mm3, including control (saline only, n=5), gambogic acid (3.0 mg/kg every two days, intravenously; n=6), CDDP (4 mg/kg every week, intravenously; n=6), and sequential combination (CDDP treatment one day before gambogic acid treatment, n=6). To help detect any additive effects of combination therapy with platinum-based agents and gambogic acid, CDDP (4 mg/kg, weekly) is typically administered at doses lower than the maximum tolerated dose. Once every two days, a caliper is used to measure the tumor's size. Once every two days, body weight is measured. The tumors are removed after 14 days, and the mice are then put to death. They are then kept at -80°C for future research.
Toxicity/Toxicokinetics
rat LD50 intraperitoneal 88 mg/kg LIVER: OTHER CHANGES Indian Journal of Experimental Biology., 5(96), 1967 [PMID:6062434]
rat LD50 intravenous 107 mg/kg LIVER: OTHER CHANGES Indian Journal of Experimental Biology., 5(96), 1967 [PMID:6062434]
mouse LD50 subcutaneous 354 mg/kg CRC Handbook of Antibiotic Compounds, Vols.1- , Berdy, J., Boca Raton, FL, CRC Press, 1980, 8(1)(331), 1982
mammal (species unspecified) LD50 unreported 55 mg/kg Zhongliu Yanjiu Cancer Review, Yu, R., et al., eds., Shanghai Science/Technology Publisher,Peop. Rep. China, 1994, -(220), 1994
References

[1]. Mol Cancer Ther. 2008 Jun;7(6):1639-46.

[2]. Bioorg Med Chem. 2004 Jan 15;12(2):309-17.

[3]. Blood. 2007 Nov 15;110(10):3517-25.

[4]. Cancer Res. 2008 Mar 15;68(6):1843-50.

[5]. Anticancer Agents Med Chem. 2012 Oct 1;12(8):994-1000.

[6]. Cell Rep. 2013 Jan 31;3(1):211-22.

[7]. Basic Clin Pharmacol Toxicol. 2006 Aug;99(2):178-84.

Additional Infomation
beta-Guttiferin has been reported in Garcinia hanburyi with data available.
Gambogic acid (2), a natural product isolated from the resin of Garcinia hurburyi tree, was discovered to be a potent apoptosis inducer using our cell- and caspase-based high-throughput screening assays. Gambogic acid was found to have an EC(50) of 0.78 microM in the caspase activation assay in T47D breast cancer cells. The apoptosis-inducing activity of gambogic acid was further characterized by a nuclear fragmentation assay and flow cytometry analysis in human breast tumor cells T47D. Gambogic acid was found to induce apoptosis independent of cell cycle, which is different from paclitaxel that arrests cells in the G2/M phase. To understand the structure-activity relationship (SAR) of gambogic acid, derivatives of 2 with modifications to different function groups were prepared. SAR studies of gambogic acid, as measured by the caspase activation assay, showed that the 9,10 carbon-carbon double bond of the alpha,beta-unsaturated ketone is important for biological activity, while the 6-hydroxy and 30-carboxy group can tolerate a variety of modifications. The importance of the 9,10 carbon-carbon double bond was confirmed by the traditional growth inhibition assay. The high potency of 2 as an inducer of apoptosis, its novel mechanism of action, easy isolation and abundant supply, as well as the fact that it is amenable to chemical modification, makes gambogic acid an attractive molecule for the development of anticancer agents.[2]
Gambogic acid (GA), the main active compound of Gamboge hanburyi, has been previously reported to activate apoptosis in many types of cancer cell lines by targeting transferrin receptor and modulating nuclear factor-kappaB signaling pathway. Whether GA inhibits angiogenesis, which is crucial for cancer and other human diseases, remains unknown. Here, we found that GA significantly inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, migration, invasion, tube formation, and microvessel growth at nanomolar concentration. In a xenograft prostate tumor model, we found that GA effectively inhibited tumor angiogenesis and suppressed tumor growth with low side effects using metronomic chemotherapy with GA. GA was more effective in activating apoptosis and inhibiting proliferation and migration in HUVECs than in human prostate cancer cells (PC3), suggesting GA might be a potential drug candidate in cancer therapy through angioprevention with low chemotoxicity. Furthermore, we showed that GA inhibited the activations of vascular endothelial growth factor receptor 2 and its downstream protein kinases, such as c-Src, focal adhesion kinase, and AKT. Together, these data suggest that GA inhibits angiogenesis and may be a viable drug candidate in antiangiogenesis and anticancer therapies. [4]
Gambogic acid (GA) is a caged xanthone that is derived from Garcinia hanburyi and functions as a strong apoptotic inducer in many types of cancer cells. The distinct effectiveness of GA has led to its characterization as a novel anti-cancer agent. There is an increasing number of research studies focused on elucidating the molecular mechanisms of GA-induced anti-cancer effects, and several critical signaling pathways have been reported to be influenced by GA treatment. In this review, we summarize the multiple functional effects of GA administration in cancer cells including the induction of apoptosis, the inhibition of proliferation and the prevention of cancer metastasis and tumor angiogenesis. [5]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C38H44O8
Molecular Weight
628.75
Exact Mass
628.303
Elemental Analysis
C, 72.59; H, 7.05; O, 20.36
CAS #
2752-65-0
Related CAS #
2752-65-0
PubChem CID
9852185
Appearance
Yellow solid powder
Density
1.3±0.1 g/cm3
Boiling Point
808.9±65.0 °C at 760 mmHg
Melting Point
88.5°C
Flash Point
251.4±27.8 °C
Vapour Pressure
0.0±3.0 mmHg at 25°C
Index of Refraction
1.627
LogP
10.3
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
8
Rotatable Bond Count
8
Heavy Atom Count
46
Complexity
1490
Defined Atom Stereocenter Count
5
SMILES
O1C(C([H])([H])[H])(C([H])([H])[H])C2([H])C([H])([H])C3([H])C([H])=C4C(C5C(=C6C([H])=C([H])C(C([H])([H])[H])(C([H])([H])C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])OC6=C(C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])C=5OC24C1(C([H])([H])C([H])=C(C(=O)O[H])C([H])([H])[H])C3=O)O[H])=O
InChi Key
GEZHEQNLKAOMCA-RRZNCOCZSA-N
InChi Code
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
Chemical Name
(Z)-4-[(1S,2S,8R,17S,19R)-12-hydroxy-8,21,21-trimethyl-5-(3-methylbut-2-enyl)-8-(4-methylpent-3-enyl)-14,18-dioxo-3,7,20-trioxahexacyclo[15.4.1.02,15.02,19.04,13.06,11]docosa-4(13),5,9,11,15-pentaen-19-yl]-2-methylbut-2-enoic acid
Synonyms
ß-Guttiferrin; ß-Guttiferrin; ß-Guttilactone; Cambogic acid; Guttatic acid; 2752-65-0; (-)-Gambogic Acid; R-gambogic acid; B''-Guttiferin; Gambogic-acid; beta-Guttiferin; Guttic acid
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: ~100 mg/mL (159 mM)
Water: <1 mg/mL (slightly soluble or insoluble)
Ethanol: N/A
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (3.98 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (3.98 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 3: 2% DMSO+40% PEG 300+2% Tween 80+ddH2O: 4mg/mL


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 1.5905 mL 7.9523 mL 15.9046 mL
5 mM 0.3181 mL 1.5905 mL 3.1809 mL
10 mM 0.1590 mL 0.7952 mL 1.5905 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

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Biological Data

  • Gambogic Acid

    Gambogic acid neutralizes ability of Bcl-2-family proteins to suppress tBid-induced mitochondrial leakage. Zhai D, et al.Mol Cancer Ther.2008 Jun;7(6):1639-46.


  • Gambogic Acid

    Gambogic acid inhibits binding of FITC-BH3 peptide to anti-apoptotic Bcl-2 family proteins.Mol Cancer Ther.2008 Jun;7(6):1639-46.

  • Gambogic Acid
    Effects of Bcl-2 over-expression or Bax/Bak DKO on Gambogic acid-induced cytotoxicity.Mol Cancer Ther.2008 Jun;7(6):1639-46.
  • Gambogic Acid
    TR-FRET assay confirms gambogic acid competes with BH3 peptide for binding to Bcl-XL.Mol Cancer Ther.2008 Jun;7(6):1639-46.
  • Gambogic Acid
    Gambogic acid induces apoptosis of cancer cells.Mol Cancer Ther.2008 Jun;7(6):1639-46.
  • Gambogic Acid
    Comparison of cytotoxic activity and BH3 peptide displacement activity of Gambogic acid and analogs.Mol Cancer Ther.2008 Jun;7(6):1639-46.
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