The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

AG-G-93501     2-[(4S)-2,2-dimethyl-5-oxo- 1,3-dioxolan-4...

Synonyms: SureCN1005092, KB-210920, FT-0667498, AC1LD3G9, AC1Q2CR7, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of acetonide

  • The efficacy of triamcinolone acetonide aerosol in the management of asthma in six patients with aspirin hypersensitivity was evaluated during a one-year trial [1].
  • The growth of L5U78Y and L1210 lymphoblasts was inhibited by a triamcinolone acetonide dose of over 0.5 to 1.0 mg/kg body weight [2].
  • Suppression of DNA synthesis in NEL-M1 human melanoma cells by triamcinolone acetonide [3].
  • We then examined the ability of the affinity gel to recognize cytosolic [3H]triamcinolone acetonide-receptor complexes from the corticoid-sensitive (CS) and -resistant strains of mouse lymphoma P1798, from CS lymphocytes of patients with chronic lymphatic leukemia, and from a CS clone of human leukemic lymphoblasts in tissue culture (CH6) [4].
  • The physical properties of the triamcinolone acetonide-binding macromolecules of the hepatomas indicate that they are specific glucocorticoid receptors [5].

Psychiatry related information on acetonide


High impact information on acetonide


Chemical compound and disease context of acetonide


Biological context of acetonide

  • The 6- to 8-fold stimulation of cell growth by insulin and transferrin was reduced to 1.75-fold when triamcinolone acetonide (10 nM) was added to the medium [16].
  • The addition of triamcinolone acetonide (10 nM) to defined medium supplemented with conditioned medium resulted in only a 1.48-fold increase in cell number [16].
  • When triamcinolone acetonide was added to a synchronized population of NEL cells, an increase in tyrosinase activity was observed at 16 hr, coinciding with the late S phase of the cell cycle [17].
  • Hydrolysis of the acetonide followed by sequential reduction of the benzyl derived protecting groups and the nitro group and debenzoylation leads to a modest yield of a 3:1 mixture of sinefungin (1) and 6'-episinefungin which can only be separated by analytical ion exchange chromatography [18].
  • The acetonide blocking groups were shown to be the best hydroxyl protecting groups, compatible with the palladium-catalyzed allylic amination reaction that afforded high yields of the 1,1'-N-linked pseudodisaccharides with a minimum amount of an elimination diene side product [19].

Anatomical context of acetonide

  • 3H-triamcinolone acetonide labeled glucocorticoid receptors in normal lymphoid tissues can be resolved into two component by DEAE chromatography: peak I elutes at 0.04 M salt and peak II is 0.22 M salt [20].
  • The binding of the purified [1,2,4-3H]triamcinolone acetonide-receptor complexes to calf thymus DNA-cellulose was increased markedly in a dose-dependent manner by low concentrations of a whole histone mixture (H2A, H2B, H3, H4, and H1 from calf thymus), but this high level of binding decreased at higher concentrations of the histone mixture [21].
  • Nuclei or cytosol fractions were prepared from lymphocytes that had been labeled at 37 or 4 degrees, respectively, with 30 nM [3H]triamcinolone acetonide ([3H]TA) [22].
  • Effect of triamcinolone acetonide on tyrosinase activity in a human melanoma cell line [17].
  • Factor 1 (10 biological units/kg body weight) itself also caused marked inhibition of the growth of these lymphoblasts without affecting the body weight or adrenal gland weight, its effect being equivalent to that of 3- to 4-mg/kg body weight doses of triamcinolone acetonide alone [2].

Associations of acetonide with other chemical compounds

  • The concentration of dexamethasone for its half-maximal stimulatory activity toward HBsAg, HBeAg and all viral transcripts was approximately 10(-8) mol/L, close to the affinity of glucocorticoid receptors to [3H]-triamcinolone acetonide in Hep3B cells (approximately 10(-8) mol/L) [23].
  • Retinoic acid, which blocks the induction of differentiation by TPA, inhibited the production of SSB by TPA; however, fluocinolone acetonide, chymostatin, catalase, or superoxide dismutase blocked neither TPA-induced SSB nor terminal differentiation [24].
  • Dilution at 0 degrees of rat liver cytosol incubated with [3H]triamcinolone acetonide provoked an enhanced binding of steroid-receptor complexes to nuclei [25].
  • METHODS: Levels of the bone turnover markers, serum osteocalcin (BGP) and urinary pyridinoline (PYD), were monitored in RA patients for 4 weeks following a single IA administration of xylocaine alone or in combination with triamcinolone acetonide [26].
  • Thus [3H]triamcinolone acetonide-receptor complexes present in a cytosol from which the inhibitor had been removed by Sephadex G-25 chromatography became spontaneously activated at low ionic strength and at 0 degrees [25].

Gene context of acetonide

  • In this minimal reconstituted system, the GR is incubated with the chaperones in the presence of [3H]triamcinolone acetonide ([3H]TA), which binds to the receptor as GR.hsp90 complexes are formed [27].
  • Triamcinolone acetonide destabilizes VEGF mRNA in Müller cells under continuous cobalt stimulation [28].
  • When the immunoprecipitated, [35S]methionine-pulse-labeled EGF receptor was analyzed by SDS-PAGE and fluorography, the newly synthesized EGF receptor was detected at the position of 170 kDa; and treatment of HSG cells with triamcinolone acetonide resulted in a 2.0-fold amplification of this 170 kDa band [29].
  • The anti-promoters fluocinolone acetonide, retinoic acid, and superoxide dismutase did not enhance TPA-induced levels of TIS1 and TIS21 mRNAs in P+ cells, suggesting that these inhibitors may act on other promotion-relevant genes [30].
  • CONCLUSION: We conclude from these results that triamcinolone acetonide increases the production of bFGF and decreases production of TGF-beta1 by human dermal fibroblasts [31].

Analytical, diagnostic and therapeutic context of acetonide

  • Concurrent titrations of [3H]progesterone and [3H]triamcinolone acetonide-binding sites demonstrated that their binding capacities were similar, considering the relative stabilities of the complexes [32].
  • Incubation of the 9S [3H]triamcinolone acetonide-labeled receptor peak with anti-hsp89 results in the immune-specific adsorption of 20% of the specifically bound radioactivity and adsorption of the 100-kilodalton receptor protein, as detected by Western-blotting, using the GR49 antireceptor monoclonal antibody as probe [33].
  • After incubation of intact GH1 cells with 10 nM [3H]triamcinolone acetonide at 37 C and subsequent cell fractionation at 4 C, three glucocorticoid receptor forms are observed: cytosolic 10 S receptor, cytosolic 4 S receptor, and nuclear receptor [34].
  • Triamcinolone acetonide, a water-insoluble corticosteroid preparation in a Freon-propelled metered-dose aerosol, was administered via a specially designed nebulizer to 22 adult patients with severe, chronic asthma [35].
  • Thirty asthmatic patients participating in a trial of triamcinolone acetonide aerosol were evaluated to determine the relationships among symptons of sore throat or hoarseness, the appearance of the throat on physical examination, and the presence of yeasts on pharyngeal culture [36].


  1. Triamcinolone aerosol. Treatment of aspirin-hypersensitive asthmatic patients. Pingleton, W.W., Bone, R.C., Kerby, G.R., Ruth, W.E. JAMA (1977) [Pubmed]
  2. Amplification of growth inhibition by glucocorticoid on L5178Y and L1210 lymphoblasts in vivo. Kido, H., Tomihara, Y., Watanabe, I., Ohsawa, N., Katunuma, N. Cancer Res. (1979) [Pubmed]
  3. Suppression of DNA synthesis in NEL-M1 human melanoma cells by triamcinolone acetonide. DiSorbo, D.M., Harris, N.A., Nathanson, L. Cancer Res. (1985) [Pubmed]
  4. Immunochemical differences between glucocorticoid receptors from corticoid-sensitive and -resistant malignant lymphocytes. Stevens, J., Eisen, H.J., Stevens, Y.W., Haubenstock, H., Rosenthal, R.L., Artishevsky, A. Cancer Res. (1981) [Pubmed]
  5. Glucocorticoid receptors in Morris hepatomas and host liver and the correlation of biological activity with receptor levels. McPartland, R.P., Milholland, R.J., Morris, H.P., Rosen, F. Cancer Res. (1977) [Pubmed]
  6. Nonhuman primates: their role in assessing developmental effects of immunomodulatory agents. Hendrickx, A.G., Makori, N., Peterson, P. Human & experimental toxicology. (2000) [Pubmed]
  7. Clinical features and treatment of peristomal pyoderma gangrenosum. Hughes, A.P., Jackson, J.M., Callen, J.P. JAMA (2000) [Pubmed]
  8. Monoclonal antibodies to the rat liver glucocorticoid receptor. Westphal, H.M., Moldenhauer, G., Beato, M. EMBO J. (1982) [Pubmed]
  9. Blocking of tumor promoter-induced AP-1 activity inhibits induced transformation in JB6 mouse epidermal cells. Dong, Z., Birrer, M.J., Watts, R.G., Matrisian, L.M., Colburn, N.H. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  10. Specific binding of phorbol ester tumor promoters to intact primary epidermal cells from Sencar mice. Solanki, V., Slaga, T.J. Proc. Natl. Acad. Sci. U.S.A. (1981) [Pubmed]
  11. Dissociation of tumor promoter-stimulated ornithine decarboxylase activity and DNA synthesis in mouse epidermis in vivo and in vitro by fluocinolone acetonide, a tumor-promotion inhibitor. Lichti, U., Slaga, T.J., Ben, T., Patterson, E., Hennings, H., Yuspa, S.H. Proc. Natl. Acad. Sci. U.S.A. (1977) [Pubmed]
  12. Mechanism of action of a steroidal antiglucocorticoid in lymphoid cells. Segnitz, B., Gehring, U. J. Biol. Chem. (1990) [Pubmed]
  13. Topical intranasal corticosteroid therapy in rhinitis. Siegel, S.C. J. Allergy Clin. Immunol. (1988) [Pubmed]
  14. Comparison of corticosteroids for treatment of respiratory syncytial virus bronchiolitis and pneumonia in cotton rats. Ottolini, M.G., Curtis, S.J., Porter, D.D., Mathews, A., Richardson, J.Y., Hemming, V.G., Prince, G.A. Antimicrob. Agents Chemother. (2002) [Pubmed]
  15. Long-term Retinal Toxicity of Intravitreal Commercially Available Preserved Triamcinolone Acetonide (Kenalog) in Rabbit Eyes. Albini, T.A., Abd-El-Barr, M.M., Carvounis, P.E., Iyer, M.N., Lakhanpal, R.R., Pennesi, M.E., Chevez-Barrios, P., Wu, S.M., Holz, E.R. Invest. Ophthalmol. Vis. Sci. (2007) [Pubmed]
  16. Effect of triamcinolone acetonide on the growth of NEL-M1 human melanoma cells cultured in the presence and absence of growth stimulatory agents. DiSorbo, D.M. Cancer Res. (1986) [Pubmed]
  17. Effect of triamcinolone acetonide on tyrosinase activity in a human melanoma cell line. DiSorbo, D.M., Harris, N.A., Nathanson, L. Cancer Res. (1984) [Pubmed]
  18. An approach to the total synthesis of sinefungin. Mock, G.A., Moffatt, J.G. Nucleic Acids Res. (1982) [Pubmed]
  19. Facile, efficient, and enantiospecific syntheses of 1,1'-N-linked pseudodisaccharides as a new class of glycosidase inhibitors. Shing, T.K., Kwong, C.S., Cheung, A.W., Kok, S.H., Yu, Z., Li, J., Cheng, C.H. J. Am. Chem. Soc. (2004) [Pubmed]
  20. Biochemical and biophysical characterization of glucocorticoid receptors in normal lymphoid tissue. McCaffrey, R., Lillquist, A., Bell, R. Blood (1981) [Pubmed]
  21. Interaction of histones in glucocorticoid receptor binding to DNA in vitro. Isohashi, F., Okamoto, K., Ueda, K., Kokufu, I., Yoshikawa, K., Sakamoto, Y. Cancer Res. (1989) [Pubmed]
  22. Physicochemical differences between glucocorticoid-binding components from the corticoid-sensitive and -resistant strains of mouse lymphoma P1798. Stevens, J., Stevens, Y.W. Cancer Res. (1979) [Pubmed]
  23. Glucocorticoid stimulates hepatitis B viral gene expression in cultured human hepatoma cells. Chou, C.K., Wang, L.H., Lin, H.M., Chi, C.W. Hepatology (1992) [Pubmed]
  24. Association of DNA strand breaks with accelerated terminal differentiation in mouse epidermal cells exposed to tumor promoters. Hartley, J.A., Gibson, N.W., Zwelling, L.A., Yuspa, S.H. Cancer Res. (1985) [Pubmed]
  25. A low molecular weight inhibitor of steroid receptor activation. Bailly, A., Sallas, N., Milgrom, E. J. Biol. Chem. (1977) [Pubmed]
  26. The systemic effect of intraarticular administration of corticosteroid on markers of bone formation and bone resorption in patients with rheumatoid arthritis. Emkey, R.D., Lindsay, R., Lyssy, J., Weisberg, J.S., Dempster, D.W., Shen, V. Arthritis Rheum. (1996) [Pubmed]
  27. Folding of the glucocorticoid receptor by the reconstituted Hsp90-based chaperone machinery. The initial hsp90.p60.hsp70-dependent step is sufficient for creating the steroid binding conformation. Dittmar, K.D., Pratt, W.B. J. Biol. Chem. (1997) [Pubmed]
  28. Triamcinolone acetonide destabilizes VEGF mRNA in Müller cells under continuous cobalt stimulation. Sears, J.E., Hoppe, G. Invest. Ophthalmol. Vis. Sci. (2005) [Pubmed]
  29. Effect of glucocorticoid on epidermal growth factor receptor in human salivary gland adenocarcinoma cell line HSG. Kyakumoto, S., Kurokawa, R., Ota, M. Biochim. Biophys. Acta (1990) [Pubmed]
  30. Preferential primary-response gene expression in promotion-resistant versus promotion-sensitive JB6 cells. Cmarik, J.L., Herschman, H., Colburn, N.H. Mol. Carcinog. (1994) [Pubmed]
  31. Triamcinolone stimulates bFGF production and inhibits TGF-beta1 production by human dermal fibroblasts. Carroll, L.A., Hanasono, M.M., Mikulec, A.A., Kita, M., Koch, R.J. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]. (2002) [Pubmed]
  32. Characteristics of progesterone-binding components in neoplastic mammary tissues of the rat. Goral, J.E., Wittliff, J.L. Cancer Res. (1976) [Pubmed]
  33. Demonstration that the 90-kilodalton heat shock protein is bound to the glucocorticoid receptor in its 9S nondeoxynucleic acid binding form. Sanchez, E.R., Meshinchi, S., Schlesinger, M.J., Pratt, W.B. Mol. Endocrinol. (1987) [Pubmed]
  34. The glucocorticoid antagonist 17 alpha-methyltestosterone binds to the 10 S glucocorticoid receptor and blocks agonist-mediated dissociation of the 10 S oligomer to the 4 S deoxyribonucleic acid-binding subunit. Raaka, B.M., Finnerty, M., Samuels, H.H. Mol. Endocrinol. (1989) [Pubmed]
  35. Triamcinolone acetonide aerosols for asthma. I. Effective replacement of systemic corticosteroid therapy. Falliers, C.J. J. Allergy Clin. Immunol. (1976) [Pubmed]
  36. Oropharyngeal candidiasis in patients treated with triamcinolone acetonide aerosol. Pingleton, W.W., Bone, R.C., Kerby, G.R., Ruth, W.E. J. Allergy Clin. Immunol. (1977) [Pubmed]
WikiGenes - Universities