| Identification | Back Directory | [Name]
AG 490 | [CAS]
133550-30-8 | [Synonyms]
AG 490
Zinc02557947
TYRPHOSTIN B42
TYROPHOSTIN AG490
TYRPHOSTIN AG 490
bis-tyrphostin B42
AG-490 (Tyrphostin B42)
AG 490 (Tyrphostin AG 490)
Tyrphostin AG 490
AG 490
AG 490(Tyrphostin AG 490,Tyrphostin B42)
A-CYANO-(3,4-DIHYDROXY)-N-BENZYLCINNAMIDE
N-BENZYL-3,4-DIHYDROXY-ALPHA-CYANOCINNAMIDE
A-CYANO-(3,4-DIHYDROXY)-N-BENZYLCINNAMAMIDE
ALPHA-CYANO-(3,4-DIHYDROXY)-N-BENZYLCINNAMIDE
N-BENZYL-3,4-DIHYDROXY-BENZYLIDENECYANOACETAMIDE
N-Benzyl-2-cyano-3-(3,4-dihydroxy-phenyl)-acrylamide
(E)-N-benzyl-2-cyano-3-(3,4-dihydroxyphenyl)acrylamide
2-cyano-3-(3,4-dihydroxyphenyl)-n-(benzyl)-2-propenamide
2-CYANO-3-[3,4-DIHYDROXYPHENYL]-N-[PHENYLMETHYL]-2-PROPENAMIDE
(E)-2-CYANO-3-(3,4-DIHYDROPHENYL)-N-(PHENYLMETHYL)-2-PROPENAMIDE
(2E)-2-Cyano-3-(3,4-dihydroxyphenyl)-N-(phenylmethyl)-2-propenamide
2-PropenaMide, 2-cyano-3-(3,4-dihydroxyphenyl)-N-(phenylMethyl)-, (2E)-
(2E)-2-Cyano-3-(3,4-dihydroxyphenyl)-N-(phenylmethyl)-2-propenamide AG-490(Tyrphostin B42) | [Molecular Formula]
C17H14N2O3 | [MDL Number]
MFCD00209833 | [MOL File]
133550-30-8.mol | [Molecular Weight]
294.3 |
| Chemical Properties | Back Directory | [Melting point ]
215°C(lit.) | [Boiling point ]
615.2±55.0 °C(Predicted) | [density ]
1.337 | [storage temp. ]
−20°C
| [solubility ]
ethanol: 5 mg/mL
| [form ]
solid
| [pka]
8.75±0.10(Predicted) | [color ]
yellow
| [biological source]
synthetic (organic) | [Stability:]
Stable for 1 year from date of purchase as supplied. Solutions in DMSO, DMF, or ethanol may be stored at -20°C for up to 1 month. | [InChIKey]
TUCIOBMMDDOEMM-ZSOIEALJSA-N |
| Hazard Information | Back Directory | [Usage]
AG 490 is a potent epidermal growth factor receptor kinase autophosphorylation inhibitor with an IC50 of 100 nM and 56.8 μM for EGFR and JAK, respectively. | [Biological Activity]
Selective inhibitor of EGF receptor tyrosine kinase (IC 50 values are 2 and 13.5 μ M for EGFR and ErbB2 respectively). Inhibitor of JAK2, JAK3/STAT, JAK3/AP-1 and JAK3/MAPK pathways and potently inhibits cytokine-independent cell growth in vitro and tumor cell invasion in vivo . | [Description]
AG-490 (133550-30-8) is a potent inhibitor of the JAK2 tyrosine kinase. In acute lymphoblastic leukemia (ALL) cells, which abundantly express JAK-2, AG-490 dose-dependently blocked cell growth, induced apoptosis and inhibited DNA synthesis. Blocks the growth of all pre-B ALL cells with no effect on normal B or T cells. Does not significantly inhibit other kinases such as Lck, Lyn, Btk, Syk and Src. Reduces liver injury in LPS-induced shock.3 AG-490 is a useful tool for exploring the role of JAK2/STAT3 pathway in physiologic processes.4 | [Uses]
AG 490 is a potent epidermal growth factor receptor kinase autophosphorylation inhibitor with an IC50 of 100 nM and 56.8 μM for EGFR and JAK, respectively. | [Definition]
ChEBI: Tyrphostin B42 is a monocarboxylic acid amide obtained by formal condensation of the carboxy group of (2E)-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enoic acid with the amino group of benzylamine. It has a role as an EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor, an antioxidant, a STAT3 inhibitor, an anti-inflammatory agent, an apoptosis inducer and a geroprotector. It is an enamide, a monocarboxylic acid amide, a nitrile, a member of catechols and a secondary carboxamide. | [Biochem/physiol Actions]
Jak-2 protein tyrosine kinase (PTK) inhibitor. Inhibits interleukin 2 (IL-2) driven mitogenesis and triggers apoptosis of tumor cells in Sezary syndrome, a leukemic variant of cutaneous T cell lymphoma. | [storage]
Room temperature | [References]
References/Citations
1) Wang et al. (1999), JAK3, STAT, and MAPK signaling pathways as novel molecular targets for the tyrphostin AG-490 regulation of IL-2-mediated T cell response; J. Immunol. 162 3897
2) Meydan et al. (1996), Inhibition of acute lymphoblastic leukaemia by Jak-2 inhibitor; Nature, 379 645
3) Gyurkovska and Ivanovaska (2015), Tyrosine kinase inhibitor tyrphostin AG490 reduces liver injury in LPS-induced shock; Eur. J. Pharmacol., 751 118
4) Wu et al. (2015), ROS generated during early reperfusion contribute to intermittent hypobaric hypoxia-afforded cardioprotection against postischemia-induced Ca(+2) overload and contractile dysfunction via the JAK2/STAT3 pathway; J. Mol. Cell. Cardiol., 81 150 |
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