Antinociceptive activity represented as percent maximum possible effect (% MPE), with MPE being a 20 s latency to tail withdrawal

Antinociceptive activity represented as percent maximum possible effect (% MPE), with MPE being a 20 s latency to tail withdrawal. a separate window Open in a separate window aResults from the mouse WWTW assay after cumulative dosing of test compound up to 10 mg/kg ip. Antinociceptive activity represented as percent maximum possible effect (% MPE), with MPE being a 20 s latency to tail withdrawal. Baseline tail withdrawal latency is ~5 s, or 25% MPE. Duration of action for compounds with full antinociceptive actviity (100% MPE) is calculated as the amount of time between administration and return to baseline following a bolus 10 mg/kg dose of compound ip. bFirst reported in reference 33. cFrom reference 34. dFrom reference 36. Compound 2D was previously reported under the name AMB-47 in reference 39. eFrom reference 35. fFrom reference 38. Test compounds (10 mg/kg cumulative dosing) were administered via Etamicastat intraperitoneal injection at 30-minute intervals, as described in the Methods section. Of the 21 novel analogues presented here, four reached the maximal possible effect (100% MPE) while six others showed partial activity (50C75% MPE); the remaining eleven compounds showed no significant difference from baseline at the doses tested. Duration of action, or the amount of time between administration of test compound and the test subjects return to baseline latency to tail flick, was measured for all of the fully active analogues. The mesyl analogues 4A and 4D were slightly shorter-acting than the lead 1A (120 min), featuring a duration of less than 90 min. Meanwhile, the benzoyl analogues 5B and 5C displayed durations of 120 to 150 min (see Figure 3). The previously reported acetyl analogues 2B and 2D remained the longest-acting ligands in this study with a duration Rabbit polyclonal to GAPDH.Glyceraldehyde 3 phosphate dehydrogenase (GAPDH) is well known as one of the key enzymes involved in glycolysis. GAPDH is constitutively abundant expressed in almost cell types at high levels, therefore antibodies against GAPDH are useful as loading controls for Western Blotting. Some pathology factors, such as hypoxia and diabetes, increased or decreased GAPDH expression in certain cell types of 240 min. Open in a separate window Figure 3. Time course data for compounds 4A (n=6), 4D (n=6), 5B (n=4), and 5C (n=3) in the 50C WWTW assay in C57BL6 male mice. Animals were injected with saline and baseline latencies were established Etamicastat 30 minutes later. Animals were then injected with test compound at 10 mg/kg ip and latency to tail flick was measured at the times indicated. Antagonist Potency of In Vivo Candidates: Compounds displaying a full antinociceptive effect and DOR antagonism were further evaluated in order to determine the potency of their DOR antagonist effects. Analogues 4D, 5B, and 5C affected a rightward shift in the EC50 of the standard DOR agonist SNC80 which equated to Ke values of 0.85 nM, 15 nM, and 8 nM respectively (calculated as described in Methods). Discussion and Conclusions Previous work in our lab has investigated the effects of various substituents at the C-6 position of the THQ core in conjunction with an unmodified and profiles. The 6-benzodioxanyl pendant, consistent with previously reported analogues featuring heteroatoms distal to the THQ core,36 decreased MOR efficacy considerably (Table 5, line E) but showed favorable MOR and DOR affinity with significantly lower KOR affinity in analogues 2E and 3E (Table 2). The 2-benzofuranyl pendant produced a wide variety of multifunctional profiles, with 1F and 4F acting as MOR agonists/DOR antagonists, 2F and 3F acting as MOR agonists/DOR partial agonists, and 5F displaying MOR partial agonist/DOR antagonist Etamicastat activity (Table 5, line F). This unpredictability, paired with high lipophilicity and limited activity at the doses tested, minimized the utility of.