product name GW842166X
Description: GW842166X is a potent and highly selective agonist of cannabinoid receptor CB2 receptor with EC50 of 63 nM, it shows little activity on CB1 receptor. GW842166X shows similar potency and efficacy for rat and human recombinant CB2 receptors with EC50 of 91 nM and 63nM, respectively. GW-842166X exhibits full agonist potency with an EC50 of 133 nM and Emax of 101% in cyclase assays. IT exhibits weak agonist potency with an EC50 of 7.780 μM and Emax of 84% in FLIPR assays.
References: J Med Chem. 2007 May 31;50(11):2597-600; Br J Pharmacol. 2008 Jan;153(2):390-401
449.25
Formula
C18H17Cl2F3N4O2
CAS No.
666260-75-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 20 mg/mL (44.5 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
30% Propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19404271
| In Vitro |
In vitro activity: GW842166X shows similar potency and efficacy for rat and human recombinant CB2 receptors with EC50 of 91 nM and 63nM, respectively. GW-842166X exhibits full agonist potency with an EC50 of 133 nM and Emax of 101% in cyclase assays. GW-842166X exhibits weak agonist potency with an EC50 of 7.780 μM and Emax of 84% in FLIPR assays. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | GW842166X has an oral bioavailability of 58% and a half-life of 3 h when dosed orally in the rat. GW842166X has extremely high potency with an oral ED50 of 0.1 mg/kg and shows full reversal of hyperalgesia at 0.3 mg/kg in the FCAa model of inflammatory pain. GW842166X orally administrated at a dose of 15 mg/kg for 8 days produced a significant reversal of the CCI induced decrease in paw withdrawal threshold in a rat model of neuropathic pain. |
| Animal model | Rat model of neuropathic pain |
| Formulation & Dosage | Dissolved in saline; 15 mg/kg; p.o. administration once daily for 8 days |
| References | J Med Chem. 2007 May 31;50(11):2597-600; Br J Pharmacol. 2008 Jan;153(2):390-401 |
Related Posts
product name GW842166X
Description: GW842166X is a potent and highly selective agonist of cannabinoid receptor CB2 receptor with EC50 of 63 nM, it shows little activity on CB1 receptor. GW842166X shows similar potency and efficacy for rat and human recombinant CB2 receptors with EC50 of 91 nM and 63nM, respectively. GW-842166X exhibits full agonist potency with an EC50 of 133 nM and Emax of 101% in cyclase assays. IT exhibits weak agonist potency with an EC50 of 7.780 μM and Emax of 84% in FLIPR assays.
References: J Med Chem. 2007 May 31;50(11):2597-600; Br J Pharmacol. 2008 Jan;153(2):390-401
449.25
Formula
C18H17Cl2F3N4O2
CAS No.
666260-75-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 20 mg/mL (44.5 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
30% Propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19404271
| In Vitro |
In vitro activity: GW842166X shows similar potency and efficacy for rat and human recombinant CB2 receptors with EC50 of 91 nM and 63nM, respectively. GW-842166X exhibits full agonist potency with an EC50 of 133 nM and Emax of 101% in cyclase assays. GW-842166X exhibits weak agonist potency with an EC50 of 7.780 μM and Emax of 84% in FLIPR assays. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | GW842166X has an oral bioavailability of 58% and a half-life of 3 h when dosed orally in the rat. GW842166X has extremely high potency with an oral ED50 of 0.1 mg/kg and shows full reversal of hyperalgesia at 0.3 mg/kg in the FCAa model of inflammatory pain. GW842166X orally administrated at a dose of 15 mg/kg for 8 days produced a significant reversal of the CCI induced decrease in paw withdrawal threshold in a rat model of neuropathic pain. |
| Animal model | Rat model of neuropathic pain |
| Formulation & Dosage | Dissolved in saline; 15 mg/kg; p.o. administration once daily for 8 days |
| References | J Med Chem. 2007 May 31;50(11):2597-600; Br J Pharmacol. 2008 Jan;153(2):390-401 |