AGN 225660
AGN 225660 is a multi-prostanoid receptor antagonist with human IC50 values of 70, 70, 5, 220 and 180 nM for EP1, EP4, TP, DP1, FP. AGN 225660 inhibits secretion of RANTES, IL-8, MCP-1, IL-12p70, and IL-23. AGN 225660 exhibits good ocular bioavailability and reduces ocular inflammation linked to phacoemulsification surgery and uveitis.
For research use only. We do not sell to patients.
- CAS No.: 1354060-46-0
- Formula: C20H27ClN2O3
- Molecular Weight:378.89
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
TP 5 nM (IC50) |
EP1 70 nM (IC50) |
EP4 70 nM (IC50) |
FP 180 nM (IC50) |
DP1 220 nM (IC50) |
IL-8 |
IL-12 |
IL-23 |
In Vitro
AGN 225660 potently antagonizes pro-inflammatory human recombinant prostanoid receptors (EP1, EP4, TP, DP1, FP) with IC50 values ranging from 5 to 220 nM, and has weak activity at anti-inflammatory receptors (EP2, EP3, IP) with IC50 values ≥1100 nM in HEK-293 transfectants[1].
AGN 225660 (1-10 μM; 24 h) dose-dependently and significantly inhibits TNFα-induced IL-8, MCP-1, and RANTES secretion in human monocyte-derived
dendritic cells[1].
AGN 225660 (1-10 μM; 18-20 h) significantly inhibits LPS (HY-D1056)-induced IL-12p70 and IL-23 secretion by 65-75% in human monocyte-derived
dendritic cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
AGN 225660 (0.1-0.3%; topical) completely inhibits leukocyte infiltration in Arachidonic acid (HY-109590)-induced uveitis in Dutch Belted rabbits at the 0.3% dose[1].
AGN 225660 (0.3%; topical; twice daily) reduces phacoemulsification surgery-induced anterior chamber flare by ~50% in African green monkeys[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:LEW/SsNHsd (male, 180-200 g, LPS-induced)[1]
-
Dosage:1%
-
Administration:topical
-
Result:Reduced aqueous humor protein concentration to <20 mg/mL vs vehicle control.
Significantly reduced leukocyte infiltration into the anterior chamber.
-
Animal Model:Dutch Belted pigmented (male/female, 2.5-3 kg, Arachidonic acid-induced)[1]
-
Dosage:0.1%; 0.3%
-
Administration:topical
-
Result:Produced marginal inhibition of leukocyte infiltration at 0.1% dose.
Totally inhibited arachidonic acid-induced leukocyte infiltration into the anterior chamber at 0.3% dose.
-
Animal Model:Chlorocebus sabaeus (8 males, 7 females, 3.2-6.7 kg, phacoemulsification surgery-induced)[1]
-
Dosage:0.3%
-
Administration:topical; twice daily
-
Result:Reduced laser flare responses by ~50% relative to PBS-treated controls on day 1 post-surgery.
Chemical Information
-
CAS No. 1354060-46-0
-
Molecular Weight 378.89
-
Formula C20H27ClN2O3
-
SMILES
O=C(CCC1=NN(CC2=CC(Cl)=CC=C2OCC(CC)CC)C(C)=C1)O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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.
-
Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
-
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)
AGN 225660 Related Classifications
HY-183037 Related Classifications
Powered by Bioz