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Merck
CN

SML3266

AMD070 hydrochloride

≥98% (HPLC)

别名:

(S)-N′-((1H-benzo[d]imidazol-2-yl)methyl)-N′-(5,6,7,8-tetrahydroquinolin-8-yl)butane-1,4-diamine hydrochloride, AMD 070 hydrochloride, AMD 11070 hydrochloride, AMD-070 hydrochloride, AMD-11070 hydrochloride, AMD11070 hydrochloride, Mavorixafor, N′-(1H-Benzimidazol-2-ylmethyl)-N′-(S)-5,6,7,8-tetrahydro-quinolin-8-yl-butane-1,4-diamine hydrochloride, X4P-001 hydrochloride

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关于此项目

经验公式（希尔记法）:
C21H27N5 · xHCl
分子量:
349.47 (free base basis)
MDL编号:
MFCD23160058
UNSPSC代码:
51111800
NACRES:
NA.77

主要文件

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质量水平

100

方案

≥98% (HPLC)

表单

powder

储存条件

desiccated

颜色

white to beige

溶解性

DMSO: 2 mg/mL, clear

储存温度

2-8°C

SMILES字符串

NCCCCN([C@@H]1C2=NC=CC=C2CCC1)CC3=NC4=C(C=CC=C4)N3.Cl

InChI

1S/C21H27N5.ClH/c22-12-3-4-14-26(15-20-24-17-9-1-2-10-18(17)25-20)19-11-5-7-16-8-6-13-23-21(16)19;/h1-2,6,8-10,13,19H,3-5,7,11-12,14-15,22H2,(H,24,25);1H/t19-;/m0./s1

InChI key

DBNMEMJSDAAGNZ-FYZYNONXSA-N

生化/生理作用

AMD070 (AMD11070) is an orally active, reversible and selective CXCR4 (CD184, fusin) antagonist (IC50 = 13 nM against 100 pM 125I-SDF-1α for binding human CD+/CXCR4+ CEM-CCRF cells) that inhibits HIV-1 replication in cultures (IC50/host cells = 2 nM/MT-4 and 26 nM/PBMCs; T-tropic HIV-1NL4.3 strain) with no host cytotoxicity even at concentrations above 23 μM.
Orally active, reversible and selective CXCR4 (CD184, fusin) antagonist that inhibits HIV-1 replication in host cell cultures.

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number
0000176054
0000176055
0000176055
0000176054

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Renato T Skerlj et al.
Journal of medicinal chemistry, 53(8), 3376-3388 (2010-03-20)
The redesign of azamacrocyclic CXCR4 chemokine receptor antagonists resulted in the discovery of novel, small molecule, orally bioavailable compounds that retained T-tropic (CXCR4 using, X4) anti-HIV-1 activity. A structure-activity relationship (SAR) was determined on the basis of the inhibition of
Ju Wang et al.
Translational neurodegeneration, 10(1), 12-12 (2021-04-02)
Currently, there is no cure for Alzheimer's disease (AD). Therapeutics that can modify the early stage of AD are urgently needed. Recent studies have shown that the pathogenesis of AD is closely regulated by an endo/lysosomal asparaginyl endopeptidase (AEP). Inhibition
Guiqin Chen et al.
Science advances, 7(16) (2021-04-18)
Netrin-1, a family member of laminin-related secreted proteins, mediates axon guidance and cell migration during neural development. T835M mutation in netrin receptor UNC5C predisposes to the late-onset Alzheimer's disease (AD) and increases neuronal cell death. However, it remains unclear how

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