research use only
Cat.No.S2666
| Related Targets | Dehydrogenase HSP Transferase P450 (e.g. CYP17) PDE phosphatase PPAR Vitamin Carbohydrate Metabolism Mitochondrial Metabolism |
|---|---|
| Other FAAH Inhibitors | Biochanin A URB597 JNJ-42165279 PF-04457845 FAAH-IN-2 JZL195 URB937 JNJ-1661010 BIA 10-2474 LY-2183240 |
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In vitro |
DMSO
: 91 mg/mL
(199.36 mM)
Ethanol : 91 mg/mL Water : Insoluble |
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In vivo |
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| Molecular Weight | 456.46 | Formula | C24H23F3N4O2 |
Storage (From the date of receipt) | |
|---|---|---|---|---|---|
| CAS No. | 1196109-52-0 | Download SDF | Storage of Stock Solutions |
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| Synonyms | N/A | Smiles | C1CN(CCC1CC2=CC(=CC=C2)OC3=NC=C(C=C3)C(F)(F)F)C(=O)NC4=CN=CC=C4 | ||
| Targets/IC50/Ki |
FAAH
230 nM(Ki)
|
|---|---|
| In vitro |
PF-3845 selectively inhibits FAAH by carbamylating FAAH's serine nucleophile. |
| In vivo |
PF-3845 treated mice (10 mg/kg, i.p.) shows rapid and complete inactivation of FAAH in the brain, as judged by competitive activity-based protein profiling (ABPP) with the serine hydrolase-directed probe fluorophosphonate (FP)-rhodamine. This compound shows a long duration of action up to 24 hour. This compound-treated mice also shows dramatic (>10-fold) elevation in brain levels of AEA and other NAEs ( [PEA] and [OEA]). FAAH is AEA-degrading enzyme fatty acid amide hydrolase. This chemical (1–30 mg/kg, oral administration [p.o.]) causes a dose dependent inhibition of mechanical allodynia with a minimum effective dose (MED) of 3 mg/kg (rats are analyzed at 4 hour post dosing with this chemical). At higher doses (10 and 30 mg/kg), this compound inhibits pain responses to an equivalent, if not greater, degree than the nonsteroidal anti-inflammatory drug naproxen (10mg/kg, p.o.). This chemical (10 mg/kg, i.p.) significantly reverses LPS-induced tactile allodynia, but doesn't modify paw withdrawal thresholds in the saline-injected paw. |
References |
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