51631-26-6

Basic information

• Product Name: Benzeneacetyl chloride, a-(1-methylethyl)-
• CAS NO: 51631-26-6
• Molecular Formula: C11H13ClO
• Molecular Weight: 196.677
• Mol File: 51631-26-6.mol
• Article Data: 13

Chemical Properties

• CAS DataBase Reference: Benzeneacetyl chloride, a-(1-methylethyl)-(CAS DataBase Reference)
• NIST Chemistry Reference: Benzeneacetyl chloride, a-(1-methylethyl)-(51631-26-6)
• EPA Substance Registry System: Benzeneacetyl chloride, a-(1-methylethyl)-(51631-26-6)

Safety Data

• Hazardous Substances Data: 51631-26-6(Hazardous Substances Data)

Upstream product

• 101-41-7 benzeneacetic acid methyl ester 
• 72615-27-1 2-phenyl-3-methylbutyric acid methyl ester 
• 140-29-4 phenylacetonitrile 
• 5558-29-2 3-methyl-2-phenyl-butyronitrile 
• 3508-94-9 3-methyl-2-phenylbutyric acid 
• 103-82-2 phenylacetic acid 

Downstream Products

• 38082-08-5 3-methyl-2-phenyl-but-1-en-1-one 
• 854779-93-4 N-hydroxy-4-[(3-methyl-2-phenylbutanoyl)amino]benzamide 
• 1430587-43-1 C₂₈H₃₄N₆O₂ 
• 1301715-23-0 C₂₆H₂₇N₃O₂ 
• 1228571-25-2 C₂₀H₂₂N₂O₃ 
• 1301715-07-0 C₂₀H₂₁NO₃ 

Relevant articles and documents

Novel Pyridine-Based Hydroxamates and 2′-Aminoanilides as Histone Deacetylase Inhibitors: Biochemical Profile and Anticancer Activity

Starting from the N-hydroxy-3-(4-(2-phenylbutanoyl)amino)phenyl)acrylamide (5 b) previously described by us as a HDAC inhibitor, we prepared four aza-analogues, 6–8, 9 b, as regioisomers containing the pyridine nucleus. Preliminary screening against mHDAC1 highlighted the N-hydroxy-5-(2-(2-phenylbutanoyl)amino)pyridyl)acrylamide (9 b) as the most potent inhibitor. Thus, we further developed both pyridylacrylic- and nicotinic-based hydroxamates (9 a, 9 c–f, and 11 a–f) and 2′-aminoanilides (10 a–f and 12 a–f), related to 9 b, to be tested against HDACs. Among them, the nicotinic hydroxamate 11 d displayed sub-nanomolar potency (IC50: 0.5 nM) and selectivity up to 34 000 times that of HDAC4 and from 100 to 1300 times that of all the other tested HDAC isoforms. The 2′-aminoanilides were class I-selective HDAC inhibitors, generally more potent against HDAC3, with the nicotinic anilide 12 d being the most effective (IC50HDAC3=0.113 μM). When tested in U937 leukemia cells, the hydroxamates 9 e, 11 c, and 11 d blocked over 80 % of cells in G2/M phase, whereas the anilides did not alter cell-cycle progress. In the same cell line, the hydroxamate 11 c and the anilide 10 b induced about 30 % apoptosis, and the anilide 12 c displayed about 40 % cytodifferentiation. Finally, the most potent compounds in leukemia cells 9 b, 11 c, 10 b, 10 e, and 12 c were also tested in K562, HCT116, and A549 cancer cells, displaying antiproliferative IC50 values at single-digit to sub-micromolar level.

Preparation of aryl alkyl ketenes

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Origins of diastereoselectivity in lewis acid promoted ketene-alkene [2 + 2] cycloadditions

A detailed analysis of a Lewis acid promoted ketene-alkene [2 + 2] cycloaddition is reported. The studies have led to a rationalization for an observed inversion of diastereoselectivity between thermally induced and Lewis acid promoted ketene-alkene [2 + 2] cycloadditions. The model is supported with both experimental and computational results.