ライフサイエンスコーパス: lobeline

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1 the privileged H-bonded conformation of (-)-lobeline.

2 responses toward the bitter-tasting compound lobeline.

3 (-)Lobeline (1) and (-)nicotine (2) bind at neuronal nicoti

4 (-)-Lobeline (2R,6S,10S), an antagonist at nicotinic acetylc

5 Structural modification of lobeline affords the defunctionalized analogues meso-tra

6 ork for GLD, we examined the effect of alpha-lobeline, an inhibitor of GALC, on D528N mutant cells.

7 tine and carbamylcholine), partial agonists (lobeline and 4-hydroxy,2-methoxy-benzylidene anabaseine)

8 oses of unlabeled epibatidine, (-)-nicotine, lobeline and cytisine significantly inhibited [18F]FPH b

9 conotoxin ImI, but wraps around the agonists lobeline and epibatidine.

10 xamined a number of abbreviated analogues of lobeline and found that removal of either one or both ox

11 s (-)-aurantioclavine, (+)-amurensinine, (-)-lobeline, and (-)- and (+)-sedamine are described.

12 1,1-dimethyl-4-phenylpiperazinium, nicotine, lobeline, and acetylcholine affinity by 120-, 86-, 85-,

13 tested, ranging from quinine to denatonium, lobeline, and caffeine.

14 ytisine, 1, 1-dimethyl-4-phenylpiperazinium, lobeline, and nicotine) were determined in competition a

15 ation by nicotinic agonists, epibatidine and lobeline, and nicotinic antagonists, methyllycaconitine,

16 e cells mediate the egg-laying attraction to lobeline, as determined by analysis of mosaic flies in w

17 ctions contribute to the high affinity of (-)lobeline at nACh receptors, it is concluded that the pre

18 oth oxygen functions reduces the affinity of lobeline by at least 25-fold; furthermore, oxidation of

19 The nicotinic receptor antagonists, alpha-lobeline, dihydro-beta-erythroidine and methyllycaconiti

20 Previous attempts to determine whether lobeline fits the currently accepted nicotinic pharmacop

21 We identified one compound, lobeline, from the Prestwick library of Food and Drug Ad

22 st 25-fold; furthermore, oxidation of the (-)lobeline hydroxyl group (to afford lobelanine) or reduct

23 for binding; that is, replacement of the (-)lobeline hydroxyl group with a chloro group had no effec

24 ain the analgesic activity and potency of (-)lobeline, indicating that there is no direct relationshi

25 ntermediate involved in the epimerization of lobeline is described.

26 the most promising structural changes to the lobeline molecule that lead to enhancement of VMAT2 affi

27 ternary ammonium group into defunctionalized lobeline molecules in the cis-series resulted in signifi

28 WFA binding and enhancement by lobeline required complex N-glycans but not O-mannose gl

29 al of either one or both oxygen functions of lobeline results in compounds that retain the analgesic

30 Cytisine and lobeline serve as full agonists at alpha4beta4-nAChR but

31 Intrathecal alpha-lobeline showed selectivity for blocking the analgesic r

32 at alpha4beta2 and alpha7 nAChRs compared to lobeline, thereby increasing selectivity for VMAT2.

33 trategy was applied to the conversion of (-)-lobeline to (-)-sedamine in high overall yield.

34 onstrated a general increase in N-glycans on lobeline-treated cells rather than specific alterations

35 rved when the nicotinic ACh receptor agonist lobeline was used.

36 ta, Ct-AChBP, in complex with varenicline or lobeline, which are both partial agonists.

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