Detail of "63-98-9"

Reference

In vitro inhibitory activities of urea analogs on bacterial urease

In vitro inhibitory activities of urea analogs on bacterial urease. Chang, Pan Sup; Suh, Byungse; Strockbine, Nancy A.; Kunin, Galvin M. (Health Sci. Cent., Temple Univ., Philadelphia, PA, USA). Arch. Pharmacal Res., 9(3), 163-7 (English) 1986. CODEN: APHRDQ. ISSN: 0253-6269. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Twenty-six urea analogs, most of which have already been approved for human use, were tested for their urease [9002-13-5] inhibitory activity in vitro. Cell-free exts. obtained from a clin. isolate of Proteus mirabilis was used as the source of enzyme. Acetohydroxamic acid [546-88-3] which is a proven potent urease inhibitor but not approved for human use was again shown to be the most active compd. among the tested. Phenacemide [63-98-9], cycloserine [68-41-7], and deferoxamine mesylate [138-14-7] were demonstrated to be moderate inhibitors. Oxytetracycline [79-57-2], trimethoprim [738-70-5], and cefamandole nafate [42540-40-9] revealed a demonstrable antiurease activity, but only at very high concns. The antiurease activity of cycloserine, trimethoprim, and cefamandole was pH dependent; only active at acidic pH. The inhibitory activity of acetohydroxamic acid however was independent of change in pH. H+ concn. plays an important role in urease activity and acidification (pH 5.5) alone eliminates ~65% of the enzymic activity. Adjustment of pH therefore appears to be an important adjunct in reducing urease activity and should always be studied to maximize the efficacy of antiurease compds. under investigation.Except for chemicals metioned above, 42540-40-9 and 61270-58-4 are also used. .

Neurotoxicity of halogenated phenylacetylureas is linked to abnormal onset of rapid axonal transport

Neurotoxicity of halogenated phenylacetylureas is linked to abnormal onset of rapid axonal transport. Nagata, Hiroshi; Brimijoin, Stephen (Dep. Pharmacol., Mayo Clin., Rochester, MN 55905, USA). Brain Res., 385(1), 136-42 (English) 1986. CODEN: BRREAP. ISSN: 0006-8993. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) A structure-activity study was performed to investigate the mechanism of neurotoxicity induced in rats by treatment with p-bromophenylacetylurea (BPAU)(I) [30241-86-2]. Phenylacetylurea [63-98-9] and 7 derivs. were tested for their ability to induce hindlimb weakness after twice weekly administration in doses of 200 mg/kg, up to a cumulative max. of 2000 mg/kg. In this test, BPAU and its chloro analog [105673-85-6] were about equipotent, but none of the other analogs displayed any evidence of neurotoxicity. Since BPAU toxicity was believed to involve abnormalities in rapid axonal transport, selected analogs were examd. in a transport expt. None of the compds. led to alterations in the maximal rate of rapid anterograde transport, as measured after intraspinal injections of [35S]methionine in rats treated with 400 mg/kg of toxicant, 7 days earlier.In this experiment, several chemicals are used like 30241-86-2 and 105673-85-6 However, both BPAU and its chloro analog caused marked shortening of the delay between isotope injection and transport onset, an effect not seen with either of the 2 nonneurotoxic analogs tested. It is hypothesized that the accelerated transport onset is a key step in development of the neuropathy, possibly causing organelle abnormalities that interfere with turnaround and recirculation of transported particles. .