71924-61-3

Upstream product

• 1089186-95-7 1-(3-fluoro-4-hydroxy-5-methoxyphenyl)-N,N,N-trimethylmethanaminium iodide 
• 103905-49-3 5-<(dimethylamino)methyl>-1-fluoro-2-hydroxy-3-methoxybenzene 
• 73943-41-6 2-fluoro-6-methoxyphenol 
• 456-49-5 1-fluoro-3-methoxybenzene 
• 71144-35-9 3-fluoro-4,5-dihydroxybenzaldehyde 
• 77-78-1 dimethyl sulfate 
• 100-97-0 hexamethylenetetramine 
• 394-64-9 1-fluoro-2,3-dimethoxybenzene 
• 79418-78-3 3-fluoro-4-hydroxy-5-methoxybenzaldehyde 
• 74-88-4 methyl iodide 

Downstream Products

• 71144-35-9 3-fluoro-4,5-dihydroxybenzaldehyde 
• 99423-94-6 (3-fluoro-4,5-dimethoxy-phenyl)-methanol 
• 102034-50-4 1-fluoro-2,3-dimethoxy-5-chloromethylbenzene 
• 476359-31-6 2-chloromethyl-1,3-difluoro-4,5-dimethoxy-benzene 
• 476359-41-8 5-fluoro-L-3,4-dimethoxyphenylalanine 
• 476359-43-0 2,6-difluoro-L-3,4-dimethoxyphenylalanine 
• 128812-04-4 2,6-difluoro-L-3,4-dihydroxyphenylalanine 
• 476359-37-2 (2R)-N-[(2S)-2-amino-2-(5'-fluoro-3',4'-dimethoxybenzyl)-ethan-1-oyl]bornane-10,2-sultam 
• 476359-39-4 (2R)-N-[(2S)-2-amino-2-(2',6'-difluoro-3',4'-dimethoxybenzyl)-ethan-1-oyl]bornane-10,2-sultam 
• 476359-33-8 (2R)-N-[(2S)-2-((diphenylmethylidene)amino)-2-(5'-fluoro-3',4'-dimethoxybenzyl)-ethan-1-oyl]bornane-10,2-sultam 
• 476359-35-0 (2R)-N-[(2S)-2-((diphenylmethylidene)amino)-2-(2',6'-difluoro-3',4'-dimethoxybenzyl)-ethan-1-oyl]bornane-10,2-sultam 
• 861995-10-0 3-fluoro-4,4',5-trimethoxy-3'-O-tert-butyldiphenylsilyl-(Z)-stilbene 
• 870274-50-3 3-fluoro-4,4',5-trimethoxy-3'-O-tert-butyldiphenylsilyl-(E)-stilbene 
• 1345017-00-6 1-methyl-4-(3-fluoro-4-methoxyphenyl)-5-(3-fluoro-4,5-dimethoxyphenyl)imidazole 

Relevant academic research and scientific papers

Chemoselective zinc/HCl reduction of halogenated β-nitrostyrenes: Synthesis of halogenated dopamine analogues

A detailed account regarding the synthesis of 2- and 5-halogenated dopamine is given. The key step is a chemoselective reduction of a nitrostyrene by Zn/HCl at 0 °C. These conditions represent a simple, low-cost alternative to reduction by water-sensitive hydride donors and two-step procedures. Under these conditions, aryl fluoride, chloride, and bromide groups are stable. However, iodine undergoes significant reductive dehalogenation.

COMPLEMENT PATHWAY MODULATORS AND USES THEREOF

The present invention provides a compound of formula I a method for manufacturing the compounds of the invention, and its therapeutic uses as inhibitor of the complement alternative pathway and particularly as inhibitor of Factor B for the treatment of e.g. age-related macular degeneration and diabetic retinopathy. The present invention further provides a combination of pharmacologically active agents and a pharmaceutical composition.

Halocombstatins and methods of synthesis thereof

The invention relates to novel compounds denominated halocombstatins. The halocombstatins are derivatives of combretastatin A-3, and include compounds that exhibit cancer growth cell inhibition against a panel of human cancer cell lines and the murine P38

Antineoplastic agents. 509. Synthesis of fluorcombstatin phosphate and related 3-halostilbenes

The present SAR study of combretastatin A-3 (3a) focused on replacement of the 3-hydroxyl group by a series of halogens. That approach with Z-stilbenes resulted in greatly enhanced (> 10-100-fold) cancer cell growth inhibition against a panel of human cancer cell lines and the murine P388 lymphocytic leukemia cell line. Synthesis of the 3-fluoro-Z-stilbene designated fluorcombstatin (11a) and its potassium 3′-O-phosphate derivative (16c) by the route 7 → 8a → 11a → 14 → 16c illustrates the general synthetic pathway. The 3′-O-phosphoric acid ester (15) of 3-bromo-Z-stilbene 13a was also converted to representative cation salts to evaluate the potential for improved aqueous solubility, and the potassium salt (16 mg/mL in water) proved most useful. The fluoro (11a), chloro (12a), and bromo (13a) halocombstatins were nearly equivalent to combretastatin A-4 (1a) as inhibitors of tubulin polymerization and of the binding of colchicine to tubulin. The tubulin binding in cell-free systems was also retained in human umbilical vein endothelial cells. All three halocombstatins retained the powerful human cancer cell line inhibitory activity of combretastatin A-4 (1a) and proved superior to combretastatin A-3 (3a). In addition, the halocombstatins targeted Gram-positive bacteria and Cryptococcus neoformans.