Name | ADL5859 HCl |
Synonyms | CS-24 ADL5859 ADL 5859 ADL-5859 ADL 5859 ADL5859 HCl ADL5859 HCL ADL5859 hydrochloride N,N-Diethyl-4-(5-hydroxyspiro[2H-1-benzopyran-2,4'-piperidin]-4-yl)benzamide hydrochloride |
CAS | 850173-95-4 |
Molecular Formula | C24H29ClN2O3 |
Molar Mass | 428.95166 |
Storage Condition | -20℃ |
In vitro study | ADL5859 independently stimulated δ-opioid receptors with 1000-fold higher specificity than μ-or κ-opioid receptors under 32nm and 37NM Ki conditions. Under 78um IC50 conditions, ADL5859 showed a weak inhibitory effect on the hERG channel. The EC50 value of ADL5859 for the δ-opioid receptor is 20nm. ADL5859 independently stimulated δ-opioid receptors with 1000-fold higher specificity than μ-or κ-opioid receptors at 32nm and 37NM K I. Under 78um IC50 conditions, ADL5859 showed a weak inhibitory effect on the hERG channel. The EC50 value of ADL5859 for the δ-opioid receptor is 20nm. |
In vivo study | Under the screening condition of 3 mg/kg orally, ADL5859 can cause 100% reversal of hyperalgesia in the inflamed paw test. The ED50 value of ADL5859 for the oral test in the FCA hyperalgesia mechanism experiment was 1.4 mg/kg. The anti-hyperalgesic phenomenon caused by ADL5859 can be reversed by pretreatment with a delta-opioid receptor antagonist (0.3 mg/kg subcutaneously injected with naltrexole), thus, it was demonstrated that δ-opioid receptors are involved in the mediated response. ADL5859(3 mg/kg P. O.) produced a strong antidepressant-like effect in the forced swimming test in rats, with a significant decrease in pause time and a significant increase in swimming time seen in rats. The bioavailability of ADL5859(3 mg/kg P. O.) was 33% in rats and 66% in dogs. ADL5859 is highly effective in reducing inflammatory responses and neuropathic pain by recruiting δ-opioid receptors expressed by peripheral nav1.8-expressing neurons. Under the screening condition of oral administration at 3 mg/kg, ADL5859 caused 100% reversal of hyperalgesia in the inflamed paw test. The ED50 value of ADL5859 for the oral test in the FCA hyperalgesia mechanism experiment was 1.4 mg/kg. The anti-hyperalgesic phenomenon caused by ADL5859 can be reversed by pretreatment with a delta-opioid receptor antagonist (0.3 mg/kg subcutaneously injected with naltrexole), thus, it was demonstrated that δ-opioid receptors are involved in the mediated response. ADL5859(3 mg/kg P. O.) produced a strong antidepressant-like effect in the forced swimming test in rats, with a significant decrease in pause time and a significant increase in swimming time seen in rats. The bioavailability of ADL5859(3 mg/kg P. O.) was 33% in rats and 66% in dogs. ADL5859 is highly effective in reducing inflammatory responses and neuropathic pain by recruiting δ-opioid receptors expressed by peripheral nav1.8-expressing neurons. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.331 ml | 11.656 ml | 23.312 ml |
5 mM | 0.466 ml | 2.331 ml | 4.662 ml |
10 mM | 0.233 ml | 1.166 ml | 2.331 ml |
5 mM | 0.047 ml | 0.233 ml | 0.466 ml |