41973-35-7

Upstream product

• 2051-07-2 bis(p-methoxybenzylidene)acetone 
• 2051-07-2 1,5-bis-(4-methoxyphenyl)-1,4-pentadien-3-one 
• 67-64-1 acetone 
• 123-11-5 4-methoxy-benzaldehyde 

Downstream Products

• 74882-32-9 1,5-bis(4-methoxyphenyl)pentan-3-one 

Relevant academic research and scientific papers

Antimicrobial Activity of Monoketone Curcuminoids Against Cariogenic Bacteria

We evaluated the antimicrobial activity of 25 monoketone curcuminoids (MKCs) against a representative panel of cariogenic bacteria in terms of their minimum inhibitory concentration (MIC) values. Curcumin A (10) displayed promising activity against Streptococcus mutans (MIC?=?50?μg/ml) and Streptococcus mitis (MIC?=?50?μg/ml) as well as moderate activity against S.?sanguinis (MIC?=?100?μg/ml), Lactobacillus casei (MIC?=?100?μg/ml), and Streptococcus salivarius (MIC?=?200?μg/ml). Results indicated higher activity of compound 10 than that of its bis-β-diketone analog. Additionally, compounds 3a (1,5-bis(4-methylphenyl)pentan-3-one) and 7b (1,5-bis(4-bromophenyl)pentan-3-ol) were moderately active against S.?mitis (MIC?=?100?μg/ml) and S.?salivarus (MIC?=?200?μg/ml).

Method and compounds for cancer treatment utilizing NFkB as a direct or ultimate target for small molecule inhibitors

A method is described for cancer treatment through NFκB inhibition. NFκB is a direct or ultimate target for small molecule inhibitors. These small molecule inhibitors are aimed at suppression of NFκB directly or by indirect suppression of IKK, SFK kinases, or other upstream kinases. The present invention includes small molecule inhibitors comprising three, five, and seven carbon unsaturated spacers having one or two carbonyls, flanked by substituted aryl rings. The small molecule inhibitors can be symmetrical or unsymmetrical.

Symmetrical bis(heteroarylmethoxyphenyl)alkylcarboxylic acids as inhibitors of leukotriene biosynthesis

Symmetrical bis(quinolylmethoxyphenyl)alkylcarboxylic acids were investigated as inhibitors of leukotriene biosynthesis and 4,4-bis(4-(2-quinolylmethoxy)phenyl)pentanoic acid sodium salt (47·Na) met our design parameters for a drug candidate (ABT-080). This compound was readily synthesized in three steps from commercially available diphenolic acid. Against intact human neutrophils, 47·Na inhibited ionophore-stimulated LTB4 formation with an IC50 = 20 nM. In zymosan-stimulated mouse peritoneal macrophages producing both LTC4 and PGE2, 47·Na showed 9000-fold selectivity for inhibition of LTC4 (IC50 = 0.16 nM) over PGE2 (IC50 = 1500 nM). Preliminary pharmacokinetic evaluation in rat and cynomolgus monkey demonstrated good oral bioavailability and elimination half-lives of 9 and 5 h, respectively. Pharmacological evaluation of leukotriene inhibition with oral dosing was demonstrated in a rat pleural inflammation model (ED50 = 3 mg/kg) and a rat peritoneal passive anaphylaxis model (LTB4, ED50 = 2.5 mg/kg; LTE4, ED50 = 1.0 mg/kg). In a model of airway constriction induced by antigen challenge in actively sensitized guinea pigs, 47·Na dosed orally blocked bronchoconstriction with an ED50 = 0.4 mg/kg, the most potent activity we have observed for any leukotriene inhibitor in this model. The mode of inhibitory action of 47·Na occurs at the stage of 5-lipoxygenase biosynthesis as it blocks both leukotriene pathways leading to LTB4 and LTC4 but not PGH2 biosynthesis. However, 47·Na does not inhibit 5-lipoxygenase catalysis in a broken cell enzyme assay; therefore it is likely that 47·Na acts as a FLAP inhibitor.