Ir-CA
Ir-CA is an antitumor agent. Ir-CA can accumulate in mitochondria and induces mitochondria dysfunction. Ir-CA induces apoptosis and autophagy. Ir-CA initiates mitophagy and cell cycle arrest to kill Cisplatin (HY-17394)-resistant A549R cells. Ir-CA can effectively inhibit metastasis by inhibiting MMP-2/MMP-9.
For research use only. We do not sell to patients.
- CAS No.: 2870682-93-0
- Formula: C43H35F6IrN5OP
- Molecular Weight:974.95
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Ir-CA shows cytotoxicity against A549, A549R, HLF, BEAS-2B, MCF-7, 4T1 cells with IC50s of 4.4, 4.5, 6.6, 2.3, 2.6, 5.7 μM respectively[1].
Ir-CA is quickly absorbed by the A549R cells (indicated by the red fluorescence after 1 h of incubation)[1].
Ir-CA (10 μM, 2 h) can accumulate in the mitochondria of living A549 and A549R cells (Co-staining experiments of Ir-CA with Mito-Tracker)[1].
Ir-CA (10 μM, 24 h) damages mitochondrial morphology and the mitochondrial function in A549R cells, and induces ROS production[1].
Ir-CA (10 μM, 24 h) induces cell apoptosis in A549R cells via a nonapoptotic/necrotic pathway, and also increases conversion from LC3-I to LC3-II, suggesting the autophagy[1].
Ir-CA (2.5 μM, 24 h) resensitizes the A549R cells to Cisplatin (HY-17394)[1].
Ir-CA (5 μM, 24 h) inhibitS the metastasis of A549R cells via down-regulation of MMPs[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Ir-CA (5 mg/kg, i.p., once every other day for 14 d) inhibits tumor growth in A549 tumor-bearing Balb/c nude mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
- Mitochondrial membrane-potential fluorescent assay
- Annexin V plus membrane-impermeant dye apoptosis staining
- BrdU Incorporation Assay
- Protocol for Cell Cycle
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Flow cytometric DNA-content cell-cycle staining
- Autophagy
- Mitochondrial membrane-potential and mitochondrial mass staining
- Apoptosis Solutions
- Lysosome and acidic-vesicle live-cell staining
- Mitophagy Solutions
- Macroautophagy Solutions
- Orthotopic Cell-Line Xenograft
Chemical Information
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CAS No. 2870682-93-0
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Molecular Weight 974.95
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Formula C43H35F6IrN5OP
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SMILES
CC1=CC2=[N](C=C1)[Ir+3]34([C-]5=C(C=CC=C5)C6=[N]3C=CC=C6)([C-]7=C(C=CC=C7)C8=[N]4C=CC=C8)[N]9=CC=C(CNC(/C=C/C%10=CC=CC=C%10)=O)C=C29.[F-][P+5]([F-])([F-])([F-])([F-])[F-]
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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
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Data Sheet (275 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Hot Topics
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Topics
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Topics Mitophagy: A Central Target in Neurodegenerative Diseases
Mitophagy is a selective form of autophagy that eliminates damaged or dysfunctional mitochondria and thereby preserves mitochondrial quality control, cellular homeostasis, and neuronal survival.
2026-06-18
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Topics When Mitophagy Becomes An Innate Immune Checkpoint
Mitophagy becomes an innate immune checkpoint when selective autophagic removal of damaged mitochondria regulates the availability of mitochondrial danger signals that activate innate immune pathways.
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Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Ir-CA Related Classifications
HY-162344 Related Classifications
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