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Suppliers of TAK-071

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AMEDCHEM [email protected] +862168061059 CHINA

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Background Information of TAK-071

TAK-071 is a potent and highly selective muscarinic M1 (M1) positive allosteric modulator (PAM), with inflection point of 2.7 nM. EC50 value of TAK-071 for M1R agonist activity is 520 nM. The muscarinic M1 receptor (M1R) is a promising target for treating cognitive impairment associated with cholinergic deficits in disorders such as Alzheimer’s disease and schizophrenia.

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Mechanism and Indications

Signaling Pathways Neuronal Signaling GPCR/G Protein
Target mAChR
Research Area Neurological Disease

Clinical Information

Product Name Sponsor & Collaborators Indications Start Date End Date Phase

Chemical Information

M.Wt Formula CAS No. Synonyms
421.46 C24H24FN3O3

Structure Information of TAK-071

Smiles C1N(C2C=CC(CC3C(C)=C(F)C4CN([[email protected]@H]5[[email protected]@H](O)CCOC5)C(=O)C=4C=3)=CC=2)N=CC=1 |&1:15,16|
InChI InChI=1S/C24H24FN3O3/c1-15-17(11-16-3-5-18(6-4-16)28-9-2-8-26-28)12-19-20(23(15)25)13-27(24(19)30)21-14-31-10-7-22(21)29/h2-6,8-9,12,21-22,29H,7,10-11,13-14H2,1H3/t21-,22-/m0/s1

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[1].Sako Y, et al. TAK-071, a novel M1 positive allosteric modulator with low cooperativity, improves cognitive function in rodents with few cholinergic side effects. Neuropsychopharmacology. 2018 Aug 1.
The muscarinic M1 receptor (M1R) is a promising target for treating cognitive impairment associated with cholinergic deficits in disorders such as Alzheimer's disease and schizophrenia. We previously reported that cooperativity (α-value) was key to lowering the risk of diarrhea by M1R positive allosteric modulators (M1 PAMs). Based on this, we discovered a low α-value M1 PAM, TAK-071 (α-value: 199), and characterized TAK-071 using T-662 as a reference M1 PAM with high α-value of 1786. Both TAK-071 and T-662 were potent and highly selective M1 PAMs, with inflection points of 2.7 and 0.62 nM, respectively. However, T-662 but not TAK-071 augmented isolated ileum motility. TAK-071 and T-662 increased hippocampal inositol monophosphate production through M1R activation and improved scopolamine-induced cognitive deficits in rats at 0.3 and 0.1 mg/kg, respectively. TAK-071 and T-662 also induced diarrhea at 10 and 0.1 mg/kg, respectively, in rats. Thus, taking into consideration the fourfold lower brain penetration ratio of T-662, TAK-071 had a wider margin between cognitive improvement and diarrhea induction than T-662. Activation of M1R increases neural excitability via membrane depolarization, reduced afterhyperpolarization, and generation of afterdepolarization in prefrontal cortical pyramidal neurons. T-662 induced all three processes, whereas TAK-071 selectively induced afterdepolarization. Combining sub-effective doses of TAK-071, but not T-662, with an acetylcholinesterase inhibitor, significantly ameliorated scopolamine-induced cognitive deficits in rats. TAK-071 may therefore provide therapeutic opportunities for cognitive dysfunction related to cholinergic deficits or reduced M1R expression, while minimizing peripheral cholinergic side effects.

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