Antitumor agent-225
Antitumor agent-225 is an orally effective and potent HDAC inhibitor with an IC50 value of 4.17 nM. Antitumor agent-225 inhibits HDAC activity by chelating zinc ions through its hydroxamic acid group, downregulates iNOS and COX-2 proteins, and suppresses the production of multiple inflammatory factors induced by LPS (HY-D1056). Antitumor agent-225 can be used for research on cancer and inflammation-related diseases.
For research use only. We do not sell to patients.
- CAS No.: 1338320-95-8
- Formula: C18H18N2O5S
- Molecular Weight:374.41
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
COX-2 |
iNOS |
IL-6 0.01 μM (IC50) |
TNF-α 0.52 μM (IC50) |
PGE2 0.52 μM (IC50) |
In Vitro
Antitumor agent-225 (compound 9) (pretreatment for 1 h, followed by LPS stimulation for 24 h) inhibits nitric oxide (NO) (IC50 = 1.07 µM), IL-6 (IC50 = 0.01 µM), PGE2 (IC50 = 0.52 µM), and TNF-a (IC50 = 0.52 µM) production in RAW 264.7 macrophages[1].
Antitumor agent-225 (0.1-10 µM; pretreatment for 30 min, followed by LPS stimulation for 24 h) significantly downregulates iNOS and COX-2 protein expression in RAW 264.7 macrophages[1].
Antitumor agent-225 inhibits HDAC enzyme activity in HeLa nuclear extracts with an IC50 of 4.17 nM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:RAW 264.7 macrophages
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Concentration:0.1, 0.3, 1, 3, 10 µM
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Incubation Time:30 min pretreatment followed by 24 h stimulation with LPS (25 ng/mL)
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Result:Significantly inhibited LPS-induced iNOS and COX-2 protein expression in a concentration-dependent manner.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar rats (7 weeks old) were injected with Carrageenan to induce acute inflammatory[1]
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Dosage:25 mg/kg
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Administration:p.o.; single dose, administered 1 hour prior to carrageenan injection; 3 h
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Result:Significantly inhibited carrageenan-induced hind-paw edema.
Caused a marked reduction in paw thickness and paw volume compared to the vehicle group.
Chemical Information
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CAS No. 1338320-95-8
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Molecular Weight 374.41
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Formula C18H18N2O5S
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SMILES
O=C(C=CC1=CC=C2C(=C1)CCN2S(=O)(=O)C3=CC=C(OC)C=C3)NO
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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.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)