13038-85-2

Upstream product

• 127099-85-8 N-Cyanoguanidine 
• 4760-34-3 N-methyl-1,2-phenylenediamine 
• 25148-68-9 N-methylbenzene-1,2-diamine dihydrochloride 
• 5418-95-1 2-guanidinobenzimidazole 
• 74-88-4 methyl iodide 
• 77-78-1 dimethyl sulfate 

Relevant academic research and scientific papers

Structure activity relationships of human galactokinase inhibitors

Classic Galactosemia is a rare inborn error of metabolism that is caused by deficiency of galactose-1-phosphate uridyltransferase (GALT), an enzyme within the Leloir pathway that is responsible for the conversion of galactose-1-phosphate (gal-1-p) and UDP-glucose to glucose-1-phosphate and UDP-galactose. This deficiency results in elevated intracellular concentrations of its substrate, gal-1-p, and this increased concentration is believed to be the major pathogenic mechanism in Classic Galactosemia. Galactokinase (GALK) is an upstream enzyme of GALT in the Leloir pathway and is responsible for conversion of galactose and ATP to gal-1-p and ADP. Therefore, it was hypothesized that the identification of a small-molecule inhibitor of human GALK would act to prevent the accumulation of gal-1-p and offer a novel entry therapy for this disorder. Herein we describe a quantitative high-throughput screening campaign that identified a single chemotype that was optimized and validated as a GALK inhibitor.

Metal-templated hydrogen bond donors as "organocatalysts" for carbon-carbon bond forming reactions: Syntheses, structures, and reactivities of 2-guanidinobenzimidazole cyclopentadienyl ruthenium complexes

The reaction of 2-guanidinobenzimidazole (GBI) and (η5-C5H5)Ru(PPh3)2(Cl) in refluxing toluene gives the chelate [(η5-C5H5)Ru(PPh3)(GBI)]+Cl- (1+Cl-; 96%). Subsequent anion metatheses yield the BF4-, PF6-, and BArf- (B(3,5-C6H3(CF3)2)4-) salts (77-85%). Reactions with CO give the carbonyl complexes [(η5-C5H5)Ru(CO)(GBI)]+X- (2+X-; X- = Cl-, BF4-, PF6-, BArf-; 87-92%). The last three salts can also be obtained by anion metatheses of 2+Cl- (77-87%), as can one with the chiral enantiopure anion P(o-C6Cl4O2)3- ((δ)-TRISPHAT-; 81%). The reaction of [(η5-C5H5)Ru(CO)(NCCH3)2]+PF6- and GBI also gives 2+PF6- (81%). The pentamethylcyclopentadienyl analogues [(η5-C5Me5)Ru(CO)(GBI)]+X- (3+X-; X- = Cl-, BF4-, PF6-, BArf-; 61-84%) are prepared from (η5-C5Me5)Ru(PPh3)2(Cl), GBI, and CO followed (for the last three) by anion metatheses. An indenyl complex [(η5-C9H7)Ru(PPh3)(GBI)]+Cl- (96%) is prepared from (η5-C9H7)Ru(PPh3)2(Cl) and GBI. All complexes are characterized by NMR (1H, 13C, 31P, 19F, 11B), with 2D spectra aiding assignments. Crystal structures of 1+PF6-·CH2Cl2 and 1+BArf-·CH2Cl2 are determined; the anion is hydrogen bonded to the cation in the former. Complexes 1-3+X- are evaluated as catalysts (10 mol %, RT) for condensations of indoles and trans-β-nitrostyrene. The chloride salts are ineffective (0-5% yields, 48-60 h), but the BArf- salts exhibit excellent reactivities (97-46% yields, 1-48 h), with the BF4- and PF6- salts intermediate. Evidence for hydrogen bonding of the nitro group to the GBI ligand is presented. GBI shows no catalytic activity; a BArf- salt of methylated GBI is active, but much less so than 2-3+BArf-.

STRUCTURE AND BASICITY OF 2-GUANIDINOBENZIMIDAZOLES

A theoretical and experimental study of the basicity of three 2-guanidinobenzimidazoles has been carried out.The most abundant tautomer, the structure of the protonated molecule, and the reason of the relatively low pKa are disscused.In addition, a careful 1H and 13C nmr study provides information about the influence of intramolecular hydrogen bonds on annular tautomeric rates.

Anti-hypertensive compositions of benzimidazole derivatives

Antihypertensive pharmaceutical compositions comprising a compound of the formula (II) SPC1 or pharmaceutically acceptable salts or solvates thereof wherein R1 is nitrile or amidino; R2 is hydrogen or lower hydrocarbon; R3