Ginnalin A
(Synonyms: Acertannin)
Ginnalin A (Acertannin) is an inducer of apoptosis and an activator of Nrf2. Ginnalin A binds to the Kelch sub-pocket of Keap1, disrupting the Keap1-Nrf2 interaction, which promotes the nuclear translocation of Nrf2 and the expression of antioxidant genes. Ginnalin A induces apoptosis and inhibits proliferation in hepatocellular carcinoma and other cancer cells; it also exhibits cytotoxicity against leukemia and melanoma cells and suppresses the growth of colon cancer. Furthermore, Ginnalin A acts as a free radical scavenger and a chelator of ferrous/cuprous ions. It inhibits TRAIL-induced apoptosis and oxidative/nitrosative stress in keratinocytes, suppresses tyrosinase activity and melanogenesis-related genes in melanoma cells, competitively inhibits collagenase (reducing MMP-13 and MMP-9 levels), and binds to amyloid-β monomers to inhibit their aggregation. Ginnalin A is a potential subject of research for hepatocellular carcinoma, colon cancer, various other cancers, Parkinson’s disease, Alzheimer’s disease, and skin aging.
For research use only. We do not sell to patients.
- CAS No.: 76746-56-0
- Formula: C20H20O13
- Molecular Weight:468.37
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Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Biological Activity
Description
Ginnalin A (Acertannin) is an inducer of apoptosis and an activator of Nrf2. Ginnalin A binds to the Kelch sub-pocket of Keap1, disrupting the Keap1-Nrf2 interaction, which promotes the nuclear translocation of Nrf2 and the expression of antioxidant genes. Ginnalin A induces apoptosis and inhibits proliferation in hepatocellular carcinoma and other cancer cells; it also exhibits cytotoxicity against leukemia and melanoma cells and suppresses the growth of colon cancer. Furthermore, Ginnalin A acts as a free radical scavenger and a chelator of ferrous/cuprous ions. It inhibits TRAIL-induced apoptosis and oxidative/nitrosative stress in keratinocytes, suppresses tyrosinase activity and melanogenesis-related genes in melanoma cells, competitively inhibits collagenase (reducing MMP-13 and MMP-9 levels), and binds to amyloid-β monomers to inhibit their aggregation. Ginnalin A is a potential subject of research for hepatocellular carcinoma, colon cancer, various other cancers, Parkinson’s disease, Alzheimer’s disease, and skin aging[1][2][3][4][5][6].
IC50 & Target
[6]|
MMP13 |
MMP-9 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HCT-116 | IC50 |
24.8 μM
|
Antiproliferative activity against human HCT116 colon cancer cells.
Antiproliferative activity against human HCT116 colon cancer cells.
|
31795145 |
| SW480 | IC50 |
22.0 μM
|
Antiproliferative activity against human SW480 colon cancer cells.
Antiproliferative activity against human SW480 colon cancer cells.
|
31795145 |
| SW-620 | IC50 |
39.7 μM
|
Antiproliferative activity against human SW620 colon cancer cells.
Antiproliferative activity against human SW620 colon cancer cells.
|
31795145 |
| SH-SY5Y | IC50 |
70 g/mL
|
Antiproliferative activity against human SH-SY5Y and mouse N18TG2 neuroblastoma cells with IC50 values ranging from 70 to 150 g/mL.
Antiproliferative activity against human SH-SY5Y and mouse N18TG2 neuroblastoma cells with IC50 values ranging from 70 to 150 g/mL.
|
37205316 |
| A-431 | IC50 |
49.5 μM
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Cytotoxicity against human A431 epidermoid carcinoma cells assessed as viability reduction incubated 48 hrs by MTT assay.
Cytotoxicity against human A431 epidermoid carcinoma cells assessed as viability reduction incubated 48 hrs by MTT assay.
|
36432019 |
In Vitro
Anti-cancerApoptosisCell Cycle RegulationOxidative StressPyroptosisAβ/Tau/α-Synuclein AggregationInnate ImmunityOthers
Anti-cancer
Ginnalin A inhibits the proliferation of SH-SY5Y and N18TG2 neuroblastoma cells, with IC50 values of 70 g/mL to 150 g/mL[2].
Ginnalin A exhibits in vitro cytotoxicity against L1210, HL-60, K562, and B16F10 cancer cell lines in the MTT assay[2].
Ginnalin A (2.5-50 μM; 24 h) shows low cytotoxicity in SH-SY5Y cells, with cell viability remaining at 91.1% at 20 μM[4].
Ginnalin A (10-20 μM; 24 h) pretreatment protects SH-SY5Y cells against 6-OHDA-induced cytotoxicity, restoring viability to 81.8-85.3% at 10-20 μM[4].
Ginnalin A (0-100 µM; 48 h) has a lower IC50 (49.5 µM) in A431 epidermoid carcinoma cells than in NTERT1 keratinocytes (99.8 µM) in the MTT assay[6].
Ginnalin A (12.5 µM; 48 h) reduces MMP-13 protein expression in A431 cells by 49.9%[6].
Ginnalin A (12.5 µM; 48 h) increases type I collagen and reduces MMP-9 protein expression by 23.7% in A431 cells[6].
Ginnalin A exhibits in vitro cytotoxicity against L1210, HL-60, K562, and B16F10 cancer cell lines in the MTT assay[2].
Ginnalin A (2.5-50 μM; 24 h) shows low cytotoxicity in SH-SY5Y cells, with cell viability remaining at 91.1% at 20 μM[4].
Ginnalin A (10-20 μM; 24 h) pretreatment protects SH-SY5Y cells against 6-OHDA-induced cytotoxicity, restoring viability to 81.8-85.3% at 10-20 μM[4].
Ginnalin A (0-100 µM; 48 h) has a lower IC50 (49.5 µM) in A431 epidermoid carcinoma cells than in NTERT1 keratinocytes (99.8 µM) in the MTT assay[6].
Ginnalin A (12.5 µM; 48 h) reduces MMP-13 protein expression in A431 cells by 49.9%[6].
Ginnalin A (12.5 µM; 48 h) increases type I collagen and reduces MMP-9 protein expression by 23.7% in A431 cells[6].
Anti-cancer
Apoptosis
Ginnalin A (Acertannin) induces apoptosis in Hep3B hepatocellular carcinoma cells and exhibits activity against HCT116, SW480, and SW620 colon cancer cells, with IC50 values of 24.8, 22.0, and 39.7 μM, respectively[1].
Ginnalin A induces the expression of apoptotic genes in Hep-3B hepatocellular carcinoma cells and upregulates CASP-3, CASP-8, CASP-9, CYCS, and p53[2].
Ginnalin A upregulates CASP-3, CASP-8, CASP-9, CYCS, FAS, and p53 in MDA-MB-231 cells, and upregulates CASP-9 and p53 while downregulating BCL-2 in MCF-7 breast cancer cells[2].
Ginnalin A induces the expression of apoptotic genes in Hep-3B hepatocellular carcinoma cells and upregulates CASP-3, CASP-8, CASP-9, CYCS, and p53[2].
Ginnalin A upregulates CASP-3, CASP-8, CASP-9, CYCS, FAS, and p53 in MDA-MB-231 cells, and upregulates CASP-9 and p53 while downregulating BCL-2 in MCF-7 breast cancer cells[2].
Anti-cancer
Apoptosis
Cell Cycle Regulation
Anti-cancer
Cell Cycle Regulation
Anti-cancer
Cell Cycle Regulation
Oxidative Stress
Anti-cancer
Oxidative Stress
Ginnalin A inhibits the expression of tyrosinase and melanogenesis genes in B16F10 mouse melanoma cells and alleviates oxidative stress[2].
Anti-cancer
Pyroptosis
Ginnalin A (24 h) pretreatment attenuates 6-OHDA-induced membrane damage in SH-SY5Y cells, manifesting as reduced LDH release[4].
Apoptosis
Oxidative Stress
Aβ/Tau/α-Synuclein Aggregation
Ginnalin A directly binds to Aβ and inhibits Aβ aggregation in a dose-dependent manner while reversing fibril formation, with its binding sites localized to Aβ residues 17-21, 35, and 38[5].
Innate Immunity
Apoptosis
Oxidative Stress
Oxidative Stress
Ginnalin A scavenges DPPH radicals and superoxide[2].
Ginnalin A activates the Nrf2 signaling pathway in 6-OHDA-exposed SH-SY5Y neuroblastoma cells, increasing NQO1, HO-1, GCLC, and glutathione[2].
Ginnalin A reduces H2O2-induced toxicity and increases the viability of HaCaT keratinocytes[2].
Ginnalin A activates the Nrf2 signaling pathway in 6-OHDA-exposed SH-SY5Y neuroblastoma cells, increasing NQO1, HO-1, GCLC, and glutathione[2].
Ginnalin A reduces H2O2-induced toxicity and increases the viability of HaCaT keratinocytes[2].
Oxidative Stress
Anti-cancer
Ginnalin A (10-20 μM; 24 h) does not increase H2O2 levels in SH-SY5Y culture medium[4].
Ginnalin A (10-20 μM; 24 h) pretreatment reduces 6-OHDA-induced intracellular ROS in SH-SY5Y cells, by 61.2% at 10 μM and by 88.5% at 20 μM[4].
Ginnalin A (10-20 μM; 24 h) pretreatment upregulates Nrf2/ARE target gene mRNA in SH-SY5Y cells[4].
Ginnalin A (10-20 μM) pretreatment increases the protein levels of NQO1, HO-1, GCLC, and nuclear Nrf2 in SH-SY5Y cells, with NQO1 increasing more than 4.6-fold at 20 μM[4].
Ginnalin A (20 μM; 24 h) promotes Nrf2 nuclear translocation in SH-SY5Y cells[4].
Ginnalin A (20 μM) pretreatment increases total GSH in SH-SY5Y cells to 229.0% of the control group[4].
Ginnalin A (10-20 μM) protection and ROS reduction in SH-SY5Y cells are abolished by Nrf2 knockdown[4].
Ginnalin A (10-20 μM; 24 h) pretreatment reduces 6-OHDA-induced intracellular ROS in SH-SY5Y cells, by 61.2% at 10 μM and by 88.5% at 20 μM[4].
Ginnalin A (10-20 μM; 24 h) pretreatment upregulates Nrf2/ARE target gene mRNA in SH-SY5Y cells[4].
Ginnalin A (10-20 μM) pretreatment increases the protein levels of NQO1, HO-1, GCLC, and nuclear Nrf2 in SH-SY5Y cells, with NQO1 increasing more than 4.6-fold at 20 μM[4].
Ginnalin A (20 μM; 24 h) promotes Nrf2 nuclear translocation in SH-SY5Y cells[4].
Ginnalin A (20 μM) pretreatment increases total GSH in SH-SY5Y cells to 229.0% of the control group[4].
Ginnalin A (10-20 μM) protection and ROS reduction in SH-SY5Y cells are abolished by Nrf2 knockdown[4].
Others
Ginnalin A (100 mg tissue; 5-20 min) is the most abundant in GT Toona sinensis leaf teas (TLTs), with a relative abundance 3.06 times higher than that in BT, and shows intermediate abundance in RT (RT/BT = 2.54)[3].
Ginnalin A (10-20 μM; 24 h) cannot reverse established 6-OHDA-induced injury in SH-SY5Y cells when added after injury[4].
Ginnalin A (50-400 µM) inhibits collagenase activity in a concentration-dependent manner, with an inhibition rate of 93.7% at 400 µM in a cell-free colorimetric assay[6].
Ginnalin A (0-400 µM; preincubation at room temperature for 15 min; kinetic reading for 30 min) is a competitive inhibitor of collagenase, increasing Km from 2.890 mM to 4.957 mM while maintaining Vmax at nearly 0.078 mM/min[6].
Ginnalin A (100-400 µM; exposure at 37°C for 30 days) reduces glycation-induced type I collagen cross-linking by 40-47.9% at 100-400 µM[6].
Ginnalin A (10-20 μM; 24 h) cannot reverse established 6-OHDA-induced injury in SH-SY5Y cells when added after injury[4].
Ginnalin A (50-400 µM) inhibits collagenase activity in a concentration-dependent manner, with an inhibition rate of 93.7% at 400 µM in a cell-free colorimetric assay[6].
Ginnalin A (0-400 µM; preincubation at room temperature for 15 min; kinetic reading for 30 min) is a competitive inhibitor of collagenase, increasing Km from 2.890 mM to 4.957 mM while maintaining Vmax at nearly 0.078 mM/min[6].
Ginnalin A (100-400 µM; exposure at 37°C for 30 days) reduces glycation-induced type I collagen cross-linking by 40-47.9% at 100-400 µM[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[4]
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Cell Line:SH-SY5Y human neuroblastoma cells
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Concentration:2.5, 5, 10, 20, and 50 μM
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Incubation Time:24 h
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Result:At 20 μM, SH-SY5Y cell viability was 91.1% of control.
At 10 μM, little toxicity was observed.
Cell Viability Assay[4]
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Cell Line:SH-SY5Y human neuroblastoma cells
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Concentration:10 and 20 μM (pretreatment); 100 μM (6-OHDA)
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Incubation Time:24 h (pretreatment); 24 h (6-OHDA)
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Result:6-OHDA alone reduced viability to 58.9%.
Viability recovered to 81.8% at 10 μM and 85.3% at 20 μM.
Real Time qPCR[4]
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Cell Line:SH-SY5Y human neuroblastoma cells
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Concentration:10 and 20 μM; 100 μM (6-OHDA)
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Incubation Time:24 h; 24 h (6-OHDA)
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Result:mRNA expression of Nrf2, NQO1, HO-1, and GCLC was upregulated at both 10 and 20 μM.
Immunofluorescence[4]
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Cell Line:SH-SY5Y human neuroblastoma cells
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Concentration:20 μM
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Incubation Time:24 h
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Result:Cytosolic Nrf2 expression was increased, and Nrf2 translocation into SH-SY5Y cell nuclei was promoted.
Western Blot Analysis[6]
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Cell Line:A431 epidermoid carcinoma cells
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Concentration:12.5 µM
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Incubation Time:48 h
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Result:MMP-13 protein expression was inhibited by 49.9% relative to the control after exposure at 12.5 µM.\nCOL1A1 protein expression increased relative to the control.
MMP-9 protein expression decreased by 23.7% relative to the control after exposure at 12.5 µM.
Related Protocols :
- RNA extraction experimental
- Mitochondrial membrane-potential fluorescent assay
- Mammalian live/dead viability and cytotoxicity staining
- Annexin V plus membrane-impermeant dye apoptosis staining
- Liver Cancer Modeling
- Amyloid: Congo Red Amyloid Staining
- Cell Viability Determination by MTT Colorimetric Assay
- Alzheimer’s Disease Modeling
- Cytoplasmic-Nuclear Fractionated Protein Extraction
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Cell Cytotoxicity Assay
- Mitochondrial membrane-potential and mitochondrial mass staining
- Apoptosis Solutions
Chemical Information
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CAS No. 76746-56-0
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Molecular Weight 468.37
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Formula C20H20O13
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SMILES
O(C(=O)C1=CC(O)=C(O)C(O)=C1)[C@@H]2[C@@H](O)[C@H](O)[C@@H](COC(=O)C3=CC(O)=C(O)C(O)=C3)OC2
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Synonyms
Acertannin
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Structure Classification
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
Select Batch:
Purity:
99.98%
Assay:
99.98%
ee.:
99.98%
References
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Ginnalin A Related Classifications
HY-N17603 Related Classifications
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