| Identification | Back Directory | [Name]
AG 957 | [CAS]
140674-76-6 | [Synonyms]
AG 957
NSC 654705
TYRPHOSTIN 957
TYRPHOSTIN AG 957
LAVENDUSTIN C ANALOG
4-AMINO-N-(2,5-DIHYDROXYBENZYL)METHYL BENZOATE
METHYL-4-[N-(2',5'-DIHYDROXYBENZYL)AMINO]BENZOATE
Benzoic acid, 4-[[(2,5-dihydroxyphenyl)methyl]amino]-, methyl ester
Lavendustin C Analog, Methyl-4-[N-(2μ,5μ-dihydroxybenzyl)amino]benzoate | [Molecular Formula]
C15H15NO4 | [MDL Number]
MFCD01074970 | [MOL File]
140674-76-6.mol | [Molecular Weight]
273.28 |
| Chemical Properties | Back Directory | [Boiling point ]
504.2±45.0 °C(Predicted) | [density ]
1.337±0.06 g/cm3(Predicted) | [storage temp. ]
−20°C | [solubility ]
DMSO: soluble | [form ]
crystalline solid | [pka]
10.30±0.43(Predicted) | [color ]
Off-white to light brown |
| Hazard Information | Back Directory | [Description]
Tyrphostins are tyrosine phosphorylation inhibitors that act by inhibiting tyrosine kinases. AG957 is a tyrphostin that targets transforming Bcr-Abl fusion proteins (p185Bcr-Abl, p210Bcr-Abl), as well as normal c-Abl (IC50s = 4.3, 1, and 7.1 μM, respectively, for human proteins). It also inhibits epidermal growth factor receptor (IC50 = 0.25 μM). As the constitutively-active 210 kDa Bcr-Abl fusion protein commonly occurs in chronic myelogenous leukemia (CML) cells, AG957 is commonly used to study Bcr-Abl signaling in the CML K562 cell line. AG957 is also used to study signaling through c-Abl. | [Uses]
Tyrphostin AG 957 is a potent tyrosine kinase inhibitor. Also, it causes metabolic alterations in K562 cells. It is a COVID19-related research product. | [Definition]
ChEBI: 4-[(2,5-dihydroxyphenyl)methylamino]benzoic acid methyl ester is an aromatic amine. | [References]
[1]. anafi m, gazit a, gilon c, et al. selective interactions of transforming and normal abl proteins with atp, tyrosine-copolymer substrates, and tyrphostins. j biol chem. 1992 mar 5;267(7):4518-23.
[2]. kaur g, gazit a, levitzki a, et al. tyrphostin induced growth inhibition: correlation with effect on p210bcr-abl autokinase activity in k562 chronic myelogenous leukemia. anticancer drugs. 1994 apr;5(2):213-22.
[3]. jamieson l, carpenter l, biden tj, et al. protein kinase ciota activity is necessary for bcr-abl-mediated resistance to drug-induced apoptosis. j biol chem. 1999 feb 12;274(7):3927-30.
[4]. fu p, usatyuk pv, lele a, et al. c-abl mediated tyrosine phosphorylation of paxillin regulates lps-induced endothelial dysfunction and lung injury. am j physiol lung cell mol physiol. 2015 may 15;308(10):l1025-38. |
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BOC Sciences
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Energy Chemical
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InvivoChem
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