• Korean Journal of Clinical Pharmacy
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• v.20 no.3
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• pp.229-234
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• 2010

섬유근통 증후군은 만성 전신 통증을 나타내며 피곤, 두통, 우울증, 수면장애 등을 동반하는 질환이다. 주로 30-50대의 여성에게서 많이 나타나며 미국에서 2-4%, 한국에서 2%의 발병률을 보이고 있다. 정확한 원인과 기전이 밝혀져 있지 않아서 진단과 치료에 많은 논란과 어려움이 있다. 현재는 증상치료에 목표를 두고 삼환계항우울약을 많이 사용하고 있으나 심각한 부작용의 문제가 있다. 이러한 문제 때문에 최근에는 selective serotonin reuptake inhibitor (SSRI) 또는 serotonin-norepinephrine reuptake inhibitor (SNRI)를 빈번히 사용하고 있다. 본 연구는 SNRI의 하나인 milnacipran의 섬유근통 증후군 치료에 대한 효능 및 안정성을 알아보기 위해, MEDLINE에 등재된 논문을 기한없이 milnacipran과 fibromyalgia로 검색하여 무작위 배정 및 이중맹검 임상연구자료들을 선별하였다. 선별된 6개의 임상연구 결과, milnacipran를 사용했을 때 일관된 효능성과 안정성이 관찰되었고 섬유근통증후군 치료와 그에 수반되는 여러증상에 효과적인 것으로 나타났다.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.10a
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• pp.139-140
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• 2003

• Bulletin of the Korean Chemical Society
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• v.25 no.11
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• pp.1703-1706
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• 2004

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.05a
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• pp.71-71
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• 2004

• Bulletin of the Korean Chemical Society
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• v.31 no.7
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• pp.1848-1858
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• 2010

Phenylaminopyrimidines represent a large group of new selective anticancer agents, the majority of which exert their action through the inhibition of specific kinases. In this study, a new series of N-substituted-2-aminopyrimidines has been designed and synthesized. A selected group of the synthesized derivatives was screened at a single dose concentration of 10 ${\mu}M$ over a panel of 60 cancer cell-lines. Compound 12e has showed great inhibitory and strong lethal effect over almost all of the 60 cell-lines and accordingly was further tested in a 5-dose testing mode to determine its $IC_{50}$ values, where it showed great efficacies with intermediate potencies over the tested cell-lines. The compound was also tested over a panel of 52 kinases to explore its kinase inhibitory profile, and was found to be a selective but moderate inhibitor over FLT3 kinase.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.249.2-250
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• 2002

Tolerance and pharmacolinetics after single-dose administration of DA-8159, a new selective PDE5 inhibitor under phase 1 study, were examined in 42 healthy male volunteers in a six-period, double-blinded placebo-controlled study. Participants received single oral tablet of DA-8159 (12.5 to 300mg) or placebo. Adverse effects and pharmacokinetic parameters were monitored during experiments. DA-8159 was well tolerated and the frequency of adverse events was dose-related. (omitted)

• BMB Reports
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• v.43 no.9
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• pp.622-628
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• 2010

Dimethyl sulfoxide (DMSO) can be reduced to dimethyl sulfide by MsrA, which stereospecifically catalyzes the reduction of methionine-S-sulfoxide to methionine. Our previous study showed that DMSO can competitively inhibit methionine sulfoxide reduction ability of yeast and mammalian MsrA in both in vitro and in vivo, and also act as a non-competitive inhibitor for mammalian MsrB2, specific for the reduction of methionine-R-sulfoxide, with lower inhibition effects. The present study investigated the effects of DMSO on the physiological antioxidant functions of methionine sulfoxide reductases. DMSO elevated hydrogen peroxide-mediated Saccharomyces cerevisiae cell death, whereas it protected human SK-Hep1 cells against oxidative stress. DMSO reduced the protein-carbonyl content in yeast cells in normal conditions, but markedly increased protein-carbonyl accumulation under oxidative stress. Using Msr deletion mutant yeast cells, we demonstrated the DMSO's selective inhibition of the antioxidant function of MsrA in S. cerevisiae, resulting in an increase in oxidative stress-induced cytotoxicity.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.88.1-88.1
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• 2003

CJ-11668 is a new potent and selective COX-2 inhibitor (IC$\sub$50/ COX-2 65nM; COX-l/COX-2 ratio 770). The pharmacokinetic profile of CJ-11668 (20 mg/kg, p.o.) in the rat was characterized by high bioavailability (90%) and long plasma half-life (11.7 hr) with low clearance (0.4 L/hr/kg). In the dog, the PK profiles (2 mg/kg, p.o.) also showed long plasma half-life (l7.9hr) with low clearance (0.5 L/hr/kg), and the bioavalability of 60%. The inhibition of CJ-11668 infive different cytochrome P450 isozymes (1A2, 2C9, 2C19, 2D6 and 3A4) was determined in vitro and had observed no significant effect. (omitted)

• Maxillofacial Plastic and Reconstructive Surgery
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• v.30 no.4
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• pp.333-344
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• 2008

The objectives of this study was to explore the growth pattern of the oral squamous cell carcinoma when overexpressed COX was inhibited, explore the pathway that COX inhibitors suppressed the proliferation of cancer cells, and then hereafter investigate the potential of COX as chemopreventive target for oral squamous cell carcinoma. For confirming the COX-dependent effect and mechanisms on growth of the oral cancer cells, we treated the nonselective NSAID, Mefenamic acid and COX-2 selective inhibitor, Celecoxib in HN4 cell line. And then the cell line was evaluated with MTT assay and growth curve, the production of PGE2, total RNA extraction and RT-PCR analysis, and TEM The results were obtained as follows: 1. After administration of medication, in the result of MTT assay, Celecoxib inoculated group inhibit the cell growth rather than Mefenamic acid inoculated group. 2. The growth curve of cell line showed as time passes by there was a dramatic cell growth in the control group, and gradual growth inhibition was found in medication inoculated group and, in Celecoxib inoculated group there was more inhibition of cell growth. 3. After the administration of medication, Celecoxib tend to inhibit the synthesis of PGE2 more than Mefenamic acid. Mefenamic acid inhibit the synthesis of PGE2 more as the concentration gets high, but Celecoxib inhibited the synthesis of PGE2 even in low concentration. 4. After the administration of medication, the revelation of COX mRNA in cell line, there was a 50% decrease in COX-1, 60% decrease in COX-2 as in $50{\mu}M$ Mefenamic acid, and in Celecoxib $50{\mu}M$ there was not much difference in COX-1 and 90% decrease in COX-2 was found. 5. HN4 cell line showed broken nucleus and tangled cytoskeleton bundles in cytoplasm which meant apoptotic features after the treatment of Celecoxib in TEM view. Depending on the above results, we estimate that the inhibition of the expression of COX-2 cause the growth suppression of the oral squamous cell carcinoma, and it get achieved through pathway of reduced PGE2 production and increased apoptosis. In addition to, because COX-2 selective inhibitor specifically act to COX-2, it is considered that COX-2 selective inhibitor has the adequate potential as chemopreventive agent for oral squamous cell carcinoma.

• Biomolecules & Therapeutics
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• v.10 no.2
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• pp.117-123
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• 2002

CJ-10882, (E)-[(3-Cyclopentyloxy-4-methoxyphenyl)methylene]hydrazine-carboxamide, is a newly developed type IV phosphodiesterase isozyme (PDE IV) inhibitor. To investigate the subacute toxic effects of CJ-10882, it was administered to both male and female dogs at 0, 25, 50, 100 or 200 mg/kg/day orally for up to 2 weeks. During the test period, clinical signs, mortality, body weight, food consumption, ophthalmoscopy, urinalysis, hematology, serum biochemistry, gross finding, organ weight, and histopathology were evacuated. Several clinical signs were observed in treated dogs at above 25 mg/kg, including salivation and vomiting. A reduction in the body weight was observed in both sexes at above 50 mg/kg. There were no treatment-related effects on mortality, ophthalmoscopy, urinalysis, hematology, sect biochemistry, necropsy findings, and histopathology in any treatment group. The results of this study demonstrate that CJ-10882, a selective Inhibitor of the type IV class of PDE, may cause effects on gastrointestinal tract and salivary glands. Therefore, these organs should be closely examined in studies with other PDE IV inhibitors.