Disease relevance of D01809

• The toxicity of these organic extracts mimics the cytotoxicity of the intact particles and could be suppressed by the synthetic sulfhydryl compounds, N-acetylcysteine and bucillamine [1].
• Bucillamine induces the synthesis of vascular endothelial growth factor dose-dependently in systemic sclerosis fibroblasts via nuclear factor-kappaB and simian virus 40 promoter factor 1 pathways [2].
• Subconjunctival administration of bucillamine suppresses choroidal neovascularization in rat [3].
• Hypoxia stimulated binding activity of BREC nuclear protein to a hypoxia responsive element (HRE), which was decreased by bucillamine [4].
• A case of rapidly progressive glomerulonephritis associated with bucillamine-treated rheumatoid arthritis [5].

High impact information on D01809

• In the ex vivo models, bucillamine treatment significantly improved portal vein blood flow and bile production, preserved normal liver architecture, and significantly reduced liver enzyme release and indices of oxidative stress [6].
• Initially, her arthritis had been well controlled with methotrexate and corticosteroids, but the RA activity became difficult to control in spite of addition of bucillamine to the treatment regimen and repeated arthrocentesis with infusion of corticosteroid into her swollen joints [7].
• Of the six agents tested, only the thiol antioxidants, BUC and NAC, were effective at preventing a decrease in intracellular reduced glutathione:glutathione disulfide ratios, protecting cells from protein and lipid oxidation, and preventing heme oxygenase 1 expression [8].
• Our data demonstrate that NAC and BUC effectively inhibited the adjuvant effects of DEP in the induction of OVA-specific IgE and IgG1 production [8].
• Furthermore, the same concentration of bucillamine inhibited transendothelial migration of PHA-activated T cells, and reduced the expression level of CD44 on T cells [9].

Chemical compound and disease context of D01809

• OBJECTIVE: To investigate the mechanism of autoimmune phenomena, occasionally seen in patients with rheumatoid arthritis treated with bucillamine (BUC) and D-penicillamine (D-Pen), by evaluating their effects on apoptosis of T cells induced by T cell receptor activation or dexamethasone [10].
• Treatment continuation rate in relation to efficacy and toxicity in long-term therapy with low-dose methotrexate, sulfasalazine, and bucillamine in 1,358 Japanese patients with rheumatoid arthritis [11].
• Withdrawal from bucillamine and prednisolone treatment made rapid improvement of pemphigus lesions [12].

Biological context of D01809

• 4. Reporter gene studies revealed that bucillamine reduced transcriptional activity in the 5'-flanking region of the VEGF gene by 74.0% [4].
• Generation of reactive oxygen species is required for bucillamine, a novel anti-rheumatic drug, to induce apoptosis in concert with copper [13].
• PURPOSE: To investigate the difference of pharmacokinetics of thiol-containing drugs in various disease states, we studies the covalent binding of SA3786, a bucillamine derivative, with proteins in patient serum compared with that in healthy serum [14].
• The molecular structure of this compound is similar to that of D-penicillamine, except that bucillamine has 2 free sulfhydryl groups in its structure whereas D-penicillamine has only one [15].
• Down-regulation by bucillamine of lamina propria leucocytes in the rat colitis model [16].

Anatomical context of D01809

• In contrast, bucillamine had no effects on T cell proliferation or any cytokine production in the cultures with anti-CD3 plus anti-CD28 mAb [9].
• Comparative inhibitory effects of bucillamine and D-penicillamine on the function of human B cells and T cells [17].
• The effects of the immunosuppressive agent bucillamine (SA 96) on fibroblasts and angiogenic factors have not been examined [2].
• We determined that bucillamine, an anti-rheumatic drug, inhibits the VEGF production induced by hypoxia in bovine retinal microcapillary endothelial cells (BREC) [4].
• Finally, in both cell lines, bucillamine and SA 981 increased the GSH content two- to three-fold [18].

Associations of D01809 with other chemical compounds

• N-acetylcysteine and Bucillamine are synthetic thiols which have been administered in experimental and clinical studies for treatment of conditions associated with oxidative stress [19].
• In the present study, we examined whether disease-modifying anti-rheumatic drugs (DMARDs), including bucillamine (BUC), gold sodium thiomalate (GST), methotrexate (MTX) and salazosulfapiridine (SASP), act by inhibiting the production of VEGF by cultured synovial cells of patients with RA [20].
• Addition of copper sulfate to bucillamine decreased significantly the percent T cell adhesion to the EC compared with bucillamine alone [21].
• PURPOSE: To investigate the effect of bucillamine for prevention of increasing blood-retinal barrier (BRB) permeability in streptozotocin (STZ)-induced diabetic rats [22].
• New information on other DMARDs is presented, ie, sulfasalazine inhibition of signal transduction, the effects of hydroxychloroquine on cytokines and lipid metabolism, and the immunosuppressive effects of bucillamine, a penicillamine-related compound [23].

Gene context of D01809

• Moreover, both bucillamine and SA 981 significantly increased the expressions of Mrp2/MRP2 and GCLC proteins in both cell lines [18].
• The present study provides the first evidence that BUC inhibits VEGF production and the expression of its mRNA in synovial cells of RA patients [20].
• Bucillamine (BUC) has been found to have beneficial effects in the treatment of rheumatoid arthritis (RA), in which the activation of endothelial cells plays an important role in the pathogenesis [24].
• Inhibitory effects of bucillamine on the expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells [24].
• And, bucillamine also inhibited IL-2-induced proliferation at the concentration of 1 x 10(-4) M, but augmented proliferation at the concentration of 1 x 10(-5) M [25].

Analytical, diagnostic and therapeutic context of D01809

• Bucillamine, a thiol antioxidant, prevents transplantation-associated reperfusion injury [6].
• We hypothesized that the antioxidant bucillamine, a potent sulfhydryl donor, would protect against I/R injury in high-risk organ transplants [6].
• Immunofluorescence analysis was also performed to analyze the effect of bucillamine on the surface expression of adhesion molecules on T cells [9].
• Histologic and immunohistochemical analyses 4, 7, and 14 days after photocoagulation demonstrated that the average size of the CNV lesions was reduced in the bucillamine-treated eyes compared with the control eyes [3].
• Effect of bucillamine (SA96) on type II collagen induced arthritis in rats [26].

References