货号:A200522
同义名:
藤黄酸 A
/ Beta-Guttiferrin; GA
Gambogic Acid激活半胱天冬酶,EC50 值为 0.78-1.64 μM,并与 Bcl-XL、Bcl-2、Bcl-W、Bcl-B、Bfl-1 和 Mcl-1 竞争性结合,IC50 值分别为 1.47、1.21、2.02、0.66、1.06 和 0.79 μM。
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| Type | HazMat fee for 500 gram (Estimated) |
| Excepted Quantity | USD 0.00 |
| Limited Quantity | USD 15-60 |
| Inaccessible (Haz class 6.1), Domestic | USD 80+ |
| Inaccessible (Haz class 6.1), International | USD 150+ |
| Accessible (Haz class 3, 4, 5 or 8), Domestic | USD 100+ |
| Accessible (Haz class 3, 4, 5 or 8), International | USD 200+ |


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|---|---|---|---|---|---|---|---|
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| 产品名称 | Bax ↓ ↑ | Bcl-2 ↓ ↑ | Bcl-B ↓ ↑ | Bcl-w ↓ ↑ | Bcl-xL ↓ ↑ | Bfl-1 ↓ ↑ | Mcl-1 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| BTSA1 | ✔ | 99%+ | |||||||||||||||||
| HA14-1 |
+
Bcl-2, IC50: 9 μM |
98% | |||||||||||||||||
| Venetoclax |
++++
Bcl-2, Ki: <0.01 nM |
99% | |||||||||||||||||
| Navitoclax | 99%+ | ||||||||||||||||||
| Obatoclax Mesylate |
+++
Bcl-2, Ki: 0.22 μM |
99% | |||||||||||||||||
| ABT-737 |
+++
Bcl-2, EC50: 30.3 nM |
+
Bcl-B, EC50: 1.82 μM |
+++
Bcl-w, EC50: 197.8 nM |
+++
Bcl-xL, EC50: 78.7 nM |
99%+ | ||||||||||||||
| Gambogic Acid |
+
Bfl-1, IC50: 1.06 μM Bcl-2, IC50: 1.21 μM |
++
Bcl-B, IC50: 0.66 μM |
++++
Bcl-w, IC50: 0.02 μM |
+
Bcl-xL, IC50: 1.47 μM |
+
Bfl-1, IC50: 1.06 μM |
++
Mcl-1, IC50: 0.79 μM |
Caspase | 99% HPLC | |||||||||||
| BH3I-1 |
+
BH3-Bcl-xL interaction, Ki: 2.4 μM |
99% | |||||||||||||||||
| A-1331852 |
++++
Bcl-xL, Ki: <0.01 nM |
99%+ | |||||||||||||||||
| A-1210477 |
++++
MCL-1, IC50: 26.2 nM |
99%+ | |||||||||||||||||
| Maritoclax | ✔ | 97% | |||||||||||||||||
| TW-37 |
+++
Bcl-2, Ki: 0.29 μM |
+
Bcl-xL, Ki: 1.11 μM |
+++
Mcl-1, Ki: 0.26 μM |
98% | |||||||||||||||
| UMI-77 |
++
Mcl-1, Ki: 490 nM |
97% | |||||||||||||||||
| (R)-(-)-Gossypol acetic acid |
++
Bcl-2, Ki: 0.32 μM |
++
Bcl-xL, Ki: 0.48 μM |
+++
Mcl-1, Ki: 0.18 μM |
99% | |||||||||||||||
| Sabutoclax |
++
Bfl-1, IC50: 0.62 μM Bcl-2, IC50: 0.32 μM |
++
Bcl-xL, IC50: 0.31 μM |
++
Bfl-1, IC50: 0.62 μM |
+++
Mcl-1, IC50: 0.20 μM |
98% | ||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 靶点 |
|
| 描述 | 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. |
| 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. |
| 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. |
| 计算器 | ||||
| 存储液制备 | ![]() |
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 |
|
| CAS号 | 2752-65-0 |
| 分子式 | C38H44O8 |
| 分子量 | 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 |
| MDL No. | MFCD16878985 |
| 别名 | 藤黄酸 A ;Beta-Guttiferrin; GA; Cambogic acid; Beta-Guttilactone; B-Guttiferrin; β-Guttiferin; Guttic Acid; Guttatic Acid |
| 运输 | 蓝冰 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Sealed in dry, 2-8°C |
| 溶解方案 |
DMSO: 80 mg/mL(127.24 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
|
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