Cantharidic acid
Cantharidic acid is a Cantharidin (HY-N0209) analog, anticancer agent, and selective Ser/thr phosphatase 1 and 2A inhibitor. Cantharidic acid induces ROS, Mitochondrial dysfunction, LDH release, cell cycle arrest, and Apoptosis. Cantharidic acid decreases Nrf2, HO-1, and GPX4, and reduces PCNA, MMP2, and MMP9. Cantharidic acid can be used in research on colorectal cancer, hepatocellular carcinoma, oral squamous cell carcinoma, and adenocarcinoma.
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- CAS. Nr.: 28874-45-5
- Formel: C10H14O5
- Molecular Weight:214.22
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
Cantharidic acid is a Cantharidin (HY-N0209) analog, anticancer agent, and selective Ser/thr phosphatase 1 and 2A inhibitor. Cantharidic acid induces ROS, Mitochondrial dysfunction, LDH release, cell cycle arrest, and Apoptosis. Cantharidic acid decreases Nrf2, HO-1, and GPX4, and reduces PCNA, MMP2, and MMP9. Cantharidic acid can be used in research on colorectal cancer, hepatocellular carcinoma, oral squamous cell carcinoma, and adenocarcinoma[1][2][3][4][5].
IC50 & Target
[1]|
MMP-2 |
MMP-9 |
HO-1 |
GPX4 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HCT-116 | IC50 |
10 μM
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Antiproliferative activity against human HCT116 colorectal cancer cells assessed as 50% inhibition of viability after 48 hrs by CCK-8 assay.
Antiproliferative activity against human HCT116 colorectal cancer cells assessed as 50% inhibition of viability after 48 hrs by CCK-8 assay.
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41589402 |
| HN12 | IC50 |
3.26-15.7 μM
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Antiproliferative activity against human OSCC cell lines UMSCC-1, UMSCC-23, HN12, and A-253 assessed as viability reduction incubated 24 hrs by ATP-based luminescent CellTiter-Glo proliferation assay.
Antiproliferative activity against human OSCC cell lines UMSCC-1, UMSCC-23, HN12, and A-253 assessed as viability reduction incubated 24 hrs by ATP-based luminescent CellTiter-Glo proliferation assay.
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25425581 |
In Vitro
Anti-cancerApoptosisCell Cycle RegulationOthers
Anti-cancer
Cantharidic acid (1.25-40 μM for FHC cells; 5-20 μM for SW480/HCT116 cells; 24-48 h) selectively reduces the viability of SW480 and HCT116 colorectal cancer cells, with an IC50 of 10 μM against HCT116 cells at 48 h, while having no obvious effect on the viability of FHC cells[1].
Cantharidic acid (5-20 μM) reduces colony formation in SW480 and HCT116 colorectal cancer cells[1].
Cantharidic acid (5-20 μM) reduces PCNA, MMP2, and MMP9 protein levels in SW480 and HCT116 colorectal cancer cells[1].
Cantharidic acid (5-20 μM; 24 h) disrupts the cell membrane integrity of SW480 and HCT116 colorectal cancer cells and increases LDH release[1].
Cantharidic acid (5-40 µM; 24 h) inhibits the proliferation of SK-Hep-1 and Huh-7 HCC cells, with 10 µM causing >59% reduction in viability and 40 µM being the most toxic concentration tested[2].
Cantharidic acid (24 h) inhibits the proliferation of UMSCC-1, UMSCC-23, HN12, and A-253 OSCC cells, with 24 h IC50 values of 3.26-15.7 µM[3].
Cantharidic acid (1-25 µM; 24-72 h) reduces LoVo cell viability in a time- and concentration-dependent manner, with 25 µM exposure for 24 h causing 40-60% viability loss and 5-10 µM exposure for 72 h causing 40% cell death[4].
Cantharidic acid (5-20 μM) reduces colony formation in SW480 and HCT116 colorectal cancer cells[1].
Cantharidic acid (5-20 μM) reduces PCNA, MMP2, and MMP9 protein levels in SW480 and HCT116 colorectal cancer cells[1].
Cantharidic acid (5-20 μM; 24 h) disrupts the cell membrane integrity of SW480 and HCT116 colorectal cancer cells and increases LDH release[1].
Cantharidic acid (5-40 µM; 24 h) inhibits the proliferation of SK-Hep-1 and Huh-7 HCC cells, with 10 µM causing >59% reduction in viability and 40 µM being the most toxic concentration tested[2].
Cantharidic acid (24 h) inhibits the proliferation of UMSCC-1, UMSCC-23, HN12, and A-253 OSCC cells, with 24 h IC50 values of 3.26-15.7 µM[3].
Cantharidic acid (1-25 µM; 24-72 h) reduces LoVo cell viability in a time- and concentration-dependent manner, with 25 µM exposure for 24 h causing 40-60% viability loss and 5-10 µM exposure for 72 h causing 40% cell death[4].
Anti-cancer
Apoptosis
Apoptosis
Cantharidic acid (5-20 µM; 24 h) increases the percentage of apoptosis in SK-Hep-1 cells[2].
Cantharidic acid (5-20 µM) activates caspase-3, caspase-8, and caspase-9 as well as PARP cleavage in SK-Hep-1 cells in a concentration-dependent manner[2].
Cantharidic acid increases Caspase-3-like activity in LoVoDx cells[4].
Cantharidic acid (5-20 µM) activates caspase-3, caspase-8, and caspase-9 as well as PARP cleavage in SK-Hep-1 cells in a concentration-dependent manner[2].
Cantharidic acid increases Caspase-3-like activity in LoVoDx cells[4].
Cell Cycle Regulation
Cantharidic acid (20 µM; 24 h) increases the subG1 and S phase cell populations and decreases the G2/M and G1 phase cell populations in SK-Hep-1 cells[2].
Others
Cantharidic acid (5-20 µM) increases p-ERK, p-JNK, and p-p38 in SK-Hep-1 cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
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Cell Line:human hepatocellular carcinoma SK-Hep-1 and Huh-7 cell lines
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Concentration:5, 10, 20, 40 µM
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Incubation Time:24 h
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Result:Suppressed SK-Hep-1 and Huh-7 cell proliferation in a dose-dependent manner.
At 10 µM, reduced cell viability by more than 59%; 40 µM was the most toxic concentration tested.
Apoptosis Analysis[2]
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Cell Line:SK-Hep-1 cells
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Concentration:5, 10, 20 µM
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Incubation Time:24 h
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Result:The percentage of apoptotic cells significantly increased with increasing Cantharidic acid concentration.
Cell Cycle Analysis[2]
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Cell Line:SK-Hep-1 cells
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Concentration:20 µM
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Incubation Time:24 h
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Result:The proportion of cells in subG1 and S phase significantly increased after 20 µM Cantharidic acid, with a corresponding reduction in cells in G2/M and G1 phases.
In Vivo
Anti-cancerApoptosisCardiovascular Regulation
Anti-cancer
Apoptosis
Cantharidic acid (0.4 mg/kg; intraperitoneal injection; daily; 21 days) inhibits the progression of colorectal cancer xenograft tumors in nude mice, reduces tumor volume and mass, inhibits proliferation, and promotes apoptosis[1].
Cardiovascular Regulation
Cantharidic acid (3 mg/kg; intragastric administration; single dose) does not induce acute cardiotoxic electrophysiological, biochemical, or histopathological changes in C57BL/6J mice[5].
Cantharidic acid (1.5 mg/kg; intragastric administration; once daily; for 14 consecutive days) does not produce subacute cardiotoxicity in C57BL/6J mice[5].
Cantharidic acid (1.5 mg/kg; intragastric administration; once daily; for 14 consecutive days) does not produce subacute cardiotoxicity in C57BL/6J mice[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (male, 4-6 weeks old, 15-20 g)[1]
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Dosage:0.4 mg/kg
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Administration:intraperitoneal injection; once daily; 21 consecutive days
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Result:Intraperitoneal injection of CA (0.4 mg/kg) markedly decreased tumor volume and mass.
TUNEL staining revealed that the TUNEL-positive cell ratio was notably increased in tumor tissues following CA administration, whereas TBHQ decreased the TUNEL-positive ratio.
Immunohistochemical findings revealed that CA administration substantially decreased Ki-67 positivity in tumor tissues, whereas TBHQ reversed the effect of CA.
Significantly downregulated the protein levels of Nrf2, HO-1, and GPX4 in tumor tissues, whereas TBHQ increased these levels.
DHE staining revealed a significant increase in ROS levels in tumor tissues after CA injection, whereas TBHQ administration reduced them.
In addition, injection of CA resulted in a remarkable reduction in MT-ATP6 levels in tumor tissues, whereas injection of TBHQ attenuated the effect of CA.
Notably, injection of CA markedly decreased MT-ATP6 and MFN1 protein levels and increased the DRP1 level in tumor tissues, but TBHQ injection reversed this phenomenon.
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Animal Model:C57BL/6J (male, 20 g)[5]
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Dosage:3 mg/kg
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Administration:i.g.; single dose
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Result:Mice receiving 3 mg/kg CTA showed no significant alterations in any measured electrophysiological parameters relative to controls.
CTA administration did not affect cardiac NKA activity, serum CK-MB and LDH levels, or histopathology.
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Animal Model:C57BL/6J (male, 20 g)[5]
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Dosage:1.5 mg/kg
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Administration:i.g.; once daily; 14 consecutive days
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Result:CTA-treated mice showed normal electrophysiology, with unchanged heart rate, QRS, QTc, JT, PR, and RR intervals.
Cardiac NKA activity was unchanged, and serum CK-MB and LDH levels were not elevated compared with vehicle.
No histopathological lesions or fibrosis were observed.
Related Protocols :
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Flow cytometric DNA-content cell-cycle staining
- PCNA Immunodetection Proliferation Assay
- Annexin V plus membrane-impermeant dye apoptosis staining
- ROS/oxidative-stress fluorescent staining
- BrdU Incorporation Assay
- Mitochondrial membrane-potential and mitochondrial mass staining
- Apoptosis Solutions
- Protocol for Cell Cycle
- Ferroptosis Solutions
- Liver Cancer Modeling
Chemical Information
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CAS. Nr. 28874-45-5
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Molecular Weight 214.22
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Formel C10H14O5
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SMILES
OC([C@@]([C@@]1(C)C(O)=O)([C@@H]2O[C@H]1CC2)C)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Select Batch:
Reinheit:
99.98%
Assay:
99.98%
ee.:
99.98%
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Molaritätsrechner
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
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Verdünnungsrechner
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Cantharidic acid Related Classifications
HY-137135 Related Classifications
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Keywords
- Cantharidic acid
- 28874-45-5
- Drug Derivative
- Reactive Oxygen Species (ROS)
- Mitochondrial Metabolism
- Lactate Dehydrogenase
- Apoptosis
- Keap1-Nrf2
- Heme Oxygenase (HO)
- Glutathione Peroxidase
- MMP
- Phosphatase
- Drug derivative
- LDH
- Heme Oxygenase
- Matrix metalloproteinases
- ATF4
- ATP production
- Atf4
- C57BL/6J mice
- CHOP
- Chop
- DNA fragmentation
- ER stress
- ERK1/2 counteraction
- GPX4
- HO-1
- JNK1/2 non-contribution
- LDH release
- MMP2
- MMP9
- Nrf2
- P-glycoprotein substrate
- PCNA
- PP1/PP2A inhibitor
- ROS
- UPR
- XBP1 splicing
- adenocarcinoma
- apoptosis inducer
- apoptosis-related gene expression
- caspase-3
- caspase-8
- caspase-9
- caspase/PARP cleavage
- cell-cycle arrest
- colony formation
- colorectal cancer
- eIF2α
- hepatocellular carcinoma
- intrinsic mitochondrial pathway
- invasion
- membrane disruption
- migration
- mitochondrial Cytc release
- mitochondrial dynamics
- mitochondrial dysfunction
- mitochondrial membrane potential
- mtDNA content
- nude mice
- oral squamous cell carcinoma
- oxidative stress
- p38 MAPK activation
- proliferation
- Inhibitor
- inhibitor
- inhibit