858929-13-2Relevant academic research and scientific papers
Synthesis of carbon-11 labeled triphenylacetamides as novel potential PET melanoma cancer imaging agents
Gao, Mingzhang,Kong, Deyuan,Clearfield, Abraham,Miller, Kathy D.,Sledge, George W.,Zheng, Qi-Huang
, p. 2301 - 2304 (2006)
New carbon-11 labeled triphenylacetamides (TPAs), N-(4-[ 11C]methoxyphenyl)-2,2,2-triphenyl-acetamide ([11C]MTA) and 3-phenyl-(R)-2-(2,2,2-triphenylacetylamino)propionic acid [ 11C]methyl ester ([11C]PAME), were
Aminolysis of allyl esters with bislithium aryl amides
Faler, Catherine A.,Joullié, Madeleine M.
, p. 7229 - 7231 (2007/10/03)
The aminolysis of allyl esters with bislithium amides is reported. Tertiary aryl amides were synthesized in a one-pot reaction with bislithium amides and a suitable electrophile in good yields. The scope of this reaction was demonstrated with a variety of anilines and aminopyridines and applied to the synthesis of triphenylmethylacetamides.
Synthesis and identification of small molecules that potently induce apoptosis in melanoma cells through G1 cell cycle arrest
Dothager, Robin S.,Putt, Karson S.,Allen, Brittany J.,Leslie, Benjamin J.,Nesterenko, Vitaliy,Hergenrother, Paul J.
, p. 8686 - 8696 (2007/10/03)
Late-stage malignant melanoma is a cancer that is refractory to current chemotherapeutic treatments. The average survival time for patients with such a diagnosis is 6 months. In general, the vast majority of anticancer drugs operate through induction of cell cycle arrest and cell death in either the DNA synthesis (S) or mitosis (M) phase of the cell cycle. Unfortunately, the same mechanisms that melanocytes possess to protect cells from DNA damage often confer resistance to drugs that derive their toxicity from S or M phase arrest. Described herein is the synthesis of a combinatorial library of potential proapoptotic agents and the subsequent identification of a class of small molecules (triphenylmethylamides, TPMAs) that arrest the growth of melanoma cells in the G1 phase of the cell cycle. Several of these TPMAs are quite potent inducers of apoptotic death in melanoma cell lines (IC50 ～ 0.5 μM), and importantly, some TPMAs are comparatively nontoxic to normal cells isolated from the bone marrow of healthy donors. Furthermore, the TPMAs were found to dramatically reduce the level of active nuclear factor κ-B (NFκB) in the cell; NFκB is known to be constitutively active in melanoma, and this activity is critical for the proliferation of melanoma cells and their evasion of apoptosis. Compounds that reduce the level of NFκB and arrest cells in the G1 phase of the cell cycle can provide insights into the biology of melanoma and may be effective antimelanoma agents.
