ライフサイエンスコーパス: diprenorphine

1 a similar affinity for the antagonist [(3)H]diprenorphine.

2 ficacy, norbuprenorphine, buprenorphine, and diprenorphine.

3 having unchanged affinity for the antagonist diprenorphine.

4 hy (PET) and the opioid receptor ligand [11C]diprenorphine.

5 [(18)F]fluoroethyl-diprenorphine, [(18)F]fluoroethyl-buprenorphine, and [(1

6 atched healthy volunteers using PET and [11C]diprenorphine, a non-selective opioid receptor radioliga

7 mutants retained binding affinities for [3H]diprenorphine, a nonselective opioid antagonist, similar

8 t, buprenorphine a low efficacy agonist, and diprenorphine an antagonist at the MOPr.

9 displayed similar binding affinity for [(3)H]diprenorphine, an antagonist, as the wild types.

10 termined the sensitivity of binding of [(3)H]diprenorphine, an antagonist, to mu, delta, and kappa op

11 ulting triple mutants were evaluated for [3H]diprenorphine and [D-Ala2,NMe-Phe4,Gly5-ol]-enkephalin (

12 ulting triple mutants were evaluated for [3H]diprenorphine and [d-Ala2,NMe-Phe4,Gly5-ol]-enkephalin (

13 mutant, retained similar affinities for [3H]diprenorphine and DAMGO as the D3.49(164)Y mutant.

14 The mutants had similar affinities for [(3)H]diprenorphine, and C7.38(321)S, C7.38(303)S, and C7.38(3

15 have shown previously that when using [(3)H]diprenorphine as radioligand, KDN21 displayed greatly en

16 binding affinities for the antagonist [(3)H]diprenorphine as the wild-type.

17 Naloxone pretreatment up-regulated [(3)H]diprenorphine binding and protein expression of the D3.4

18 [3H]Diprenorphine binding increased 3-fold from 1-15 days in

19 Western blot and [(3)H]diprenorphine binding showed that approximately 70% of M

20 epresent approximately 70 +/- 11% of the [3H]diprenorphine binding sites, as indicated by saturation

21 +/- 3% and approximately 5 +/- 2% of the [3H]diprenorphine binding sites, respectively.

22 tment with MTSEA significantly inhibited [3H]diprenorphine binding to 11 of 22 mutants of the rat mu

23 eatment with SUPERFIT potently inhibited [3H]diprenorphine binding to delta, mu/delta 1, delta/mu 3,

24 methanethiosulfonate (MTSEA) inhibited [(3)H]diprenorphine binding to eight deltaOR and eight kappaOR

25 OFQ competed with [3H]diprenorphine binding to mu-, delta- or kappa-opioid rec

26 593 and naloxone competitively inhibited [3H]diprenorphine binding with Ki values of 2.0, 18 and 18 n

27 with MTSEA dose-dependently inhibited [(3)H]diprenorphine binding with MTSEA sensitivity in the orde

28 SUPERFIT inhibited [3H]diprenorphine binding with much higher affinity for the

29 r MTS ethylsulfonate (MTSES) inhibited [(3)H]diprenorphine binding with the potency order of MTSEA >

30 tant displayed little or no detectable [(3)H]diprenorphine binding, and pretreatment with naloxone gr

31 n (DAMGO) binding and effect of MTSEA on [3H]diprenorphine binding.

32 n (DAMGO) binding and effect of MTSEA on [3H]diprenorphine binding.

33 lular loop did not alter the affinity of [3H]diprenorphine but caused a dramatic decrease in the affi

34 onized by the opioid antagonists naloxone or diprenorphine, despite their very poor affinity for the

35 48) and N150(3.35), whilst buprenorphine and diprenorphine did not.

36 ad reading epilepsy and six controls had 11C-diprenorphine (DPN) positron-emission-tomography (PET) s

37 lective opioid receptor PET radioligand [11C]diprenorphine (DPN), quantified as a volume-of-distribut

38 y-015 enkephalin (DAGO) (mu-agonist) and [3H]diprenorphine (general opiate antagonist) binding sites

39 Equilibrium binding of [3H]diprenorphine onto membranes from cells grown for 13-15

40 ignificant alteration in the affinity of [3H]diprenorphine or etorphine for the receptor or the poten

41 nondyskinetic patients were studied with 11C-diprenorphine PET, the former showed a significant reduc

42 Naloxone or diprenorphine protected all sensitive mutants, except th

43 In the presence of diprenorphine, the magnitude of adenylyl cyclase superac

44 ange of intrinsic activities, the antagonist diprenorphine, the partial agonist buprenorphine, and th

45 eflecting the volume of distribution of [11C]diprenorphine to assess changes in cerebral receptor bin

46 The Kd for [3H]diprenorphine was 1.1+/-0.2 nM, and the Bmax was 2.6+/-0

47 a deletion of 37 COOH-terminal residues bind diprenorphine with comparable affinities and show simila