Heterocyclic Building Blocks-Benzothiophene

Homberg, J C published the artcileDrug-induced hepatitis associated with anticytoplasmic organelle autoantibodies., Recommanded Product: 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, the main research area is .

A study from five hepatology units documenting 157 cases of drug-induced hepatitis and a second study from a laboratory of immunology which tested more than 100,000 sera permitted us to establish the frequency of antiorganelle antibodies and their diagnostic value in drug-induced hepatitis. In drug-induced hepatitis caused by a heterogenous group of drugs consisting of ajmaline, aminopterine, isaxonine, isoniazid, perhexiline, phenylbutazone and troleandromycine, antiorganelle antibodies were absent or rare. In drug-induced hepatitis caused by another heterogenous group of drugs, including clometacin, fenofibrate, oxyphenisatin and papaverine, antismooth muscle, antinucleus and antimitochondria antibodies were found in isolation or in different combinations in 70% of cases. From the presence of antismooth muscle antibodies in sera, we could trace 30 cases of clometacin-induced hepatitis. The third group included drug-induced hepatitis with special antibody:iproniazid-induced hepatitis with antimitochondrial antibody 6 and tienilic acid (ticrynafen)-induced hepatitis with antiliver/kidney microsome antibody 2 (anti-LKM2). These two antibodies are rare in routine sera and were absent in patients who received the drug and had no liver damage. From the presence of corresponding antibodies, we detected six cases of iproniazid-induced hepatitis and 67 cases of tienilic acid-induced hepatitis. Antiorganelle antibodies found in high titers disappeared in 2 to 24 months following withdrawal of the offending drug. The fourth group was represented by halothane-induced hepatitis; antiliver/kidney microsome antibody 1 was weak and infrequent. Similarities between drug-induced hepatitis of the second group and lupoïd hepatitis suggest that drugs may reveal this spontaneous disorder.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatology (Baltimore, Md.) published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Recommanded Product: 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Zimmerman, H J published the artcileEffects of ticrynafen on hepatic excretory function in the isolated perfused rat liver., Application of 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, the main research area is .

Ticrynafen, a uricosuric diuretic agent which causes hepatocellular injury in man as an apparent idiosyncratic reaction, was found to impair the function of the isolated perfused rat liver. At concentrations in the perfusate equivalent to those produced in the blood of man by therapeutic doses, the drug led to a striking reduction in bile flow and sulfobromophthalein excretion and release of aspartate aminotransferase into the perfusate. These adverse effects were enhanced by treatment of rats with phenobarbital prior to removal of the liver, indicating that the adverse effect of ticrynafen is probably caused by a metabolite produced in the cytochrome P-450 system.

Hepatology (Baltimore, Md.) published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Application of 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Liu, Zhang-Xu published the artcileImmune-mediated drug-induced liver disease., Product Details of C13H8Cl2O4S, the main research area is .

Drug-induced immune-mediated hepatic injury is an adverse immune response against the liver that results in a disease with hepatitic, cholestatic, or mixed clinical features. Drugs such as halothane, tienilic acid, dihydralazine, and anticonvulsants trigger a hepatitic reaction, and drugs such as chlorpromazine, erythromycins, amoxicillin-calvulanic acid, sulfonamides and sulindac trigger a cholestatic or mixed reaction. Unstable metabolites derived from the metabolism of the drug may bind to cellular proteins or macromolecules, leading to a direct toxic effect on hepatocytes. Protein adducts formed in the metabolism of the drug may be recognized by the immune system as neoantigens. Immunocyte activation may then generate autoantibodies and cell-mediated immune responses, which in turn damage the hepatocytes. Cytochromes 450 are the major oxidative catalysts in drug metabolism, and they can form a neoantigen by covalently binding with the drug metabolite that they produce. Autoantibodies that develop are selectively directed against the particular cytochrome isoenzyme that metabolized the parent drug. The hapten hypothesis proposes that the drug metabolite can act as a hapten and can modify the self of the individual by covalently binding to proteins. The danger hypothesis proposes that the immune system only responds to a foreign antigen if the antigen is associated with a danger signal, such as cell stress or cell death. Most clinically overt adverse hepatic events associated with drugs are unpredictable, and they have intermediate (1 to 8 weeks) or long latency (up to 12 months) periods characteristic of hypersensitivity reactions. Immune-mediated drug-induced liver disease nearly always disappears or becomes quiescent when the drug is removed. Methyldopa, minocycline, and nitrofurantoin can produce a chronic hepatitis resembling AIH if the drug is continued.

Clinics in liver disease published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Product Details of C13H8Cl2O4S.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Weidmann, P published the artcileDiuretic treatment and serum lipoproteins: effects of tienilic acid and indapamide., Application of 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, the main research area is .

Treatment with the commonly used diuretic, chlorthalidone, has previously been found to increase the serum low-density-lipoprotein cholesterol (LDL-C) fraction. Therefore, the effects of two new agents, tienilic acid (a combined diuretic-uricosuric) and indapamide on serum lipid and lipoprotein levels were assessed. Six weeks of treatment with tienilic acid, 250 mg/day, markedly decreased serum uric acid and significantly increased LDL-C and triglycerides in 16 men. In contrast, indapamide 2.5 mg/day, had no apparent influence on serum lipids or lipoproteins in 18 men.

Klinische Wochenschrift published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Application of 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Riegelman, R K published the artcileWhat to do until the FDA arrives., Application In Synthesis of 40180-04-9, the main research area is .

The need for clinical monitoring to assure drug safety despite reliance on Food and Drug Administration testing is illustrated. The need to temper theory with clinical experience is exemplified by the recent examples of swine flu, resistant gonorrhea, and resistant pneumococcal infection. The potential for adverse effects to escape detection in animal studies and small-scale human trials is illustrated by the examples of ticrynafen, chloramphenicol, and diethylstilbestrol. The potential for unexpected side effects when established drugs are used in new ways is demonstrated by the examples of retrolental fibroplasia and vitamin D toxicity. The responsibilities of the medical profession and the individual practitioner include a healthy skepticism of newly introduced treatments, active participation in clinical monitoring, and maintenance of a system for chart retrieval when drugs are recalled or new effects reported.

Postgraduate medicine published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Application In Synthesis of 40180-04-9.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Powers, D published the artcileTicrynafen-induced acute renal failure., HPLC of Formula: 40180-04-9, the main research area is .

Two cases of acute renal failure associated with ticrynafen administration are reported. Both patients had received hydrochlorothiazide prior to the institution of ticrynafen therapy and were mildly hyperuricemic. Flank pain, oliguria, and azotemia developed after the institution of ticrynafen in both cases. Clinical and laboratory features were consistent with acute uric acid nephropathy in both patients. In addition, a newly formed collection of radiolucent material was found by intravenous urography in the renal pelvis of one of the patients. Both patients were treated with intravenous fluids and sodium bicarbonate. One of the patients received allopurinol as well. Complete recovery of renal function was observed in both patients. Ticrynafen-induced hyperuricosuria in these previously volume-depleted and hyperuricemic subjects is felt to have been responsible for intrarenal and extrarenal deposition of uric acid in our patients.

Clinical toxicology published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, HPLC of Formula: 40180-04-9.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Matsuda, O published the artcileA case of familial renal hypouricemia associated with increased secretion of para-aminohippurate and idiopathic edema., Computed Properties of 40180-04-9, the main research area is .

A 42-year-old housewife had hypouricemia (serum uric acid ranging from 0.5 to 1.5 mg/dl; 30-89 mumol/l), increased uric acid clearance (47.6-83.0 ml/min), increased maximum tubular secretory capacity for para-aminohippurate, and idiopathic edema. Urate excretion was only minimally suppressed by pyrazinamide, and paradoxically decreased by probenecid. Uric acid clearance did not show any appreciable change after long-term administration of ticrynafen. In response to an increment of extracellular volume by hypertonic saline infusion or long-term 9 alpha-fluorohydrocortisone administration, urate clearance did not show any substantial increase. These data may suggest that not only presecretory but possibly also postsecretory reabsorption of urate is impaired in this patient. No other renal tubular abnormalities were detected. Family study revealed that her renal hypouricemia is hereditary. She was unable to increase urinary excretion of sodium during hypertonic saline infusion and failed to change the response to the sodium-retaining action of 9 alpha-fluorohydrocortisone, presumably accounting for her edema.

Nephron published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Computed Properties of 40180-04-9.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Lant, A published the artcileDiuretics. Clinical pharmacology and therapeutic use (Part II)., Safety of 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, the main research area is .

25 years have elapsed since the introduction of the first effective oral diuretic, chlorothiazide. Diuretics are now amongst the most widely prescribed drugs in clinical practice worldwide. Availability of these drugs has not only brought therapeutic benefit to countless numbers of patients but it has at the same time provided valuable research tools with which to investigate the functional behaviour of the kidney and other electrolyte-transporting tissues. Despite many remaining gaps in our knowledge of the biochemical processes involved in diuretic drug action, available compounds can be divided into 5 groups on the basis of their preferential effects on different segments of the nephron involved in tubular reabsorption of sodium chloride and water. Firstly, there is a heterogeneous group of chemicals that share the common property of powerful, short-lived diuretic effects that are complete within 4 to 6 hours. These agents act on the thick ascending limb of Henle’s loop and are known as ‘high ceiling’ or ‘loop’ diuretics. The second group are the benzothiadiazines and their many related heterocyclic variants, all of which localise their effects to the early portion of the distal tubule. The third group comprises the potassium-sparing diuretics which act exclusively on the Na+-K+/H+ exchange mechanisms in the late distal tubule and cortical collecting duct. The action of drugs in groups 2 and 3 is prolonged to between 12 and 24 hours. The fourth group consists of diuretics that are chemically related to ethacrynic acid but have the unusual property of combining within the same molecule the property of saluresis and uricosuria. These compounds have actions, to different individual extents, in the proximal tubule, thick ascending limb, and early distal tubule and are known as ‘polyvalent’ diuretics. Finally, there is a mixed group of weak or adjunctive diuretics which includes the vasodilator xanthines such as aminophylline, and the osmotically active compounds such as mannitol. The metabolic consequences of continued diuretic usage are considered along with non-metabolic sequelae such as ototoxicity or interactions with other concurrent treatments. The relationships between the clinical benefits conferred and the potential harms generated by long term diuretic therapy are also discussed.

Drugs published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Safety of 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Johnson, M W published the artcileThe risks of asymptomatic hyperuricaemia and the use of uricosuric diuretics., Recommanded Product: 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, the main research area is .

Introduction of new uricosuric diuretics will be accompanied by the unknown risk factors associated with the use of any new drug, as demonstrated by reports of hepatic toxicity associated with ticrynafen. In addition to unexpected reactions, there are potential risks related to induction of uricosuria, which are serious and have been reported to occur. More importantly, the risk of developing clinical gout or coronary heart disease due to mild asymptomatic hyperuricaemia appears minimal, so indications for the use of uricosuric diuretics are limited. If a uricosuric diuretic is thought necessary (and is available), it would seem prudent to measure the daily excretion rate of uric acid to identify those patients with hyperuricaemia related to overproduction of uric acid. A uricosuric diuretic should be avoided in those patients, as well as in patients with uric acid stones, and possibly in those with calcium stones. A uricosuric diuretic might be useful for patients with hypertension who also have hyperuricaemia due to a low excretion of uric acid.

Drugs published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Recommanded Product: 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Kosman, M E published the artcileEvaluation of a new uricosuric diuretic–ticrynafen., Computed Properties of 40180-04-9, the main research area is .

Ticrynafen is an orally administered diuretic that is similar to the thiazides in its therapeutic actions, but unlike the thiazides, it increases urate excretion and lowers serum uric acid levels. Ticrynafen is useful in the treatment of hypertension and in selected cases of chronic congestive heart failure. At present, it appears to be indicated primarily in patients with these disorders who have a history of gout. Patients who are currently receiving a thiazide should not have their therapy arbitrarily changed to ticrynafen because of asymptomatic hyperuricemia.

JAMA published new progress in MEDLINE about 40180-04-9, 40180-04-9 belongs to class benzothiophene, name is 2-(2,3-Dichloro-4-(thiophene-2-carbonyl)phenoxy)acetic acid, and the molecular formula is C13H8Cl2O4S, Computed Properties of 40180-04-9.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem