N8289
NBI-31772 hydrate
≥98% (HPLC)
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关于此项目
经验公式（希尔记法）:
C17H11NO7 · xH2O
化学文摘社编号:
分子量:
341.27 (anhydrous basis)
UNSPSC Code:
51111800
PubChem Substance ID:
MDL number:
InChI
1S/C17H11NO7.H2O/c19-11-2-1-7(4-12(11)20)16(23)15-9-6-14(22)13(21)5-8(9)3-10(18-15)17(24)25;/h1-6,19-22H,(H,24,25);1H2
SMILES string
O.OC(=O)c1cc2cc(O)c(O)cc2c(n1)C(=O)c3ccc(O)c(O)c3
InChI key
QHAUFGIHMBUQKN-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
solid
storage condition
protect from light
storage temp.
−20°C
Biochem/physiol Actions
NBI-31772 is an insulin-like growth factor-1 binding proteins (IGFBPs) inhibitor; IGF-1 potentiator.
NBI-31772 is an insulin-like growth factor-1 binding proteins (IGFBPs) inhibitor; IGF-1 potentiator. NBI-31772 is an air/DMSO DOPA oxidation product, which inhibits IGF binding to IFGFB′s. NBI-31772 displaces IGF-1 from IGF1:IGFBP complex. Thus, it increases circulating level of IGF-1. NBI-31772 does not bind to IGFR.
存储类别
13 - Non 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
Jessica E Malberg et al.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 32(11), 2360-2368 (2007-03-08)
The present studies were conducted to determine if increasing central levels of the neurotrophic factor insulin-like growth factor-1 (IGF-I) either directly or indirectly produces anxiolytic and antidepressant-like effects in the mouse. Central levels of IGF-I can be increased directly, by
X J Liu et al.
The Journal of biological chemistry, 276(35), 32419-32422 (2001-07-11)
Insulin-like growth factor-I (IGF-I) has both metabolic and mitogenic activities mediated through interaction with the type 1 IGF receptor. The circulation of IGF-I in blood and interstitial fluid is not free but bound mostly to a family of six high
Jonathan D Schertzer et al.
The American journal of pathology, 171(4), 1180-1188 (2007-09-08)
Administration of recombinant human insulin-like growth factor-I (rhIGF-I) has beneficial effects in animal models of muscle injury and muscular dystrophy. However, the results of these studies may have been confounded by interactions of rhIGF-I with endogenous IGF-binding proteins (IGFBPs). To
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