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Chemical Structure| 2752-65-0 Chemical Structure| 2752-65-0

Structure of Gambogic Acid
CAS No.: 2752-65-0

Chemical Structure| 2752-65-0

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Gambogic acid activates caspases with EC50 of 0.78-1.64 μM and competitively inhibits Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50 of 1.47, 1.21, 2.02, 0.66, 1.06 and 0.79 μM, respectively.

Synonyms: Beta-Guttiferrin; GA; Cambogic acid

4.5 *For Research Use Only !

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Product Citations

Product Citations

Krueger, Nadine ; Kronenberger, Thales ; Xie, Hang ; Rocha, Cheila ; Poehlmann, Stefan ; Su, Haixia , et al.

Abstract: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has forced the development of direct-acting antiviral drugs due to the coronavirus disease 2019 (COVID-19) pandemic. The main protease of SARS-CoV-2 is a crucial enzyme that breaks down polyproteins synthesized from the viral RNA, making it a validated target for the development of SARS-CoV-2 therapeutics. New chem. phenotypes are frequently discovered in natural goods. In the current study, we used a fluorogenic assay to test a variety of natural products for their ability to inhibit SARS-CoV-2 Mpro. Several compounds were discovered to inhibit Mpro at low micromolar concentrations It was possible to crystallize robinetin together with SARS-CoV-2 Mpro, and the X-ray structure revealed covalent interaction with the protease's catalytic Cys145 site. Selected potent mols. also exhibited antiviral properties without cytotoxicity. Some of these powerful inhibitors might be utilized as lead compounds for future COVID-19 research.

Keywords: COVID-19 ; antivirals ; coronavirus ; covalent drugs ; dynamic light scattering ; inhibitors ; main protease ; natural products

Alternative Products

Product Details of Gambogic Acid

CAS No. :2752-65-0
Formula : C38H44O8
M.W : 628.75
SMILES Code : 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
Synonyms :
Beta-Guttiferrin; GA; Cambogic acid
MDL No. :MFCD16878985

Safety of Gambogic Acid

GHS Pictogram:
Signal Word:Danger
Hazard Statements:H301-H315-H319-H335
Precautionary Statements:P261-P301+P310-P305+P351+P338
Class:6.1
UN#:2811
Packing Group:

Isoform Comparison

Biological Activity

Target
  • Bcl-xL

    Bcl-xL, IC50:1.47 μM

  • Bcl-B

    Bcl-B, IC50:0.66 μM

  • Bcl-w

    Bcl-w, IC50:0.02 μM

  • Bfl-1

    Bfl-1, IC50:1.06 μM

In Vitro:

Cell Line
Concentration Treated Time Description References
HCT-15P cells 0.0625-0.5 µM 7 days Inhibited cell proliferation and induced apoptosis Int J Oncol. 2015 Nov;47(5):1663-71.
Human prostate cancer cells (PC3) 100 nM 7-10 hours Inhibited PC3 cell migration Cancer Res. 2008 Mar 15;68(6):1843-50.
HCT-15R cells 0.0625-0.5 µM 9 days Inhibited cell proliferation and induced apoptosis Int J Oncol. 2015 Nov;47(5):1663-71.
Human prostate cancer cells (PC3) 400 nM Inhibited PC3 cell proliferation Cancer Res. 2008 Mar 15;68(6):1843-50.
HCT-15P cells 2 µM 6-24 hours Induced G1 phase cell cycle arrest Int J Oncol. 2015 Nov;47(5):1663-71.
FRT-Cx43 cells 1, 2, 5, 10 µM 10 minutes To validate the inhibitory effect of D-GA on GJIC via Gap-FRAP assay, results showed that D-GA significantly inhibited fluorescence recovery. Front Pharmacol. 2018 Jul 30;9:814.
LN215 cells 20 µM 10 minutes To evaluate the inhibitory effect of D-GA on gap junctional intercellular communication (GJIC), results showed that D-GA significantly inhibited GJIC. Front Pharmacol. 2018 Jul 30;9:814.
CT26 1 µM 12 hours GA induces pyroptosis through the caspase-3/GSDME-dependent pathway, significantly reducing cell viability. Cancers (Basel). 2022 Nov 9;14(22):5505.
HCT116 2 µM 12 hours GA induces pyroptosis through the caspase-3/GSDME-dependent pathway, significantly reducing cell viability. Cancers (Basel). 2022 Nov 9;14(22):5505.
Human prostate cancer PC3 cells 0.125–0.5 µM 12 hours (migration assay) or 24 hours (invasion assay) To investigate the inhibitory effect of gambogic acid on TNF-α-induced migration and invasion of PC3 cells. Results showed that GA significantly inhibited TNF-α-induced migration and invasion of PC3 cells. Acta Pharmacol Sin. 2012 Apr;33(4):531-41.
SW1990 cells 0.0, 0.5, 1.0, 2.0 µM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid effectively inhibited the growth of SW1990 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
MIA PaCa-2 cells 0.0, 0.5, 1.0, 2.0 µM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid effectively inhibited the growth of MIA PaCa-2 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
BxPC-3 cells 0.0, 0.5, 1.0, 2.0 µM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid effectively inhibited the growth of BxPC-3 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
PANC-1 cells 0.0, 0.5, 1.0, 2.0 µM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid effectively inhibited the growth of PANC-1 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
Human umbilical vein endothelial cells (HUVECs) 50-100 nM 12-16 hours Inhibited HUVEC tube formation Cancer Res. 2008 Mar 15;68(6):1843-50.
PPC1 cells 0.5, 1, 2, 5, 10 µM 20 hours To evaluate the apoptosis-inducing effect of Gambogic Acid on PPC1 cells, results showed significant activation of caspase-3. Mol Cancer Ther. 2008 Jun;7(6):1639-46.
Jurkat cells 0.1, 0.2, 0.5, 2, 5 µM 20 hours To evaluate the apoptosis-inducing effect of Gambogic Acid on Jurkat cells, results showed significant induction of apoptosis. Mol Cancer Ther. 2008 Jun;7(6):1639-46.
HL-60 cells 0.1, 0.2, 0.5, 2, 5 µM 20 hours To evaluate the apoptosis-inducing effect of Gambogic Acid on HL-60 cells, results showed significant induction of apoptosis. Mol Cancer Ther. 2008 Jun;7(6):1639-46.
CT26 cells 0, 25, 50 μg/mL 24 hours Evaluate NPs@GA-induced apoptosis, showing NPs@GA has superior capacity to induce tumor cell apoptosis than free GA. Mater Today Bio. 2025 Feb 24;31:101611.
SNU-668 cells 1.41 µM (IC50) 24 hours To assess the cytotoxic effects of GA, it was found that GA induced similar cellular responses, including vacuolation and subsequent cell death. Cell Death Dis. 2019 Feb 22;10(3):187.
SNU-449 cells 1.62 µM (IC50) 24 hours To assess the cytotoxic effects of GA, it was found that GA induced similar cellular responses, including vacuolation and subsequent cell death. Cell Death Dis. 2019 Feb 22;10(3):187.
NCI-H460 cells 2.35 µM (IC50) 24 hours To assess the cytotoxic effects of GA, it was found that GA induced similar cellular responses, including vacuolation and subsequent cell death. Cell Death Dis. 2019 Feb 22;10(3):187.
BxPC-3 cells 1.68 µM (IC50) 24 hours To assess the cytotoxic effects of GA, it was found that GA induced similar cellular responses, including vacuolation and subsequent cell death. Cell Death Dis. 2019 Feb 22;10(3):187.
MDA-MB 435S cells 1.33 µM (IC50) 24 hours To assess the cytotoxic effects of GA, it was found that GA dose-dependently reduced cell viability and induced progressive cytoplasmic vacuolation and subsequent cell death. Cell Death Dis. 2019 Feb 22;10(3):187.
MDA-MB 468 cells 2.35 µM (IC50) 24 hours To assess the cytotoxic effects of GA, it was found that GA dose-dependently reduced cell viability and induced progressive cytoplasmic vacuolation and subsequent cell death. Cell Death Dis. 2019 Feb 22;10(3):187.
MDA-MB 453 cells 1.5 µM (IC50) 24 hours To assess the cytotoxic effects of GA, it was found that GA dose-dependently reduced cell viability and induced progressive cytoplasmic vacuolation and subsequent cell death. Cell Death Dis. 2019 Feb 22;10(3):187.
NCI-H1299 cells 1 µM 24 hours To evaluate the growth inhibitory and apoptosis-inducing effects of gambogic acid on NCI-H1299 cells. Results showed that gambogic acid significantly inhibited cell growth and induced apoptosis. Br J Cancer. 2014 Jan 21;110(2):341-52.
NCI-H460 cells 4 µM 24 hours To evaluate the growth inhibitory and apoptosis-inducing effects of gambogic acid on NCI-H460 cells. Results showed that gambogic acid significantly inhibited cell growth and induced apoptosis. Br J Cancer. 2014 Jan 21;110(2):341-52.
A549 cells 3.5 µM 24 hours To evaluate the growth inhibitory and apoptosis-inducing effects of gambogic acid on A549 cells. Results showed that gambogic acid significantly inhibited cell growth and induced apoptosis. Br J Cancer. 2014 Jan 21;110(2):341-52.
Human umbilical vein endothelial cells (HUVECs) 40 nM 4 hours Inhibited HUVEC invasion Cancer Res. 2008 Mar 15;68(6):1843-50.
HCT-15R cells 2 µM 6-24 hours Induced G1 phase cell cycle arrest Int J Oncol. 2015 Nov;47(5):1663-71.
BxPC-3 cells 1 µM 24 hours Gambogic acid induced autophagy in BxPC-3 cells, as evidenced by increased LC3-II expression and degradation of P62 protein. Cancer Cell Int. 2019 Jan 5;19:7.
PANC-1 cells 1 µM 24 hours Gambogic acid induced the conversion of LC3-I to LC3-II in PANC-1 cells, increased the number of autophagic vacuoles, and confirmed autophagy through the formation of acidic vesicular organelles (AVOs). Cancer Cell Int. 2019 Jan 5;19:7.
HT-29 human colon cancer cells 0.00, 0.31, 0.62, 1.25, 2.50, 5.00 or 10.00 µM 24, 48 or 72 hours Gambogic acid inhibited the proliferation of HT-29 cells in a dose- and time-dependent manner and induced apoptosis. World J Gastroenterol. 2015 May 28;21(20):6194-205.
U266 cells 0.2 µM 4 hours To assess the effect of GA on the PI3K/Akt/mTOR signaling pathway. The results showed that GA significantly inhibited the phosphorylation of Akt and mTOR in U266 cells under hypoxia. Cancer Sci. 2014 Aug;105(8):1063-70.
Primary monocytes from CML patients 0.58–0.82 µM (IC50) 48 hours Gambogic acid significantly decreased cell viability and induced apoptosis in primary monocytes from CML patients Clin Cancer Res. 2014 Jan 1;20(1):151-63.
K562 cells 0.40 µM (IC50) 48 hours Gambogic acid decreased cell viability in a dose-dependent manner, induced apoptosis and proliferation inhibition Clin Cancer Res. 2014 Jan 1;20(1):151-63.
KBM5-T315I cells 0.35 µM (IC50) 48 hours Gambogic acid decreased cell viability in a dose-dependent manner, induced apoptosis and proliferation inhibition Clin Cancer Res. 2014 Jan 1;20(1):151-63.
KBM5 cells 0.32 µM (IC50) 48 hours Gambogic acid decreased cell viability in a dose-dependent manner, induced apoptosis and proliferation inhibition Clin Cancer Res. 2014 Jan 1;20(1):151-63.
Murine hepatocarcinoma H22 cells 0.4 µM 48 hours To evaluate the effect of GA alone or in combination with proteasome inhibitors on cell viability. Results showed that GA alone had a weak inhibitory effect on cell viability, but when combined with proteasome inhibitors MG132 or MG262, the inhibitory effect was significantly enhanced. Cancer Lett. 2011 Feb 28;301(2):221-8.
Human leukemia K562 cells 0.4 µM 48 hours To evaluate the effect of GA alone or in combination with proteasome inhibitors on cell viability. Results showed that GA alone had a weak inhibitory effect on cell viability, but when combined with proteasome inhibitors MG132 or MG262, the inhibitory effect was significantly enhanced. Cancer Lett. 2011 Feb 28;301(2):221-8.
SKBR3 0 to 10 µM 6 hours Assess the effect of Gambogic Acid on Hsp90-dependent client proteins Proc Natl Acad Sci U S A. 2016 Aug 16;113(33):E4801-9.
Human umbilical vein endothelial cells (HUVECs) 10 nM 7-10 hours Inhibited HUVEC migration Cancer Res. 2008 Mar 15;68(6):1843-50.
U266 cells 0.05–0.2 µM 8 hours To evaluate the effect of GA on hypoxia-induced VEGF expression and secretion. The results showed that GA significantly inhibited VEGF expression and secretion in U266 cells under hypoxia. Cancer Sci. 2014 Aug;105(8):1063-70.
U266 cells 0.025–6.4 µM 8 hours To determine potential cytotoxic and anti-proliferative effects of GA. The results showed that treatment with GA at concentrations above 0.4μM led to a significant dose-dependent inhibition of U266 cell growth under normoxia and hypoxia. Cancer Sci. 2014 Aug;105(8):1063-70.
CHO-TRVb-hTfR1 cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA in cells expressing hTfR1, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
CHO-TRVb-neo cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA in cells without TfR expression, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
HS-SULTAN cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA on malignant hematopoietic cells, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
Human prostate cancer cells (PC3) 400 nM Inhibited PC3 cell proliferation Cancer Res. 2008 Mar 15;68(6):1843-50.
Human prostate cancer cells (PC3) 100 nM 7-10 hours Inhibited PC3 cell migration Cancer Res. 2008 Mar 15;68(6):1843-50.
Human umbilical vein endothelial cells (HUVEC) 40 nM 4 hours Inhibited HUVEC invasion Cancer Res. 2008 Mar 15;68(6):1843-50.
RAJI cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA on malignant hematopoietic cells, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
RAMOS cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA on malignant hematopoietic cells, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
U266 cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA on malignant hematopoietic cells, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
IM-9 cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA on malignant hematopoietic cells, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
HL-60 cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA on malignant hematopoietic cells, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
JURKAT cells 0.3 μM 48 hours To evaluate the cytotoxic effect of GA on malignant hematopoietic cells, results showed that GA at 0.3 μM significantly inhibited cell proliferation and induced apoptosis. Leukemia. 2009 Jan;23(1):59-70.
SW1990 cells 0.0, 0.5, 1.0, 2.0 μM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid inhibited the growth of SW1990 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
MIA PaCa-2 cells 0.0, 0.5, 1.0, 2.0 μM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid inhibited the growth of MIA PaCa-2 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
BxPC-3 cells 0.0, 0.5, 1.0, 2.0 μM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid inhibited the growth of BxPC-3 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
PANC-1 cells 0.0, 0.5, 1.0, 2.0 μM 12, 24, 48 hours To evaluate the effect of gambogic acid on the growth of pancreatic cancer cells. Results showed that gambogic acid inhibited the growth of PANC-1 cells in a dose- and time-dependent manner. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
Human umbilical vein endothelial cells (HUVEC) 50-100 nM 12-16 hours Inhibited HUVEC tube formation Cancer Res. 2008 Mar 15;68(6):1843-50.
Human umbilical vein endothelial cells (HUVEC) 10 nM 7-10 hours Inhibited HUVEC migration Cancer Res. 2008 Mar 15;68(6):1843-50.
SNU-668 cells 1.41 μM 24 hours To assess the cytotoxic effects of GA on different types of cancer cells, it was found that GA induced similar cellular responses, including cytoplasmic vacuolation and subsequent cell death Cell Death Dis. 2019 Feb 22;10(3):187.
SNU-449 cells 1.62 μM 24 hours To assess the cytotoxic effects of GA on different types of cancer cells, it was found that GA induced similar cellular responses, including cytoplasmic vacuolation and subsequent cell death Cell Death Dis. 2019 Feb 22;10(3):187.
NCI-H460 cells 2.35 μM 24 hours To assess the cytotoxic effects of GA on different types of cancer cells, it was found that GA induced similar cellular responses, including cytoplasmic vacuolation and subsequent cell death Cell Death Dis. 2019 Feb 22;10(3):187.
BxPC-3 cells 1.68 μM 24 hours To assess the cytotoxic effects of GA on different types of cancer cells, it was found that GA induced similar cellular responses, including cytoplasmic vacuolation and subsequent cell death Cell Death Dis. 2019 Feb 22;10(3):187.
MDA-MB 435S cells 1.33 μM 24 hours To assess the cytotoxic effects of GA, it was found that GA dose-dependently reduced cell viability and induced cytoplasmic vacuolation and subsequent cell death Cell Death Dis. 2019 Feb 22;10(3):187.
MDA-MB 468 cells 2.35 μM 24 hours To assess the cytotoxic effects of GA, it was found that GA dose-dependently reduced cell viability and induced cytoplasmic vacuolation and subsequent cell death Cell Death Dis. 2019 Feb 22;10(3):187.
MDA-MB 453 cells 1.5 μM 24 hours To assess the cytotoxic effects of GA, it was found that GA dose-dependently reduced cell viability and induced cytoplasmic vacuolation and subsequent cell death Cell Death Dis. 2019 Feb 22;10(3):187.
293T cells 1 µM 5 hours Induced apoptosis, correlated with TfR expression levels Proc Natl Acad Sci U S A. 2005 Aug 23;102(34):12095-100.
T47D cells 2 µM 15 minutes Interfered with TfR internalization, increased cell surface TfR expression Proc Natl Acad Sci U S A. 2005 Aug 23;102(34):12095-100.
Jurkat cells 5 µM 24 hours Induced apoptosis, observed membrane blebbing by electron microscopy Proc Natl Acad Sci U S A. 2005 Aug 23;102(34):12095-100.
Murine hepatocarcinoma H22 cells 0.4 µM 48 hours GA as a single agent inhibited cell viability by less than 20%, but when combined with proteasome inhibitors MG262 or MG132, the inhibitory effect was significantly enhanced. Cancer Lett. 2011 Feb 28;301(2):221-8.
Human leukemia K562 cells 0.4 µM 48 hours GA as a single agent inhibited cell viability by less than 20%, but when combined with proteasome inhibitors MG262 or MG132, the inhibitory effect was significantly enhanced. Cancer Lett. 2011 Feb 28;301(2):221-8.
Normal bone marrow mononuclear cells 0.5, 1, 2 μg/mL 24 hours GA did not affect apoptosis in normal bone marrow cells at low concentration (<2.0 μg/mL). Chin J Cancer Res. 2013 Apr;25(2):183-91.
JeKo-1 cells 0.0625-4 μg/mL 12, 24, 36 hours GA significantly inhibited the growth of JeKo-1 cells in a dose- and time-dependent manner. The maximum GA-induced cytotoxity was evident at 36 hrs exposure to 4 μg/mL GA. Chin J Cancer Res. 2013 Apr;25(2):183-91.
U937 cells 1.0 mg/L 24 hours GA could correct the disrupted distribution of Nup88 in U937 cells and decrease the protein level by inhibiting gene transcription, leading to apoptosis. Acta Pharmacol Sin. 2013 Feb;34(2):191-8.
Primary monocytes from CML patients 0.58–0.82 µmol/L (IC50) 48 hours Gambogic acid significantly inhibited the cell viability of primary monocytes from CML patients with IC50 values of 0.58–0.82 µmol/L Clin Cancer Res. 2014 Jan 1;20(1):151-63.
K562 cells 0.40 µmol/L (IC50) 48 hours Gambogic acid decreased the viability of K562 cells in a dose-dependent manner with an IC50 value of 0.40 µmol/L Clin Cancer Res. 2014 Jan 1;20(1):151-63.
KBM5-T315I cells 0.35 µmol/L (IC50) 48 hours Gambogic acid decreased the viability of KBM5-T315I cells in a dose-dependent manner with an IC50 value of 0.35 µmol/L Clin Cancer Res. 2014 Jan 1;20(1):151-63.
KBM5 cells 0.32 µmol/L (IC50) 48 hours Gambogic acid decreased the viability of KBM5 cells in a dose-dependent manner with an IC50 value of 0.32 µmol/L Clin Cancer Res. 2014 Jan 1;20(1):151-63.

In Vivo:

Species
Animal Model
Administration Dosage Frequency Description References
C57BL/6 mice Matrigel plug model Subcutaneous injection 0.1-0.2 μM Single injection, analyzed after 7 days Inhibited angiogenesis in vivo Cancer Res. 2008 Mar 15;68(6):1843-50.
KMF mice H22 allograft model Intraperitoneal injection 1 mg/kg (GA) and 2 mg/kg (MG132) Once daily for 7 consecutive days To evaluate the inhibitory effect of GA in combination with the proteasome inhibitor MG132 on tumor growth. Results showed that the combination treatment significantly inhibited tumor growth without apparent systemic toxicity. Cancer Lett. 2011 Feb 28;301(2):221-8.
BALB/c nude mice U266 cell xenograft model Intravenous injection 2 mg/kg and 4 mg/kg Once every other day for 14 days To evaluate the anti-tumor and anti-angiogenic activity of GA in vivo. The results showed that GA significantly inhibited tumor growth and angiogenesis, and reduced the expression of HIF-1α and VEGF in tumor tissues. Cancer Sci. 2014 Aug;105(8):1063-70.
BALB/c mice CT26 tumor model Intravenous injection 2 mg/kg and 8 mg/kg Every two days for 11 days GA significantly inhibited tumor growth by inducing GSDME-dependent pyroptosis and enhancing the antitumor immune response. Cancers (Basel). 2022 Nov 9;14(22):5505.
Nude mice KBM5 and KBM5-T315I xenograft model Intraperitoneal injection 3 mg/kg/2 days Every 2 days for 17 days Gambogic acid significantly inhibited the growth of KBM5 and KBM5-T315I xenografts and reduced tumor weight Clin Cancer Res. 2014 Jan 1;20(1):151-63.
SCID mice A549 xenograft model Intravenous injection 3.0 mg/kg Every 2 days for 14 days To evaluate the antitumor effects of gambogic acid combined with cisplatin on A549 xenograft models. Results showed that the combination therapy significantly inhibited tumor growth and induced apoptosis. Br J Cancer. 2014 Jan 21;110(2):341-52.
BALB/c nude mice MDA-MB 435S cell xenograft model Intraperitoneal (i.p.) injections 4 or 8 mg/kg Twice (day 0 and day 2), lasting for 14 days To evaluate the in vivo antitumor effect of GA, it was found that GA dose-dependently reduced tumor size and cellular vacuolation was observed in tumor tissues. Cell Death Dis. 2019 Feb 22;10(3):187.
Balb/c mice CT26 colorectal cancer model Peritumoral injection 5 mg/kg Single injection, observed until day 21 Evaluate the antitumor effect of Gel-NPs@GA, showing significant tumor growth inhibition and immune cell infiltration. Mater Today Bio. 2025 Feb 24;31:101611.
BALB/c nude mice HT-29 cell xenograft model Caudal vein injection 5, 10 or 20 mg/kg Twice weekly for four weeks Gambogic acid significantly inhibited the growth of HT-29 xenograft tumors in a dose-dependent manner. World J Gastroenterol. 2015 May 28;21(20):6194-205.
BALB/c nude mice Pancreatic cancer xenograft model Intraperitoneal injection 8 mg/kg Once every 3 days for 27 days Combination treatment of gambogic acid and chloroquine significantly inhibited the growth of pancreatic cancer xenografts, reduced Ki-67 expression, and increased TUNEL-positive cells. Cancer Cell Int. 2019 Jan 5;19:7.
Balb/c female nude mice Xenograft tumor model of pancreatic cancer Intraperitoneal injection 8 mg/kg (GA), 100 mg/kg (gemcitabine) Once every 3 days for 26 days To evaluate the synergistic effects of gambogic acid combined with gemcitabine in a xenograft tumor model of pancreatic cancer. Results showed that the combination treatment significantly repressed tumor growth with a tumor inhibition rate of 72.9%. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
Balb/c female nude mice Xenograft tumor model of pancreatic cancer Intraperitoneal injection 8 mg/kg Once every 3 days for 26 days To evaluate the synergistic effects of gambogic acid and gemcitabine combination therapy on the xenograft tumor model of pancreatic cancer. Results showed that the combination treatment significantly inhibited tumor growth. J Exp Clin Cancer Res. 2017 Aug 10;36(1):107.
Nude mice KBM5 and KBM5-T315I xenograft model Intraperitoneal injection 3 mg/kg/2 days Every 2 days for 17 days Gambogic acid significantly inhibited the growth of both Bcr-Abl wild-type and Bcr-Abl-T315I mutant xenografts, with significantly reduced tumor weights compared to the vehicle-treated group Clin Cancer Res. 2014 Jan 1;20(1):151-63.
BALB/c nude mice MDA-MB 435S cell xenograft model Intraperitoneal (i.p.) injections 4 or 8 mg/kg Twice (day 0 and day 2), for 14 days To evaluate the in vivo antitumor effect of GA, it was found that GA dose-dependently reduced tumor size and cellular vacuolation was observed in tumor tissues Cell Death Dis. 2019 Feb 22;10(3):187.
KMF mice H22 cell allograft model Intraperitoneal injection 1 mg/kg Once daily for 7 consecutive days Combination treatment with GA and MG132 significantly inhibited tumor growth without apparent systemic toxicity. Cancer Lett. 2011 Feb 28;301(2):221-8.

Protocol

Bio Calculators
Preparing Stock Solutions 1mg 5mg 10mg

1 mM

5 mM

10 mM

1.59mL

0.32mL

0.16mL

7.95mL

1.59mL

0.80mL

15.90mL

3.18mL

1.59mL

Dissolving Methods
Please choose the appropriate dissolution scheme according to your animal administration guide.For the following dissolution schemes, clear stock solution should be prepared according to in vitro experiments, and then cosolvent should be added in turn:

in order to ensure the reliability of the experimental results, the clarified stock solution can be properly preserved according to the storage conditions; The working fluid for in vivo experiment is recommended to be prepared now and used on the same day;

The percentage shown in front of the following solvent refers to the volume ratio of the solvent in the final solution; If precipitation or precipitation occurs in the preparation process, it can be assisted by heating and/or ultrasound.
Protocol 1
Protocol 2

References

 

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