Synthesis and antitubercular activity of some mannich bases derived from isatin isonicotinic acid hydrazone

The purpose of this study based on the design and synthesis of a new series of 4-[1-[substitutedaminomethyl]]-2-oxo-2,3-dihydro-1H-3-indolylidene-pyridine- carboxylic acid hydrazones [2a-g] in a trial to overcome the resistance developed with the therapeutic uses of isonicotinic acid hydrazide [isoniazid, INH]. The new compounds were prepared by reacting isatin isonicotinic acid hydrazone with formalin and the appropriate secondary amines. The structures of the newly synthesized compounds were elucidated using different spectral data [IR, 1 HNMR, and 13 CNMR] as well as elemental methods of analyses. The lipophilicity of the synthesized compounds supercedes that of INH as expressed by Clog P.The new compounds [2a-g] as well as INH as a reference drug were tested for their antitubercular activity against bovine Mycobacterium tuberculosis at a dose level of 10 micromol. The tested compounds exhibited comparable inhibitory activity against the tested TB strain comparing to INH a reference drug

Electrochemical behavior of dopamine at the poly (isonicotinic acid) modified glassy carbon electrode / 药学学报

<p><b>AIM</b>To study the determination of dopamine (DA) in the presence of ascorbic acid (AA) using poly (isonicotinic acid) film modified electrode.</p><p><b>METHODS</b>The cyclic voltammetry and differential pulse voltammetry were used to study the electrochemical behavior of DA at the poly (isonicotinic acid) film modified electrode.</p><p><b>RESULTS</b>The poly (isonicotinic acid) film modified electrode showed an electrocatalytic effect on DA, and shifted the oxidation of AA to negative potential. The difference between the oxidation potentials of DA and AA was 204 mV, thus, AA did not interfere with the determination of DA. The linear range between the anodic currents and DA concentration was: 1.0 x 10(-7)-2.0 x 10(-5) and 2.0 x 10(-5)-1.0 x 10(-4) mol.L-1. The detection limit was 8.0 x 10(-9) mol.L-1.</p><p><b>CONCLUSION</b>The useful life period of the modified electrode is three weeks at least. The modified electrode can be used to the determination of DA in the sample.</p>

Isatin isonicotinoyl hydrazone complexes of tervalent metals Ti, Zr, Sn, Pt, and Th

Two forms of isatin isonicotinoyl hydrazone have been prepared. Analytical, t.g.a., electronic, i.r. and n.m.r. results show that the orange form [H.G.] is the anti-tautomer hydrazone whereas the yellow form [H.Y]. 1/2H[2]O is a mixture of imide-imidol of the syn one stabilized by H-bond through H-chelates. The complexes of Ti, Zr, Sn, Pt and Th with HG and HY were prepared and characterized using a variety of analytical, spectral and thermal measurements. The analytical data showed that 1:1 or 1:2 molar compounds were obtained. The title hydrazone behaved as a neutral or monobasic bidentate ligand coordinating through the azomethine N and isatin O or eventually as tridentate coordinating through O, N and pyridine N

Acute Isoniazid Intoxication-As an Unusual Cause of Fatal Status Epilepticus-

Isoniazid (INH), a hydrazide of isonicotinic acid, has been used for more than 30 years for the treatment of tuberculosis and is one of the most effective anti-tuberculous agents so far. In spite of the widespread use of INH, very few accidental or suicidal poisonings have been reported, Acute INH intoxication is characterized by hyperpyrexia, respiratory distress, coma seizure, metabolic acisosis, hyperglycemia and acetonuria Especially metabolic acidosis is not corrected by alkali therapy in which usual dose of bicarbonate supply, and seizure attacks also has not controlled by common anti-epileptic drugs, so it needed a large quantity of intravenous pyridoxine and diazepam infusion. This report describes an adult who ingested large amount of INH with the intent of suicide and was presented with the fatal status epilepticus and severe metabolic acidosis.

Hepatitis and multi-drug therapy in leprosy with special reference to prothionamide.

Hepatotoxicity in two drug regimens was studied at Central Leprosy Teaching and Research Institute, Chengalpattu (Tamil Nadu) during 1983-84. In 'P' regimen-prothionamide 350 mg daily, dapsone 100 mg daily and rifampicin 600 mg at monthly intervals were given. In' C' regimen-dapsone 100 mg daily, rifampicin 600 mg once a month and clofazimine 300 mg once a month and 100 mg alternate day were given. Trial was started with fifty multibacillary adult leprosy patients in each group. Enzymatic hepatic dysfunction was noted in 52-58 per cent of the cases even before the therapy was started. In 'P' regimen, four cases of clinical jaundice and six cases of high bilirubinaemia was noticed during the trial as against two cases each of clinical jaundice and high bilirubinaemia in 'C regimen. Of the two cases of clinical jaundice in 'C' regimen, one turned out to be a case of HBV infection. The study which is in progress, indicated higher hepatotoxicity in 'P' regimen which is probably explained by the simultaneous use of two hepatotoxic drugs. Viral hepatitis is endemic in this area and might have aggravated the hepatotoxicity observed.

Prothionamide and dapsone therapy in leprosy--a clinical study.

Combined therapy with prothionamide and dapsone was instituted in fifteen active untreated lepromatous leprosy cases for a period of 18 months. Clinical improvement was good with attainment of zero morphological index in about 66% cases. Bacteriological improvement was rather unsatisfactory as one case only reached zero level. Side effects were observed in few cases necessitating withdrawal of combined therapy and patients' prothionamide compliance was rather unimpressive.