Tag: M.W=200-350

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

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

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

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 artcileTicrynafen-associated hepatic injury: analysis of 340 cases., Related Products of benzothiophene, the main research area is .

Ticrynafen, a uricosuric diuretic, was withdrawn from clinical use in the United States in 1980 after having been implicated as the cause of a number of instances of serious hepatic injury. In this report, we analyze 340 cases of ticrynafen-associated hepatic disease reported to the manufacturer from the time of initial marketing until shortly after the drug had been recalled. Jaundice was recorded in 246 of 287 patients with sufficient clinical information, and 25 (10.2%) of these icteric patients died. The high levels of serum aminotransferase and the case fatality rate are consistent with the hepatocellular injury that was evident in all of the histologic material. In three-fourths of the cases available to us for histologic study, the lesion was that of acute hepatocellular injury. In the remaining cases there was evidence of chronic active hepatitis and/or cirrhosis. Comparison of demographic characteristics of the total population exposed to ticrynafen with the subset developing hepatic injury suggests a proportionately higher risk of injury for females over the age of 60 years. The variable and unusually prolonged latent period and lack of reported eosinophilia or rash generally suggest a mechanism other than hypersensitivity. However, the recurrence of hepatic injury in 15 of the 16 patients challenged with the drug and the prominence of eosinophils in hepatic tissue in some of the cases suggests that hypersensitivity may also play a pathogenetic role. Accordingly, there is reason to incriminate both metabolic idiosyncrasy and hypersensitivity in the mechanism of injury.

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, Related Products of benzothiophene.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

Noble, R E published the artcileLong-term usage of tienilic acid in essential hypertension., HPLC of Formula: 40180-04-9, the main research area is .

The purpose of this double-blind study was to compare the effects on blood pressure of tienilic acid and hydrochlorothiazide in patients with essential hypertension. The biochemical effects of tienilic acid in relation to those of hydrochlorothiazide were also determined over a long-term period of therapy. Sixty-six outpatients with mild to moderate essential hypertension were treated for seven months with either 250 mg of tienilic acid or 50 mg of hydrochlorothiazide after a 3 week placebo period. When warranted, dosage was increased to a maximum of 500 mg of tienilic acid and 100 mg of hydrochlorothiazide daily. Results indicate that tienilic acid reduced blood pressure significantly and to the same extent as hydrochlorothiazide. No significant side effects were observed. The effects on potassium, blood urea nitrogen and creatinine were comparable in both groups. However, serum uric acid rose with hydrochlorothiazide but fell with tienilic acid. In view of this effect, tienilic acid may have certain advantages over thiazide therapy in the treatment of hypertension.

Postgraduate medical journal 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

Okun, R published the artcileA double-blind study of tienilic acid with two year follow-up of patients with mild to moderate essential hypertension., Application In Synthesis of 40180-04-9, the main research area is .

In a double-blind study, thirty patients having mild to moderate essential hypertension were randomly assigned to a six week regimen of either tienilic acid, hydrochlorothiazide, or placebo. Blood pressure was significantly reduced with tienilic acid and hydrochlorothiazide although more so with tienilic acid. Serum uric acid declined strikingly with tienilic acid and increased significantly with hydrochlorothiazide. Serum potassium declined slightly with tienilic acid but more so with hydrochlorothiazide. Serum creatinine and blood urea nitrogen increased slightly more with tienilic acid than with hydrochlorothiazide. There were no clinical adverse effects to any of the medications during this study. Twenty-four months of continuous administration of tienilic acid revealed maintenance of blood pressure effect, but with slight increases in blood urea nitrogen, serum creatinine and uric acid and slight decreases in serum potassium as compared to six weeks administration. Tienilic acid appears to be a useful new antihypertensive agent. The hypouricaemic effect is profound and strongly suggests the need for continuing evaluation of this compound because of its unique combination of diuretic, antihypertensive and hypouricaemic properties.

Postgraduate medical journal 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

Andersson, O published the artcileTienilic acid in mild to moderate hypertension., Computed Properties of 40180-04-9, the main research area is .

Tienilic acid has blood pressure lowering properties alone and in combined treatment with beta-adrenergic blocking agents; 250 mg of tienilic acid seems to correspond to 50 mg of hydrochlorothiazide. Tienilic acid effectively reduces serum urate and has no marked or rapid effect on potassium balance. During short-term treatment, no impairment of glucose tolerance was found.

Postgraduate medical journal 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

Morgan, A published the artcileThe use of tienilic acid in nephrotic syndrome: a clinical study., Application In Synthesis of 40180-04-9, the main research area is .

The diuretic and uricosuric activities of tienilic acid 250–50 mg daily over a minimum six week period have been studied in seven patients with the nephrotic syndrome secondary to glomerulonephritis proven by renal biopsy. Tienilic acid failed to control oedema in one patient who had to be withdrawn. In the six other patients a hypouricaemic effect with increased urate clearance was noted. No consistent effects were noted with respect to the serum cholesterol and triglyceride concentrations. No side effects were observed. It is concluded that in nephrotic patients tienilic acid behaves as a mild diuretic with consistent hypouricaemic and uricosuric effects.

Postgraduate medical journal 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

Pearson, R M published the artcilePropranolol and tienilic acid in essential hypertension., Quality Control of 40180-04-9, the main research area is .

Sixteen patients with moderately severe essential hypertension completed a double-blind crossover trial with four treatment periods each lasting for six weeks. They received in random order, placebo; tienilic acid 250 mg/day; propranolol 80 mg b.d.; and tienilic acid 250 mg/day and propranolol 80 mg b.d. in combination. Mean blood pressure in the lying position was 169/98 mmHg on placebo, 157/94 mmHg on tienilic acid, 159/90 mmHg on propranolol and 142/86 mmHg on the combination of tienilic acid and propranolol. The effects of tienilic acid and propranolol on blood pressure were additive and there was no evidence of any interaction. The onset of the hypotensive effect of tienilic acid was gradual while the effect of propranolol was maximal within 2 weeks of the start of treatment. Tienilic acid produced a significant reduction in serum urate from 0.33 mmol/l to 0.18 mmol/l. The combination of tienilic acid and propranolol in the doses used in the trial was effective and acceptable in the reduction of raised blood pressure.

Postgraduate medical journal 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, Quality Control of 40180-04-9.

Referemce:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem