更新于：2024-11-01

nAChRα9&α10 x CHRNB4

更新于：2024-11-01

基本信息

关联

项与 nAChRα9&α10 x CHRNB4 相关的药物

ACV-1

靶点

CHRNB4 x nAChRα9&α10

作用机制

CHRNB4抑制剂 [+1]

在研机构-

原研机构

University of Melbourne

在研适应症-

非在研适应症

神经痛 [+1]

最高研发阶段终止

首次获批国家/地区-

首次获批日期1800-01-20

项与 nAChRα9&α10 x CHRNB4 相关的临床试验

ACTRN12607000201471 / Suspended临床2期

A randomised, double-blind, placebo-controlled study to assess the safety, tolerability, pharmacodynamics and pharmacokinetics of subcutaneous doses of ACV1 in patients with diabetic peripheral neuropathic pain or post-herpetic neuralgia.

开始日期2007-04-10

申办/合作机构-

ACTRN12606000456550 / Completed临床2期

A randomised, double-blind, placebo-controlled study to assess the safety, tolerability, pharmacodynamics and pharmacokinetics of subcutaneous doses of ACV1 in patients with neuropathic sciatic pain

开始日期2006-09-29

申办/合作机构-

ACTRN12605000408684 / Completed临床1期

A Randomised, Placebo-Controlled, Double-Blind, Single and Multiple Ascending Dose Study to Assess the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of Subcutaneous Doses of ACV1 in Healthy Adult Male Subjects.

开始日期2005-06-23

申办/合作机构-

100 项与 nAChRα9&α10 x CHRNB4 相关的临床结果

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100 项与 nAChRα9&α10 x CHRNB4 相关的转化医学

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0 项与 nAChRα9&α10 x CHRNB4 相关的专利（医药）

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项与 nAChRα9&α10 x CHRNB4 相关的文献（医药）

2009-10-01·Molecular Psychiatry1区 · 医学

Differential contribution of genetic variation in multiple brain nicotinic cholinergic receptors to nicotine dependence: recent progress and emerging open questions

1区 · 医学

Review

作者: L Greenbaum ; B Lerer

Nicotine dependence (ND), a major public health challenge, is a complex, multifactorial behavior, in which both genetic and environmental factors have a role. Brain nicotinic acetylcholine receptor (nAChR)-encoding genes are among the most prominent candidate genes studied in the context of ND, because of their biological relevance as binding sites for nicotine. Until recently, most research on the role of nAChRs in ND has focused on two of these genes (encoding the alpha4- and beta2-subunits) and not much attention has been paid to the possible contribution of the other nine brain nAChR subunit genes (alpha2-alpha3, alpha5-alpha7, alpha9-alpha10, beta3-beta4) to the pathophysiology and genetics of ND. This situation has changed dramatically in the last 2 years during which intensive research had addressed the issue, mainly from the genetics perspective, and has shown the importance of the CHRNA5-CHRNA3-CHRNB4 and CHRNA6-CHRNB3 loci in ND-related phenotypes. In this review, we highlight recent findings regarding the contribution of non-alpha4/beta2-subunit containing nAChRs to ND, based on several lines of evidence: (1) human genetics studies (including linkage analysis, candidate-gene association studies and whole-genome association studies) of several ND-related phenotypes; (2) differential pharmacological and biochemical properties of receptors containing these subunits; (3) evidence from genetically manipulated mice; and (4) the contribution of nAChR genes to ND-related personality traits and neurocognitive profiles. Combining neurobiological genetic and behavioral perspectives, we suggest that genetic susceptibility to ND is not linked to one or two specific nAChR subtype genes but to several. In particular, the alpha3, alpha5-6 and beta3-4 nAChR subunit-encoding genes may play a much more pivotal role in the neurobiology and genetics of ND than was appreciated earlier. At the functional level, variants in these subunit genes (most likely regulatory) may have independent as well as interactive contributions to the ND phenotype spectrum. We address methodological challenges in the field, highlight open questions and suggest possible pathways for future research.