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.
JZL195 is a selective and efficacious dual FAAH/MAGL inhibitor with IC50 of 13 nM and 19 nM for mouse brain FAAH and MAGL respectively.IC50 value: 13 nM/19 nM (mouse brain FAAH/MAGL) [1]Target: dual FAAH/MAGL inhibitorin vitro: JZL195 shows only modest and incomplete inhibitory activity against NTE (IC50 >5 uM). At higher concentrations, JZL195 inhibited ABHD6 but not any of the other brain serine hydrolases detected in our competitive ABPP assays. JZL195 also inhibited rat and human FAAH and MAGL enzymes with IC50 values in the range of 10–100 nM based on competitive ABPP assays [1].in vivo: A time course analysis of mice given one administration ofJZL195 (20 mg/kg, i.p.) revealed that blockade of FAAH andMAGL lasted at least 10 h as judged by gel-based ABPP or AEAand 2-AG hydrolysis assays [1]. The effect of systemic injections of a range of doses of JZL195 and the pan-cannabinoid receptor agonist WIN55212 were performed 1 day following intraplantar injection of CFA in C57BL/6 mice. JZL195 and WIN55212 both reduced mechanical allodynia and thermal hyperalgesia, and produced catalepsy and sedation in a dose dependent manner. Unlike WIN55212, JZL195 reduced allodynia at doses below those at which side-effects were observed [2].
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[1][2][3].
Dual FAAH/sEH-IN-1 (compound 3) is a high affinity dual sEH (soluble epoxide hydrolase) and FAAH (fatty acid amide hydrolase) inhibitor, with IC50 values of 9.6 and 7 nM, respectively. Dual FAAH/sEH-IN-1 shows antinociception against the inflammatory phase[1].
WWL154, an analog of JZL184 that maintains the SH-reactive p-nitrophenyl carbamate group, is a FAAH-4 inhibitor[1].
N-Benzylpalmitamide is a macamide isolated from Lepidium meyenii, acts as an inhibitor of fatty acid amide hydrolase (FAAH).
FAAH-IN-8 (compound 11) is a competitive inhibitor of FAAH with an IC50 value of 6.7 nM and a Ki value of 5 nM. FAAH-IN-8 has high blood-brain permeability and a significant antioxidant profile with no neurotoxicity[1].
11C-MK-3168 is a potent, reversible and blood/brain barrier penetrated fatty acid amide hydrolase (FAAH) inhibitor, with IC50s of 1.0, 1.7 and 5.5 nM for human, rat and rhesus FAAH, respectively.
MAGL-IN-5 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[1][2].
FAAH/MAGL-IN-4 (Compound 13) is a potent fatty acid amide hydrolase (FAAH) and monoglyceride lipase (MGL) inhibitor with IC50s of 9.1 nM and 7.9 μM, respectively. FAAH/MAGL-IN-4 can be used for the research of pain and CNS disorders[1].
Carprofen-13C,d3 is the deuterium and 13C labeled Carprofen[1]. 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[2][3][4].
SA 47 is a selective and potent inhibitor of fatty acid amide hydrolase (FAAH) and carbamate[1].
PF 750 is a selective and covalent fatty acid amide hydrolase (FAAH) inhibitor, with IC50s varied from 16.2-595 nM in different pre-incubation times. Covalently modifies the enzyme’s active site serine nucleophile[1].
TC-F2 is a reversible non-covalent binding inhibitor of fatty acid amide hydrolase (FAAH) with an IC50 of 28 nM. FAAH is involved in many human diseases, particularly cancer, pain and inflammation as well as neurological, metabolic and cardiovascular disorders[1].
URB597 is a potent, orally bioavailable FAAH inhibitor with IC50 of 4.6 nM, with no activity on other cannabinoid-related targets.IC50 value: 4.6 nM [1]Target: FAAH in vitro: URB597 binds in the hydrophobic pocket and catalytic core of FAAH that connects the active site residues to the membrane surface of FAAH [1]. URB597 reduces the expression of the LPS-induced enzymes cyclo-oxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS; NOS2) in primary rat microglial cell, with a concomitant reduction in the release of the inflammatory mediators prostaglandin E2 (PGE2) and (NO) nitric oxide [2]. in vivo: URB597 inhibits [3H]anandamide hydrolysis in rat brain membranes with a parallel increase in brain anandamide, OEA, and PEA content by inhibition of FAAH. URB597 enhances the hypothermia effect induced by ethanolamide by inhibiting FAAH [3]. When delivered intraperitonealy (0.3 mg/kg) URB597 reduces allodynia and hyperalgesia through cannabinoid CB1 and CB2 receptor-mediated analgesia in rats with inflammatory pain [4].
Carpro-AM1 is a dual-acting FAAH/substrate-selective COX inhibitor with an IC50 value of 94 nM for FAAH[1].