SML3770
BMS-466442
≥98% (HPLC)
别名:
(S)-Methyl 3-(1-benzyl-1H-imidazol-4-yl)-2-(6-benzyloxy-5-methoxy-1H-indole-2-carboxamido)propanoate, BMS 466442, BMS466442, N-[[5-Methoxy-6-(phenylmethoxy)-1H-indol-2-yl]carbonyl]-1-(phenylmethyl)-L-histidine methyl ester
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关于此项目
经验公式（希尔记法）:
C31H30N4O5
化学文摘社编号:
分子量:
538.59
UNSPSC Code:
12352200
MDL number:
NACRES:
NA.21
产品名称
BMS-466442, ≥98% (HPLC)
InChI key
UUCAHZCMRZOTNF-MHZLTWQESA-N
SMILES string
COC([C@H](CC1=CN(C=N1)CC2=CC=CC=C2)NC(C(NC3=C4)=CC3=CC(OC)=C4OCC5=CC=CC=C5)=O)=O
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
-10 to -25°C
Quality Level
Biochem/physiol Actions
Potent and selective alanine serine cysteine transporter-1 (ASC-1; SLC7A10) inhibitor that effectively blocks ASC-1-mediated cellular D-Ser uptake.
BMS-466442 is a selective alanine serine cysteine transporter-1 (ASC-1) inhibitor (D-Ser uptake IC50 = 36.8 nM and 19.7 nM using HEK human ASC-1 transfectants or primary rat embryonic cortical cultures, respectively) with good selectivity over >40 other targets, including LAT-2 or ASCT-2 (IC50 >10 μM).
BMS-466442 is a selective alanine serine cysteine transporter-1 (ASC-1) inhibitor (D-Ser uptake IC50 = 36.8 nM and 19.7 nM using HEK human ASC-1 transfectants or primary rat embryonic cortical cultures, respectively) with good selectivity over >40 other targets, including LAT-2 or ASCT-2 (IC50 >10 μM).
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Rini Arianti et al.
FEBS letters, 595(16), 2085-2098 (2021-07-02)
Brown and beige adipocytes dissipate energy by uncoupling protein 1 (UCP1)-dependent and UCP1-independent thermogenesis, which may be utilized to develop treatments against obesity. We have found that mRNA and protein expression of the alanine/serine/cysteine transporter-1 (ASC-1) was induced during adipocyte
Inhibition of the Alanine-Serine-Cysteine-1 Transporter by BMS-466442
ACS Chemical Neuroscience, 10(5), 2510-2517 (2019)
Jeffrey M Brown et al.
Journal of neurochemistry, 129(2), 275-283 (2013-11-26)
NMDA receptor hypofunction is hypothesized to contribute to cognitive deficits associated with schizophrenia. Since direct activation of NMDA receptors is associated with serious adverse effects, modulation of the NMDA co-agonists, glycine or D-serine, represents a viable alternative therapeutic approach. Indeed
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