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AG-879

structure given in first source
Also Known As:
2-propenethioamide, 3-(3,5-bis(1,1-dimethylethyl)-4- hydroxyphenyl)-2-cyano-, (E)-; AG 879; AG879
Networked: 17 relevant articles (4 outcomes, 6 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1. Baell, Jonathan: 2 articles (01/2007 - 01/2004)
2. Hirokawa, Yumiko: 2 articles (01/2007 - 01/2004)
3. Lessene, Guillaume: 2 articles (01/2007 - 01/2004)
4. Levitzki, Alexander: 2 articles (01/2007 - 01/2004)
5. Maruta, Hiroshi: 2 articles (01/2007 - 01/2004)
6. Brattain, Michael G: 2 articles (01/2006 - 07/2005)
7. Zhou, Yunfei: 2 articles (01/2006 - 07/2005)
8. Linher-Melville, Katja: 1 article (01/2018)
9. Miladinovic, Tanya: 1 article (01/2018)
10. Popovic, Snezana: 1 article (01/2018)

Related Diseases

1. Neoplasms (Cancer)
2. Colonic Neoplasms (Colon Cancer)
3. Cholangiocarcinoma
4. Dermatitis
5. Sarcoma (Soft Tissue Sarcoma)
01/01/2004 - "AG 879, in combination of PP1 (an inhibitor specific for Src kinase family), suppresses almost completely the growth of RAS-induced sarcomas in nude mice. "
01/08/2007 - "Furthermore, we and others have demonstrated that the growth of mouse RAS-induced sarcomas allografts in mice is almost completely suppressed by either FK228 or a combination of two complimentary Tyr-kinase inhibitors, PP1 and AG 879, all of which block the RAS-induced activation of PAK1. "
09/01/2006 - "In conclusion, our data have a novel preclinical potential for revealing a possible therapeutical utility in targeting in-vivo nerve growth factor/TrKA by AG879 or neutralizing antibody anti-TrKA in cancer proliferation and in muscle sarcomas, in particular."
05/01/2001 - "To understand the biologic significance of RAS-induced up-regulation of these ligands in both RAS-induced PAK activation and malignant transformation, we have conducted the following studies, based on the previous observations that (1) the N-terminal SH3 domain of PIX selectively binds a Pro-rich domain of 18 amino acids of PAKs, CDC42/Rac-dependent Ser/Thr kinase family, and (2) this specific interaction is essential for both PAK activation and membrane ruffling Using four distinct, cell-permeable, and highly specific inhibitors, namely WR-PAK18, which blocks the PAK-PIX interaction; AG 1478, which inhibits ErbB1 kinase activity; and AG 825 or AG 879, which inhibits ErbB2 kinase activity, we demonstrate that (1) the PAK-PIX interaction is essential for v-Ha-RAS-induced malignant transformation; (2) v-Ha-RAS requires not only ErbB1 but also ErbB2, which are activated through two independent autocrine pathways to induce both the PIX/Rac/CDC42-dependent PAK activation and malignant transformation in vitro; and (3) a combination of AG 879 and the Src family kinase-specific inhibitor PP1 suppresses almost completely the growth of RAS-induced sarcomas in nude mice. "

Related Drugs and Biologics

1. Tyrosine Kinase Inhibitors
2. Lapatinib (GW572016)
3. Phosphotransferases (Kinase)
4. RTKI cpd
5. Neutralizing Antibodies
6. Intercellular Signaling Peptides and Proteins (Growth Factors)
7. Nerve Growth Factor (NGF)
8. staurosporine aglycone (K252a)
9. Tyrphostins
10. tyrphostin AG825

Related Therapies and Procedures

1. Therapeutics