23593-68-2

Upstream product

• 693-98-1 2-methylimidazole 
• 596-43-0 bromo-triphenyl-methane 
• 15469-97-3 N-tritylimidazole 
• 74-88-4 methyl iodide 
• 76-83-5 trityl chloride 
• 87941-55-7 4-bromo-1-(triphenylmethyl)-1H-imidazole 

Downstream Products

• 121816-83-9 4-bromo-2-methyl-1-tritylimidazole 
• 258873-62-0 2-[1-(triphenylmethyl)-1H-imidazol-2-yl]acetaldehyde 
• 1143535-26-5 1-(4-chlorophenyl)-2-(1-trityl-1H-imidazol-2-yl)ethanol 
• 172499-78-4 3-[N-Triphenylmethyl-imidazol-2-yl]-propan-1-ol 
• 1555939-34-8 N₁-[3-phenyl-3-(thiazol-2-yl)propanoyl]-N₂-[3-(1-trityl-1H-imidazol-2-yl)propyl]guanidine 
• 1555939-32-6 N₁-(3,3-diphenylpropanoyl)-N₂-[3-(1-trityl-1H-imidazol-2-yl)propyl]guanidine 
• 1555939-30-4 N₁-[3-(thiophen-2-yl)butanoyl]-N₂-[3-(1-trityl-1H-Imidazol-2-yl)propyl]guanidine 
• 1555939-28-0 N₁-(3-phenylbutanoyl)-N₂-[3-(1-trityl-1H-imidazol-2-yl)propyl]guanidine 
• 1555938-77-6 N-[3-(1-trityl-1H-imidazol-2-yl)propyl]guanidine 
• 1555938-57-2 N₁,N₂-bis(benzyloxycarbonyl)-N₁-[3-(1-trityl-1H-imidazol-2-yl)propyl]guanidine 
• 1000517-17-8 C₂₄H₂₀N₂O₂ 
• 161398-29-4 1-(3-Chlorophenyl)-2-(1-triphenylmethylimidazol-2-yl)ethyl alcohol 
• 258873-65-3 C₅₂H₇₀N₁₀O₉ 
• 258873-63-1 {7-tert-butoxycarbonylamino-6-oxo-1-[2-(1-trityl-1H-imidazol-2-yl)-ethyl]-[1,5]diazocan-3-yl}-carbamic acid tert-butyl ester 

Relevant academic research and scientific papers

FERROPORTIN INHIBITORS AND METHODS OF USE

The subject matter described herein is directed to Ferroportin inhibitor compounds of Formula I and pharmaceutical salts thereof, methods of preparing the compounds, pharmaceutical compositions comprising the compounds and methods of administering the compounds for prophylaxis and/or treatment of diseases caused by a lack of hepcidin or iron metabolism disorders, particularly iron overload states, such as thalassemia, sickle cell disease and hemochromatosis.

PYRROLO [2,3-D] PYRIMIDIN DERIVATIVES AS PROTEIN KINASE B INHIBITORS

The invention relates to a novel group of compounds of Formula (I) or salts thereof: wherein Y, Z1, Z2, R1, R4, R5 and n are as described in the specification, which may be useful in the treatment or prevention of a disease or medical condition mediated through protein kinase B (PKB) such as cancer. The invention also relates to pharmaceutical compositions comprising said compounds, methods of treatment of diseases mediated by PKB using said compounds and methods for preparing compounds of Formula (I)

BENZOTRIAZEPINONE DERIVATIVES

The present invention is concerned with benzotriazepinone derivatives, their intermediates, uses thereof and processes for their production. In particular, the present invention relates to parathyroid hormone (PTH) and parathyroid hormone related protein (PTHrp) receptor ligands, (PTH-I or PTH/PTHrp receptor ligands). The invention also relates to methods of preparing such ligands and to compounds which are useful as intermediates in such methods.

N-HETEROCYCLYL-SUBSTITUTED AMINO-THIAZOLE DERIVATIVES AS PROTEIN KINASE INHIBITORS

Aminothiazole compounds with N-containing cycloalkyl at the 2-amino position which are represented by the Formula (I), or a pharmaceutically acceptable prodrug of said compound, or pharmaceutically acceptable salt of said compound, modulate and/or inhibit the cell proliferation and activity of protein kinases.

Properties of a binaphthyl-bridged porphyrin - Iron complex bearing hydroxy groups inside its cavity

Hydrogen-bond formation with the terminal oxygen atom is considered to be the basis of dioxygen molecule activation by cytochrome P450. In order to verify the effect of this hydrogen bond, we have undertaken the synthesis of a model complex: a binaphthyl-

Influence of some novel N-substituted azoles and pyridines on rat hepatic CYP3A activity

A series of N-substituted heteroaromatic compounds structurally related to clotrimazole was synthesized, and the effects of these compounds on ethosuximide clearance in rats were determined as a measure of their abilities to induce cytochrome P4503A (CYP3A) activity. Ethosuximide clearance and in vitro erythromycin N-demethylase activity were shown to correlate. In this series, imidazole or other related heteroaromatic 'head groups' were linked to triphenylmethane or other phenylmethane derivatives. Within the series, it was found that 1-triphenylmethane-substituted imidazoles elicited the greatest increase in CYP3A activity, and that among the triphenylmethyl-substituted imidazoles, the highest activities were achieved by the substitution of F- or Cl- in either the meta or para position of one of the phenyl rings. Diphenylmethylsubstituted pyridine was effectively devoid of activity. Compounds eliciting the largest increase in CYP3A activity (viz. 1-[(3-fluorophenyl)diphenylmethyl]imidazole, 1-[(4- fluorophenyl)diphenylmethyl]imidazole, and 1-[tri-(4- fluorophenyl)methyl]imidazole) produced little or no increase in ethoxyresorufin O-dealkylase (EROD) activity (i.e. CYP1A), whereas benzylimidazole, which elicited only a small increase in CYP3A activity, produced an almost 9-fold increase in CYP1A activity. For a series of eleven compounds exhibiting a wide range of influence on CYP3A activity, a positive correlation was found between ethosuximide clearance and hepatic CYP3A mRNA levels.

Synthesis and Reactions of Brominated 2-Nitroimidazoles

Various approaches to the synthesis of the hitherto-unknown 4(5)-bromo-2-nitroimidazole (5) are reported.Direct bromination of 2-nitroimidazole with N-bromosuccinimide gave the unreported 4,5-dibromo-2-nitroimidazole (10) in quantitative yield, but this could be selectively debrominated to give compound (5).While 1-methyl-2-nitroimidazole readily gave 4-bromo-1-methyl-2-nitroimidazole (15) on bromination, this could not be demethylated to give (5), and bromination of various other N-protected 2-nitroimidazoles was also unsuccessful.Lithiation of 4-bromo-1-tritylimidazole (21) followed by quenching with propyl nitrate gave (after detritylation and methylation) a mixture of a dimer (28) and compound (15), indicating that the desired product (5) is produced in this reaction although it can only be isolated in derivatized form.The proposed route for formation of the dimer suggests a general reaction between 1-alkyl-4-bromo-2-nitroimidazoles and strong C- and N-nucleophiles, resulting in substitution at the 5-position.

2,5-Dilithiation of N-Protected Imidazoles. Syntheses of 2,5-Disubstituted Derivatives of 1-Methoxymethyl-, 1-Triphenylmethyl-, and 1-(N,N-Dimethylsulphonamido)-imidazole

The conditions previously established for the dilithiation of 1-methylimidazole are shown to be applicable to 1-methoxymethyl- and 1-triphenylmethyl-imidazole allowing good-yielding syntheses of 1,2,5-trisubstituted imidazole derivatives.The suitability of the 1-substituted (and of other groups) for the N-protection of imidazoles in dilithiation experiments is discussed and the use of the N,N-dimethylsulphamoyl protecting group is proposed. 1-Sulphamoylimidazole undergoes mono- and 2,5-di-lithiation quantitatively at low temperatures and in short reaction times.The results of work-up of the 2,5-dilithio intermediate with 1 mol equiv. of iodomethane or dimethyl sulphate indicate selectivity in favour of reaction at the 5-position.

Liposomal Heme as Oxygen Carrier under Semi-physiological Conditions

A meso-5,10,15,20-tetra(o-pivalamidophenyl)porphyrinatoiron(II) complex of a 2-methylimidazole, substituted in the 1-position with a hydrophobic group, was incorporated into a lipid bilayer of phosphatidylcholine (liposomal heme).The liposomal heme reversibly bound molecular oxygen in neutral aqueous media at 37 deg C, and the half-life of the oxygen adduct was half a day.The oxygen-binding affinity (p1/2) for the liposomal heme was ca. 50 mmHg, which is similar to that of hemoglobin in blood.The incorporation and structure of the liposomal heme were confirmed by physico-chemical methods, which indicated that the hydrophobic environment of the inner region of liposome protected the oxygen adduct from its proton-driven oxidation.