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Design and optimization of selective azaindole amide M1 positive allosteric modulators.

アザインドールアミド系M1受容体正アロステリック調節薬の設計と最適化

other not specified not assessed

Abstract

Selective modulation of the M1 muscarinic receptor through positive allosteric mechanisms represents an emerging strategy for addressing cognitive deficits in schizophrenia and Alzheimer's disease. This study describes a novel class of azaindole amide compounds and characterizes their key pharmacophoric features. A critical structural element is the nitrogen atom within the azaindole core, which establishes an intramolecular hydrogen bond with the amide N-H group, thereby stabilizing the bioactive conformation consistent with published structure-activity relationships and homology modeling data. A representative compound (compound 25) demonstrated potent and selective M1 PAM activity, favorable physicochemical characteristics, sufficient brain penetration, acceptable pharmacokinetic profiles, and in vivo efficacy. These combined attributes support the further advancement of this chemical series.

Mechanism

The nitrogen atom of the azaindole core forms an intramolecular hydrogen bond with the amide N-H, stabilizing the bioactive conformation required for selective M1 receptor positive allosteric modulation.

Bibliographic

Authors
Davoren JE, O'Neil SV, Anderson DP, Brodney MA, Chenard L, Dlugolenski K, et al.
Journal
Bioorg Med Chem Lett
Year
2016 (2016-01-15)
PMID
26631313
DOI
10.1016/j.bmcl.2015.11.053

Tags

Disease:アルツハイマー病 認知機能低下

Delivery context

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

Safety notes

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

See also:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 26631313. https://h2-papers.org/en/papers/26631313
Source: PubMed PMID 26631313