213685-60-0

Upstream product

• 96315-18-3 2-nitro-4-phenylmethoxy-phenol 
• 75-15-0 carbon disulfide 
• 102580-07-4 2-Amino-4-benzyloxy-phenol 
• 140-89-6 potassium ethyl xanthogenate 

Downstream Products

• 213684-85-6 6-((5-(benzyloxy)benzo[d]oxazol-2-yl)thio)-N-(2,6-diisopropylphenyl)hexanamide 
• 213684-86-7 N-(2,6-diisopropylphenyl)-6-((5-hydroxybenzo[d]oxazol-2-yl)thio)hexanamide 
• 114997-09-0 3-[N-(5-Benzyloxy-benzooxazol-2-yl)-hydrazino]-propionitrile 
• 38519-88-9 (5-benzyloxy-benzooxazol-2-yl)-[4-(2-diethylamino-ethoxy)-phenyl]-amine 
• 213684-87-8 9-(5-hydroxybenzoxazol-2-ylthio)-N-(2,6-diisopropylphenyl)nonanamide 

Relevant academic research and scientific papers

Design, synthesis and pharmacology of aortic-selective acyl-CoA: Cholesterol O-acyltransferase (ACAT/SOAT) inhibitors

We describe our molecular design of aortic-selective acyl-coenzyme A:cholesterol O-acyltransferase (ACAT, also abbreviated as SOAT) inhibitors, their structure–activity relationships (SARs) and their pharmacokinetic (PK) and pharmacological profiles. The connection of two weak ligands—N-(2,6-diisopropylphenyl)acetamide (50% inhibitory concentration [IC50] = 8.6 μM) and 2-(methylthio)benzo[d]oxazole (IC50 = 31 μM)—via a linker comprising a 6 methylene group chains yielded a highly potent molecule, 9-(benzo[d]oxazol-2-ylthio)-N-(2,6-diisopropylphenyl)nonanamide (3h) that exhibited high potency (IC50 = 0.004 μM) toward aortic ACAT. This head-to-tail design made it possible to markedly enhance the activity to 2150- to 7750-fold and to discriminate the isoform-selectivity based on the double-induced fit mechanism. At doses of 1 and 3 mg/kg, 3h significantly decreased the lipid-accumulation areas in the aortic arch to 74 and 69%, respectively without reducing the plasma total cholesterol level in high fat- and cholesterol-fed F1B hamsters. Here, we demonstrate the antiatherosclerotic effect of 3h in vivo via its direct action on aortic ACAT and its powerful modulator of cholesterol level. This molecule is a potential therapeutic agent for the treatment of diseases involving ACAT-1 overexpression.

Anilide compounds and drugs containing the same

The invention relates to a novel anilide compound and a pharmaceutical composition comprising the same. The invention relates to a compound represented by the following general formula: represents a divalent residue of benzene with a substituent(s), heterocycle-condensed benzene which may or may not have a substituent, pyridine which may or may not have a substituent, cyclohexane or naphthalene or Ar represents an aryl group which may or may not have a substituent; X represents —NH—, oxygen atom or sulfur atom; Y represents —NR4—, oxygen atom, sulfur atom, sulfoxide or sulfone; Z represents single bond or —NR5—; R4represents hydrogen atom, a lower alkyl group, an aryl group or a silylated lower alkyl group which may or may not have a substituent; R5represents hydrogen atom, a lower alkyl group, an aryl group or a silylated lower alkyl group which may or may not have a substituent; and n represents an integer of 0 to 15. The inventive compounds are useful in the form of pharmaceutical composition, specifically as acyl coenzyme A cholesterol acyltransferase (ACAT) inhibitor.

Benzoxazoline and benzimidazoline derivatives as novel aldose reductase inhibitors, part 2: Lead optimization

We designed novel aldose reductase inhibitors, benzoxazoline and benzimidazoline derivatives, based on lead evolution from spiroquinazolinones. In order to optimize in vivo activity in the lens, variously substituted derivatives were synthesized. The relationship between structure and in vitro activity was also analyzed by comparative molecular field analysis. The optimized compound exhibited high potency in the lens.

3-[1-(2-Benzoxazolyl)hydrazino]propanenitrile derivatives: Inhibitors of immune complex induced inflammation

3-[1-(2-Benzoxazolyl)hydrazino]propanenitrile derivatives were evaluated in the dermal and pleural reverse passive Arthus reactions in the rat. In the pleural test these compounds were effective in reducing exudate volume and accumulation of white blood cells. This pattern of activity was similar to that of hydrocortisone and different from that of indomethacin. The structural requirements for inhibiting the Arthus reactions were studied by systematic chemical modification of 1. These structure-activity relationship studies revealed that nitrogen 1' of the hydrazino group is essential for activity and must be electron rich, whereas chemical modifications of other sites of 1 had only a modest effect on activity.