产品名称

GNE 7915

产品货号

Axon 2348 CAS [1351761-44-8] MF C19H21F4N5O3MW 443.40 Purity: 99% Soluble in DMSO Description Highly potent, selective, metabolically stable, and brain-penetrable LRRK2 inhibitor (IC50 value 9 nM for phospho-LRRK2 in vitro). GNE 7915 is selective across 187 screened kinases, and >3200 and 53 times selective over JAK2 and TTK, respectively. GNE 7915 does not suppress LPS-stimulated TNFα and CXCL10 levels in LPS-treated primary wild-type (WT) or knockout (KO) astrocyte cultures, and is not reported to cause cellular or genetic toxicity. References Certificates Categories Extra info A.A. Estrada et al. Discovery of highly potent, selective, and brain-penetrable leucine-rich repeat kinase 2 (LRRK2) small molecule inhibitors. J. Med. Chem. 2012, 55, 9416-9433. G.C. Luerman et al. Phosphoproteomic evaluation of pharmacological inhibition of leucine-rich repeat kinase 2 reveals significant off-target effects of LRRK-2-IN-1. J. Neurochem. 2014, 128, 561-576. M.E. Kavanagh et al. The development of CNS-active LRRK2 inhibitors using property-directed optimisation. Bioorg. Med. Chem. Lett. 2013, 23, 3690-3696. Certificate of Analysis Material Safety Data Sheet Apoptosis Cell Signaling & Oncology CNS Pain & Inflammation LRRK2 Ubiquitin EC 2.7.11.1 Potent, selective, metabolically stable, and brain-penetrable LRRK2 inhibitor Chemical name (4-(4-(ethylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-2-fluoro-5-ethoxyphenyl)(morpholino)methanone Parent CAS No. [1351761-44-8] Order Size Unit Price Stock 10 mg €110.00 In Stock

产品价格

现货询价，电话：010-67529703

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产品品牌

axonmedchem

产品概述

产品详情

GNE 7915

Based on 14 reference(s) in Google Scholar 8 10 14

Axon 2348

CAS [1351761-44-8]

MF C19H21F4N5O3
MW 443.40

Purity: 99%
Soluble in DMSO

GNE 7915

Description

Highly potent, selective, metabolically stable, and brain-penetrable LRRK2 inhibitor (IC50 value 9 nM for phospho-LRRK2 in vitro). GNE 7915 is selective across 187 screened kinases, and >3200 and 53 times selective over JAK2 and TTK, respectively. GNE 7915 does not suppress LPS-stimulated TNFα and CXCL10 levels in LPS-treated primary wild-type (WT) or knockout (KO) astrocyte cultures, and is not reported to cause cellular or genetic toxicity.