1. Signaling Pathways
  2. Metabolic Enzyme/Protease
    Neuronal Signaling
  3. FAAH


Fatty acid amide hydrolase

FAAH (Fatty acid amide hydrolase) is a membrane-bound protein belonging to serine hydrolase family of enzymes.FAAH is responsible for the hydrolysis of a number of important endogenous fatty acid amides, including the endogenous cannabimimetic agent anandamide (AEA), the sleep-inducing compound oleamide, and the putative anti-inflammatory agent palmitoylethanolamide (PEA). FAAH plays a significant role in termination of signalling of a class of bioactive lipids called fatty acid amides (FAAs) both in the central nervous system (CNS) and peripheral tissues.

FAAH belongs to the amidase signature (AS) superfamily and is widely distributed in multicellular eukaryotes. FAAH has a key role in the control of the cannabinoid signaling, through the hydrolysis of the endocannabinoids anandamide and in some tissues 2-arachidonoylglycerol.

FAAH Related Products (47):

Cat. No. Product Name Effect Purity
  • HY-B1227
    Inhibitor 99.76%
    Carprofen is a nonsteroid anti-inflammatory agent, acts as a multi-target FAAH/COX inhibitor, with IC50s of 3.9 μM, 22.3 μM and 78.6 μM for COX-2, COX-1 and FAAH, respectively.
  • HY-14595
    Biochanin A
    Inhibitor 99.01%
    Biochanin A is a naturally occurring fatty acid amide hydrolase (FAAH) inhibitor, which inhibits FAAH with IC50s of 1.8, 1.4 and 2.4 μM for mouse, rat, and human FAAH, respectively.
  • HY-14376
    Inhibitor 99.89%
    Redafamdastat (PF-04457845) is a highly efficacious and selective FAAH inhibitor with IC50 values is 7.2±0.63 nM and 7.4±0.62 nM for hFAAH and rFAAH, respectively.
  • HY-15250
    Inhibitor 99.81%
    JZL195 is a selective and efficacious dual fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) inhibitor with IC50s of 2 and 4 nM, respectively.
  • HY-119283
    Inhibitor 99.73%
    MAGL-IN-5 (CAY10499) is a non-selective lipase inhibitor with IC50 values of 144, 90, and 14 nM for human recombinant monoacylglycerol lipase(MAGL),hormone sensitive lipase(HSL), and fatty acid amide hydrolase(FAAH) respectively.
  • HY-155773
    VU534 is a NAPE-PLD activator, with an EC50 of 0.30 μM. VU534 is dual inhibitors of FAAH and sEH (IC50 of 1.2 μM). VU534 increases efferocytosis in a NAPE-PLD dependent manner. VU534 has the potential for cardiometabolic diseases study [1] .
  • HY-10864
    Inhibitor 98.96%
    URB-597 (KDS-4103) is an orally bioavailable and selective FAAH inhibitor. URB-597 inhibits FAAH activity with an IC50s of approximately 5 nM in rat brain membranes, 0.5 nM in intact rat neurons, 3 nM in human liver microsomes. Antidepressant-like effects. Analgesic activity.
  • HY-14380
    Inhibitor 99.90%
    PF-3845 is a potent, selective, irreversible and orally active inhibitor of fatty acid amide hydrolase (FAAH), with a Ki of 0.23 µM. PF-3845 is a covalent inhibitor that carbamylates FAAH's serine nucleophile. PF-3845 can reduce pain sensation, inflammation, and anxiety/depression without substantial effects on motility or cognition.
  • HY-19740
    BIA 10-2474
    Inhibitor 99.39%
    BIA 10-2474 is an inhibitor of fatty acid amide hydrolase (FAAH) with IC50 values of 50 to 70mg/kg in various rat brain regions.
  • HY-79511
    Inhibitor 98.17%
    FAAH-IN-2 (O-Desmorpholinopropyl Gefitinib) is a potent FAAH(fatty acid amide hydrolase) inhibitor extracted from Patent WO/2008/100977A2.
  • HY-10865
    Inhibitor 98.02%
    LY2183240 is a highly potent blocker of anandamide uptake (IC50= 270 pM; Ki=540 nM). LY2183240 is a potent, covalent inhibitor of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) with an IC50 of 12.4 nM. LY2183240 inactivates FAAH by carbamylation of the enzyme's serine nucleophile. LY2183240 also inhibits several other brain serine hydrolases with IC50s of 5.3, 0.09, 8.2 nM for MAG lipase, bh6 and KIAA1363, respectively .
  • HY-N7062
    Inhibitor 98.99%
    JNJ-1661010 (Takeda-25) a potent and selective fatty acid amide hydrolase (FAAH) inhibitor with IC50s of 34 and 33 nM for rat FAAH and human FAAH, respectively. JNJ-1661010 can cross the blood-brain barrier and used as broad-spectrum analgesics.
  • HY-19636
    Inhibitor 99.87%
    JNJ-42165279 is a FAAH inhibitor with IC50 of 70 ± 8 nM and 313 ± 28 nM for hFAAH and rFAAH, respectively.
  • HY-18544
    Inhibitor 99.89%
    AA38-3 is a serine hydrolase (SH) inhibitor. AA38-3 can inhibit three SHs, ABHD6, ABHD11, and FAAH.
  • HY-N2512
    Inhibitor ≥98.0%
    1-Monomyristin, extracted from Serenoa repens, inhibits the hydrolysis of 2-oleoylglycerol (IC50=32 μM) and fatty acid amide hydrolase (FAAH) activity (IC50=18 μM). 1-Monomyristin shows antibacterial activity against Staphylococcus aureus and Aggregatibacter actinomycetemcomitans and also antifungal activity against Candida albicans.
  • HY-136924
    FP-biotin is a potent organophosphorus toxicant, well-suited for searching for new biomarkers of organophosphorus toxicants exposure. FP-Biotin quantifies FAAH, ABHD6, and MAG-lipase activity. FP-biotin is used for studies with plasma because biotinylated peptides are readily purified by binding to immobilized avidin beads.
  • HY-103337
    Inhibitor ≥98.0%
    N-Arachidonoylserotonin (Arachidonyl serotonin; AA-5-HT) is a potent fatty acid amide hydrolase (FAAH) inhibitor with an IC50 value of 1~12 µM. N-Arachidonoylserotonin acts also as an antagonist of transient receptor potential vanilloid-type 1 (TRPV1) channels (IC50=70~100 nM). N-Arachidonoylserotonin is analgesic in rodents .
  • HY-N2365
    Inhibitor 98.39%
    N-Benzylpalmitamide is a macamide isolated from Lepidium meyenii, acts as an inhibitor of fatty acid amide hydrolase (FAAH).
  • HY-116477
    Inhibitor 99.86%
    URB937 is an orally active and peripherally restricted FAAH inhibitor (IC50=26.8 nM) and increases anandamide levels. URB937 fails to affect FAAH activity in the brain (not penetrate the blood-brain barrier).
  • HY-18080
    SA 47
    Inhibitor ≥99.0%
    SA 47 is a selective and potent inhibitor of fatty acid amide hydrolase (FAAH) and carbamate.