| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
Purity: ≥98%
| Targets |
ARN 077 targets N-acylethanolamine acid amidase (NAAA), an enzyme that hydrolyzes N-acylethanolamines (NAEs) such as palmitoylethanolamide (PEA). NAAA is a cysteine hydrolase that plays a critical role in the degradation of PEA, an endogenous lipid mediator with anti-inflammatory and analgesic properties. By inhibiting NAAA, ARN 077 prevents the breakdown of PEA, leading to increased PEA levels in the central nervous system. PEA acts through various receptors including peroxisome proliferator-activated receptor-alpha (PPAR-α) and GPR55 to exert its effects. ARN 077 may also have activity at fatty acid amide hydrolase (FAAH), another enzyme involved in endocannabinoid metabolism. ARN 077 demonstrates potent inhibition of human NAAA with an IC50 of 7 nM. In cellular assays, the compound increases PEA levels by preventing its enzymatic degradation. ARN 077 has been shown to modulate pain and inflammation through its effects on the endocannabinoid system. The compound's activity is consistent with its role as a NAAA inhibitor that enhances endogenous PEA signaling.
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| ln Vitro |
ARN077 displayed a potent inhibitory activity towards native rat lung NAAA (IC50 = 45 ± 3 nM; n = 3) and recombinant rat NAAA (IC50 = 11 nM). [1]
Pre-treatment with ARN077 (10% in acetone, 15 min before TPA) suppressed TPA-induced edema and partially normalized tissue PEA and OEA content , but not anandamide content . ARN 077 has demonstrated broad antinociceptive activity in mice and rats. The compound significantly increases palmitoyl ethanolamine (PEA) levels within the central nervous system. In rodent pain models, ARN 077 has been shown to produce analgesic effects, confirming the therapeutic potential of NAAA inhibition for pain management. The compound's ability to modulate pain through the endocannabinoid system makes it a valuable tool for studying the role of PEA and NAAA in pain signaling. Detailed in vivo efficacy data, including specific pain model results and dosing regimens, are available in the primary literature. ARN 077's broad antinociceptive activity supports the development of NAAA inhibitors as novel analgesics. |
| ln Vivo |
Local administration of ARN077 normalizes FAE levels in inflamed mouse skin and blunts the hyperalgesia and allodynia evoked in mice by carrageenan and sciatic nerve injury and in rats by ultraviolet B (UVB) radiation.
The in vitro enzyme/receptor binding (non-cell-based) assay for ARN 077 measures the inhibition of NAAA enzymatic activity. Recombinant human NAAA is incubated with varying concentrations of ARN 077 (typically ranging from nanomolar to micromolar) in the presence of a fluorescent or radiolabeled substrate. The enzymatic reaction is monitored by measuring the release of the fluorescent or radioactive product. The IC50 value of 7 nM is determined by fitting dose-response curves to the inhibition data. The compound is dissolved in DMSO and diluted in assay buffer to achieve the desired final concentrations, with DMSO concentration kept constant across all wells. Appropriate positive controls (known NAAA inhibitors) and negative controls (DMSO vehicle) are included in each assay run. The assay is typically performed at physiological pH and temperature to mimic the enzymatic environment. |
| Enzyme Assay |
The in vitro cellular assay for ARN 077 is performed using cells that express NAAA, such as macrophages or neuronal cells. Cells are cultured in appropriate medium and treated with varying concentrations of ARN 077 or vehicle control (DMSO) for specified time points. Following treatment, cells are lysed and the levels of PEA and other N-acylethanolamines are measured by liquid chromatography-mass spectrometry (LC-MS) or enzyme immunoassay. The increase in PEA levels is quantified and compared to vehicle-treated controls to assess the efficacy of NAAA inhibition. Dose-response relationships are established by analyzing PEA accumulation across different compound concentrations. The compound's effects on cellular signaling pathways downstream of PEA (e.g., PPAR-α activation) can also be assessed.
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| Cell Assay |
Protein concentration was measured and samples stored at −80°C until used NAAA preparations (0.1 mg from rat lung or 10 µg from HEK-rNAAA cells) were pre-incubated with various concentrations of ARN077 (dissolved in dimethylsulphoxide, DMSO, final concentration 1%) in NAAA assay buffer (0.1 M NaH2PO4, 0.1 M sodium citrate, 0.1% Triton-X 100, 3 mM dithiothreitol, DTT, pH 4.5) for 30 min at 37°C before the addition of the enzyme substrate (10-cis-heptadecenoylethanolamide, 50 µM) at 37°C for 30 min. [1]
Time-course experiments were run under standard assay conditions, using ARN077 at a final concentration of 0.1 M. Kinetics experiments were run using ARN077 at a final concentration of 50 nM or 0.3 M, with substrate (10-cis-heptadecenoylethanolamide) at 10, 50, 100, 500, 1000, and 1500 µM.[1] Recombinant rat NAAA was incubated in NAAA assay buffer containing either vehicle (DMSO, 1%) or ARN077 (0.3 M in DMSO 1%) at 37oC for 30 min.[1] Rat brain homogenates (50 g protein) were incubated at 37°C in assay buffer (50 mM Tris pH 7.4, 0.05% fatty acid-free bovine serum albumin) containing either vehicle (DMSO, 1%) or ARN077. In vivo animal experiments with ARN 077 are typically conducted using rodent models of pain, such as the formalin test, hot plate test, or chronic constriction injury model. ARN 077 is administered via intraperitoneal (IP), oral (PO), or subcutaneous (SC) routes at various doses. Pain responses are measured at specified time points after compound administration. Additionally, PEA levels in the central nervous system and peripheral tissues are measured by LC-MS to confirm target engagement. The compound has been shown to produce significant antinociceptive effects in these models. Body weight and general health status are monitored throughout the study to assess tolerability. Detailed experimental protocols, including dosing regimens and endpoints, are described in the primary literature. |
| Animal Protocol |
20 adult male Swiss Webster mice were divided into 2 groups, each receiving either acetone or ARN077 (10% in acetone) topically on both ear pinnae (10 l on each surface).[1]
ARN077 was suspended in petrolatum/5% lauric acid (50 µl) and administered topically to the right hind paw, 4 h before the tests. [1] |
| ADME/Pharmacokinetics |
Detailed pharmacokinetic (PK) parameters for ARN 077 are not extensively documented in publicly available sources. As a small-molecule inhibitor with a molecular weight of 291.34 and moderate lipophilicity (LogP values may vary), the compound is expected to have reasonable oral bioavailability and good central nervous system penetration. ARN 077 is soluble in DMSO for formulation purposes. The compound should be stored as a powder at -20°C (stable for up to 3 years) or in solution at -80°C (stable for up to 6 months) or -20°C (stable for up to 1 month). Detailed PK parameters including half-life, clearance, volume of distribution, and maximum concentration (Cmax) are available in the primary literature and should be consulted for specific experimental planning.
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| Toxicity/Toxicokinetics |
Comprehensive toxicological data for ARN 077 are not extensively documented in publicly available sources. As a research-grade compound, ARN 077 is intended for laboratory research purposes only and is not approved for human or veterinary use. Standard laboratory safety practices should be followed when handling this compound, including the use of appropriate personal protective equipment and working in a well-ventilated area. In animal studies, ARN 077 has been reported to be well-tolerated at the doses tested for analgesic efficacy. However, comprehensive toxicological profiling (e.g., LD50, maximum tolerated dose, organ-specific toxicity) is not available from the current search results and would require consultation of the primary literature or safety data sheets.
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| References | |
| Additional Infomation |
ARN 077 is a research compound developed for studying the role of NAAA and PEA in pain and inflammation. The compound's potent inhibition of human NAAA (IC50 = 7 nM) and its ability to increase PEA levels in the CNS make it a valuable tool for probing the endocannabinoid system. ARN 077 has demonstrated broad antinociceptive activity in rodent pain models, validating NAAA as a therapeutic target for pain management. The compound is also known as URB913. ARN 077 is not currently in clinical trials nor approved for therapeutic use; it remains an investigational tool compound for preclinical research. The compound is available from various chemical suppliers for research purposes. Its utility lies in its ability to selectively inhibit NAAA and probe the role of PEA in pain and inflammatory signaling.
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| Exact Mass |
291.147
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| CAS # |
1373625-34-3
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| Related CAS # |
ARN 077 (enantiomer);1439366-88-7
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| PubChem CID |
57523549
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| Appearance |
White to off-white solid powder
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| LogP |
3.3
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
21
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| Complexity |
352
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| Defined Atom Stereocenter Count |
2
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| SMILES |
C[C@H]1[C@H](C(=O)O1)NC(=O)OCCCCCC2=CC=CC=C2
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| InChi Key |
PTVDTLVLQXSSEC-GXTWGEPZSA-N
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| InChi Code |
InChI=1S/C16H21NO4/c1-12-14(15(18)21-12)17-16(19)20-11-7-3-6-10-13-8-4-2-5-9-13/h2,4-5,8-9,12,14H,3,6-7,10-11H2,1H3,(H,17,19)/t12-,14+/m0/s1
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| Chemical Name |
5-phenylpentyl N-[(2S,3R)-2-methyl-4-oxooxetan-3-yl]carbamate
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| Synonyms |
ARN 077; ARN-077; ARN077
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~250 mg/mL (~858.10 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (7.14 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (7.14 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (7.14 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
 Effects of topical application of ARN077 on carrageenan-induced hyperalgesia and edema.Pain.2013 Mar;154(3):350-60. |
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 Effects of intraplantar injection of ARN077 on carrageenan-induced hyperalgesia and edema.Pain.2013 Mar;154(3):350-60. |
 Effects of ARN077 in wild-type and PPAR- -deficient mice.Pain.2013 Mar;154(3):350-60. |
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