Relevant bibliographies by topics / CDDOBA

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Academic literature on the topic 'CDDOBA'

Author: Grafiati
Published: 11 September 2023

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Journal articles on the topic "CDDOBA"

1

Konopleva, Marina, Ismael Samudio, Twee Tsao, Steven M. Kornblau, Yue-Xi Shi, Teresa McQueen, Rooha Contractor, et al. "Mechanisms and Activity of PPARγ-Active Triterpenoids CDDO and CDDO-Me in Leukemias." Blood 106, no. 11 (November 16, 2005): 2460. http://dx.doi.org/10.1182/blood.v106.11.2460.2460.

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Abstract First-line therapy of acute myeloid leukemia (AML) consists of combinations of cytarabine and an anthracycline. While initial complete remissions are frequent, most patients succumb to resistant disease underlining the need for novel, more effective agents. The most striking progress in AML therapy was achieved by targeting the nuclear receptor RARα with ATRA. Research in our laboratory has demonstrated that the novel synthetic triterpenoid CDDO (2-cyano-3,12- dioxooleana-1,9-dien-28-oic acid) and its more active C28 methyl ester derivative CDDO-Me inhibit growth and induce apoptosis in a variety of cancers including AML, CLL and blast crisis CML. CDDO and to a much higher degree CDDO-Me are potent activators of the nuclear transcription factor Peroxisome Proliferator-Activated Receptor gamma (PPARγ). In a mammalian two-hybrid assay, the CDDO and CDDO-Me induced activation of PPARγ was associated with a marked increase in multiple coactivator recruitment (SRC-1, SRC-2, SRC-3, TRAP220/DRIP205, CARM-1 and PGC-1) that is qualitatively different from that induced by other PPARγ ligands. CDDO induced a higher degree of myelo-monocytic differentiation in DRIP205-overexpressing HL-60 cells suggesting that high cellular levels of DRIP205 co-activator modulate differentiation response to PPARγ ligation. CDDO induced p21 mRNA and protein in leukemic cells and transactivation of the p21 promoter in a p53-independent fashion. We have recently identified the PPARγ-independent depletion of mitochondrial glutathione (GSHm) as a novel mechanism of action resulting in redox disbalance and mitochondrial damage as mechanisms of pro-apoptotic effects of CDDO and CDDO-Me. Gene expression studies using cDNA arrays demonstrate that CDDO induces genes involved in the antioxidant response (AR) including phase II detoxifying enzymes (glutamate cysteine ligase, GSH transferase, etc.) and antioxidant enzymes (heme oxygenase 1, thioredoxin reductase). Cotreatment with the GSH precursor, n-acetyl cystein prevented apoptosis and loss of viability induced by CDDOs, whereas alkylation of intracellular thiols by diethylmaleate decreased the accumulation of a biotinylated derivative of CDDO, TP-301, in U937 leukemic cells suggesting that intracellular reduced thiols are functional targets of CDDO and its derivatives. The in vivo studies using liposomal CDDO-Me in a conditional leukemia model demonstrated significant reduction of leukemia burden as measured by bioluminescence imaging and prolongation of survival. Based on the ample pre-clinical evidence of anti-leukemia effects and on the favorable PK/toxicity profile of the parental compound, CDDO will enter Phase I clinical trials in hematologic malignancies in 3Q 2005 and CDDO-Me in 1Q 2006.
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Setiawan, A. M., A. A. Syafrianno, R. Rahmat, and Supari. "High-Resolution North Sulawesi Drought Hazzard Mapping Based on Consecutive Dry Days (CDD)." IOP Conference Series: Earth and Environmental Science 893, no. 1 (November 1, 2021): 012018. http://dx.doi.org/10.1088/1755-1315/893/1/012018.

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Abstract North Sulawesi is one of the Province in northern Indonesia with high spatial annual rainfall variations and influenced by global climate anomaly that can lead to extreme events and disaster occurrence, such as flood, landslide, drought, etc. The purpose of this study is to generate high-resolution meteorological hazard map based on long-term historical consecutive dry days (CDD) over the North Sulawesi region. CDD was calculated based on observed daily precipitation data from Indonesia Agency for Meteorology, Climatology, and Geophysics (BMKG) surface observation station network (CDDobs) and the daily-improved Climate Hazards group Infrared Precipitation with Stations (CHIRPS) version 2.0 (CDDCHIRPS) during 1981 – 2010 period. The Japanese 55-year Reanalysis (JRA-55) data obtained from iTacs (Interactive Tool for Analysis of the Climate System) with the same time scale period also used to explain physical – dynamical atmospheric properties related to drought hazard over this region. The Geostatistical approach using regression kriging method was applied as spatial interpolation technique to generate high resolution gridded (0.05° × 0.05°) drought hazard map. This method combines a regression of CDDobs as dependent variable (target variable) on CDDCHIRPS as predictors with kriging of the prediction residuals. The results show that most of the areas were categorized as medium drought hazard level with CDD values ranging from 80-100 days. Meanwhile, small islands around main Sulawesi island such as Sangihe and Karakelong island are dominated by low drought hazard levels with CDD values ranging from 50-60 days. The highest levels of drought hazard area are located in South Bolaang Mongondow Regency.
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Panwar, Kuldeep, Dinesh Prasad, Mayank Srivastava, and Zainab Haseeb. "New Current Mode Lossy Integrator Employing CDDITA." Circuits and Systems 09, no. 08 (2018): 117–23. http://dx.doi.org/10.4236/cs.2018.98012.

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Wang, Yongping, Weston W. Porter, Nanjoo Suh, Tadashi Honda, Gordon W. Gribble, Lisa M. Leesnitzer, Kelli D. Plunket, et al. "A Synthetic Triterpenoid, 2-Cyano-3,12-dioxooleana-1,9-dien-28-oic Acid (CDDO), Is a Ligand for the Peroxisome Proliferator-Activated Receptor γ." Molecular Endocrinology 14, no. 10 (October 1, 2000): 1550–56. http://dx.doi.org/10.1210/mend.14.10.0545.

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Abstract A novel synthetic triterpenoid, 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO), previously reported to have potent differentiating, antiproliferative, and antiinflammatory activities, has been identified as a ligand for the peroxisome proliferator-activated receptor γ (PPARγ). CDDO induces adipocytic differentiation in 3T3-L1 cells, although it is not as potent as the full agonist of PPARγ, rosiglitazone. Binding studies of CDDO to PPARγ using a scintillation proximity assay give a Ki between 10−8 to 10−7m. In transactivation assays, CDDO is a partial agonist for PPARγ. The methyl ester of CDDO, CDDO-Me, binds to PPARγ with similar affinity, but is an antagonist. Like other PPARγ ligands, CDDO synergizes with a retinoid X receptor (RXR)-specific ligand to induce 3T3-L1 differentiation, while CDDO-Me is an antagonist in this assay. The partial agonism of CDDO and the antagonism of CDDO-Me reflect the differences in their capacity to recruit or displace cofactors of transcriptional regulation; CDDO and rosiglitazone both release the nuclear receptor corepressor, NCoR, from PPARγ, while CDDO-Me does not. The differences between CDDO and rosiglitazone as either partial or full agonists, respectively, are seen in the weaker ability of CDDO to recruit the coactivator CREB-binding protein, CBP, to PPARγ. Our results establish the triterpenoid CDDO as a member of a new class of PPARγ ligands.
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Ikeda, Takashi, Yukiko Nakata, Fumihiko Kimura, Ken Sato, Kenneth Anderson, Kazuo Motoyoshi, Michael Sporn, and Donald Kufe. "Induction of redox imbalance and apoptosis in multiple myeloma cells by the novel triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid." Molecular Cancer Therapeutics 3, no. 1 (January 1, 2004): 39–45. http://dx.doi.org/10.1158/1535-7163.39.3.1.

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Abstract The synthetic oleanane triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) and its chemical derivatives induce differentiation and apoptosis of human leukemia cells. The precise mechanisms responsible for the effects of CDDO, however, remain unclear. In the present study, we examined the effects of CDDO and its C-28 imidazolide ester (CDDO-Im) on apoptosis of multiple myeloma (MM) cells. The results show that both CDDO and CDDO-Im are potent inducers of MM cell apoptosis and that CDDO-Im is more active than CDDO. CDDO-Im treatment was associated with (a) depletion of glutathione, (b) increases in reactive oxygen species, (c) a reduction of the Fas-associated death domain (FADD)-like interleukin-1-converting enzyme (FLICE) inhibitory protein, (d) activation of caspase-8, and (e) a decrease of the mitochondrial transmembrane potential. The reducing agents, N-acetyl-l-cysteine, DTT, and catalase inhibited each of these CDDO-Im-induced proapoptotic signals. Inhibition of caspase-8 with z-IETD-fmk also abrogated CDDO-Im-induced decreases of the mitochondrial transmembrane potential and inhibited apoptosis. These results demonstrate that CDDO-Im disrupts intracellular redox balance and thereby activates the extrinsic caspase-8-dependent apoptotic pathway. We further show that CDDO-Im induces apoptosis of primary MM cells at submicromolar concentrations and that MM cells are more sensitive to this agent than normal bone marrow mononuclear cells. These results suggest that CDDO compounds have potential as new agents for the treatment of MM.
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Koh, Eun-Young, Keun-Sik Kim, Hee-Bin Park, Jong-Seok Kim, and Pyung-Hwan Kim. "Active Targeting of Versatile Nanocomplex Using the Novel Biomarker of Breast Cancer Stem Cells." International Journal of Molecular Sciences 24, no. 1 (December 30, 2022): 685. http://dx.doi.org/10.3390/ijms24010685.

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Breast cancer in women is one of the most common life-threatening malignancies. Despite of the development for the improved treatment, there are still many limitations to overcome. Among them, cancer stem cells (CSCs) are well known for tumor formation, development, cellular heterogeneity, and cancer recurrence. Therefore, to completely cure breast cancer, treatment of both cancer and CSC is required. To selectively target CSCs, we generated a liposome-based smart nano complex using CEACAM 6 (CD66c) antibody (Ab), a novel cell-surface biomarker of breast-derived CSCs (BCSCs) discovered in our previous research. Selective and increased cellular uptake was observed in BCSCs treated with CD66c Ab-conjugated rhodamine-labeled liposomes (CDRHOL) depending on the expression level of CD66c. CD66c Ab-conjugated doxorubicin (DOX)-loaded liposomes (CDDOXL) selectively showed increased cell killing effects in BCSCs with high CD66c expression levels. In an in vivo animal study, CDRHOL showed enhanced accumulation in xenografted BCSC tumors with low delivery into non-target organs. Moreover, mice treated with CDDOXL have assessed the decreased induction ability of immune response by low expression levels of pro-inflammatory cytokines and reduced liver toxicity by histopathological analysis. Finally, the improved antitumor effect of CDDOXL was evaluated in a metastatic BCSC mouse model via systemic administration. Collectively, our study is the first to demonstrate that a multi-functional nano complex using a novel surface biomarker of BCSC may be a more effective therapeutic agent for the treatment of cancer and CSCs.
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Kress, Christina L., Marina Konopleva, Maryla Krajewska, Vanesa Martinez-Garcia, Sophie Lefebvre, Marc L. Hyer, Teresa McQueen, Michael Andreeff, John C. Reed, and Juan Zapata. "Triterpenoids Display Single Agent Activity in a Mouse Model of CLL/SBL." Blood 108, no. 11 (November 16, 2006): 2530. http://dx.doi.org/10.1182/blood.v108.11.2530.2530.

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Abstract The synthetic triterpenoid 2-Cyano-3,12-Dioxooleana-1,9-Dien-28-Oic Acid (CDDO) induces apoptosis of leukemia cells through a novel mechanism and has recently entered Phase I human clinical trials. We studied the effects of CDDO and its imidazolide derivative (CDDO-Im) on cultured human chronic lymphocytic leukemia (CLL) cells and on B cells from TRAF2DN/Bcl-2 transgenic mice, a new mouse model of CLL and small B cell lymphoma (SBL). Both triterpenoids efficiently induced death of malignant human and mouse B-cells ex vivo, although CDDO-Im was over 10-fold more potent than CDDO. Treating TRAF2DN/Bcl-2 mice that had developed leukemia with liposome-formulated CDDO or CDDO-Im resulted in significant reductions of B cells in blood, spleen and lung, with CDDO-Im more potent than CDDO, while treatment with empty liposomes had no impact on disease. Analysis of blood cells recovered from treated mice showed that CDDO-Im is a potent inducer of cell dead in vivo. Furthermore, CDDO-Im efficiently eradicated mouse CLL cells but had a lesser effect on the viability of normal B cells. These results demonstrate that triterpenoids CDDO and CDDO-Im reduce leukemia and lymphoma burden in vivo in a transgenic mouse model of CLL/SBL and suggest that CDDO-based synthetic triterpenoids should be tested for clinical activity in patients with CLL. Our results also provide evidence of the suitability of our mouse model of CLL/SBL as a preclinical platform for chemotherapeutic drug testing.
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Brookes, Paul, Andrew Tompkins, Kimberly Morse, Shannon Hilchey, Suhail Salim, Denise Ray, Richard Phipps, and Steven H. Bernstein. "The Triterpenoids 2-cyano-3,12-dioxooleana-1,9-dien-28-oic Acid (CDDO) and Their Imidazole (CDDO-Im) and Dinitrile Derivatives (DI-CDDO) Elicit Apoptosis through a Novel Mitochondrial Pathway." Blood 106, no. 11 (November 16, 2005): 2426. http://dx.doi.org/10.1182/blood.v106.11.2426.2426.

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Abstract We have recently shown that B-cell non Hodgkin’s lymphoma express the transcription factor PPARγ and undergo apoptosis upon exposure to PPARγ ligands. The synthetic triterpenoid CDDO is a specific ligand for PPARγ, and CDDO and its derivatives, CDDO-Im and DI-CDDO, induce diffuse large cell lymphoma (DLCL) death (OCI Ly10 and OCI Ly19 cells), with a potency of DI-CDDO>CDDO-Im>CDDO, suggesting that such agents have therapeutic potential in lymphoma. The natural PPARγ ligand, 15d-PGJ2 (which also elicits DLCL death), has previously been shown to inhibit mitochondrial complex I, enhance mitochondrial reactive oxygen species (ROS) generation, and react with protein thiols. Given that CDDO is structurally similar to 15d-PGJ2 we hypothesized that CDDO-induced cell death may similarly be mediated via complex I inhibition, ROS generation, thiol oxidation, and opening of a large membrane pore complex in the mitochondrial membrane, termed the “permeability transition” (PT) pore. Studies on isolated rat liver mitochondria however showed that none of the CDDO-derivatives inhibited complex I activity or affected mitochondrial protein thiols. However, all three compounds did induce PT pore opening and mitochondrial swelling, with a concurrent loss of mitochondrial membrane potential, in a Ca2+ dependent manner (potency DI-CDDO>CDDO-Im>CDDO). This is consistent with a previously shown role for Ca2+ in CDDO-induced cell death. Interestingly, this mitochondrial swelling was not inhibited by the classical PT pore inhibitor cyclosporin A (CsA). This is supported by our findings that the induction of OCI-Ly19 cell death by CDDO was also not inhibited by CsA, or by another classical PT pore inhibitor, nortriptyline. These phenomena may be partially explained by invoking the “unregulated PT pore”. In addition to the classical PT pore, a non-CsA sensitive “unregulated PT pore” also exists, which is generated by the aggregation of misfolded mitochondrial membrane proteins that are induced by oxidants and thiol reactive agents. That exposure of mitochondria to CDDO results in the formation of “unregulated PT pores” is supported by our findings that the proteosome inhibitor PS341, potentiates CDDO-induced cell death, suggesting the involvement of a protein folding response. The temporal role of ROS in CDDO-induced cell death was also investigated, and it was found that the antioxidant N-acetyl-cysteine did not inhibit PT pore opening, but did inhibit cell death. This is consistent with our observation that ROS generation in isolated mitochondria was not immediately triggered by CDDO, but rather increased at delayed time points, placing it downstream of PT pore opening. This proposes the following novel model of a direct mitochondrial effect of CDDO and its derivatives: \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \[CDDO{\rightarrow}\ mitochondrial\ protein\ misfolding\ {\rightarrow}\ unregulated\ PT\ pore\ formation\ {\rightarrow}\ ROS\ {\rightarrow}\ cell\ death\] \end{document} In summary: CDDO and its derivatives have direct effects on mitochondria, and represent novel therapeutic approaches for the treatment of patients with DLCL; and combinations of CDDO and its derivatives with proteosome inhibitors represent a rational combination to test in the context of clinical trials.
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Elsawa, Sherine F., Anne J. Novak, Marina Konopleva, Michael Andreeff, Thomas E. Witzig, and Stephen M. Ansell. "Preferential Inhibition of Malignant Cell Growth by CDDO in Waldenström Macroglobulinemia." Blood 108, no. 11 (November 16, 2006): 2528. http://dx.doi.org/10.1182/blood.v108.11.2528.2528.

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Waldenström macroglobulinemia (WM) is a B cell disorder with a highly variable clinical outcome, where some patients remain asymptomatic, while others have significant symptoms and require therapeutic intervention. Clinical symptoms include infiltration of lymphoplasmacytic cells into the bone marrow, production of a monoclonal IgM protein, anemia, lymphadenopathy, and serum hyperviscosity. Despite the introduction of multiple chemotherapeutic regimens over the past several decades, WM remains an incurable disease. 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) and its methyl ester derivative (CDDO-Me) and imidazolide derivative (CDDO-Im) are synthetic triterpenoids derived from oleanolic acid. These compounds have been shown to induce apoptosis of several tumor cell types including breast cancer, lung cancer, ovarian cancer, melanoma, osteosarcoma, leukemia, and multiple myeloma cells. The goal of this study was to evaluate the potential role of synthetic triterpenoids in WM. Preliminary studies on malignant B cells indicated that CDDO-Im induced the greatest amount of cell death and we therefore used this derivative of CDDO for our studies. CD19+ CD138+ cells from bone marrow biopsy specimens obtained from WM patients were isolated by positive selection and were treated with varying concentrations of CDDO-Im (62.5 nM to 750 nM ) and cell viability was determined after 24 hours (n=3). Compared to the nil control 47% of the malignant cells remained viable at a CDDO-Im concentration of 62.5 nM and only 11% remained viable at 125 nM CDDO-Im. To determine if CDDO-Im had specific toxic effects on non-malignant cells, we cultured CD19- CD138- cells from WM patient bone marrows with CDDO-Im and found that non-malignant cells were less sensitive to the drug, 80% being viable at 62.5 nM and 65% being viable at 125 nM. Similarly, we found that normal peripheral blood B cells and CD19+ CD138+ bone marrow B cells from healthy donors were less sensitive to CDDO-Im. Compared to the nil control 93% of the CD19+ CD138+ bone marrow B cells and 70% of the peripheral blood B cells remained viable at a CDDO-Im concentration of 62.5 nM and 95% and 68% remained viable at 125 nM CDDO-Im respectively. We next examined the effect of CDDO-Im on WM cell proliferation and found that CDDO-Im inhibited cell proliferation in a dose-dependent manner. Similar to the viability assays, there was a differential effect of CDDO-Im on malignant and non-malignant cells. Compared to the nil control, at 125 nM, there was a complete inhibition of malignant cell growth, while approximately 40% of the non-malignant cells remained proliferative. To determine the mechanism of cell death, CD19+ CD138+ cells were cultured in the presence or absence of various doses of CDDO-Im for 6 hours and cell lysates were examined for cleavage of PARP. There was evidence of PARP cleavage in a dose-dependent manner, suggesting that CDDO-Im induced malignant cell death occurs through a caspase-dependent mechanism. In summary, the synthetic triterpenoid CDDO-Im decreased the viability of WM B cells in a dose-dependent manner, and CDDO-Im had a greater effect on the viability of the malignant cells compared to non-malignant cells from the same WM patients. CDDO-Im also inhibited malignant cell growth in a dose-dependent manner and the mechanism of CDDO-Im mediated cell death appears to be a caspase-mediated event. Overall, our data indicate that CDDO-Im may have potential efficacy in WM patients.
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Konopleva, Marina, Twee Tsao, Peter Ruvolo, Irina Stiouf, Zeev Estrov, Clinton E. Leysath, Shourong Zhao, et al. "Novel triterpenoid CDDO-Me is a potent inducer of apoptosis and differentiation in acute myelogenous leukemia." Blood 99, no. 1 (January 1, 2002): 326–35. http://dx.doi.org/10.1182/blood.v99.1.326.

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It has been shown that the novel synthetic triterpenoid CDDO inhibits proliferation and induces differentiation and apoptosis in myeloid leukemia cells. In the current study the effects of the C-28 methyl ester of CDDO, CDDO-Me, were analyzed on cell growth and apoptosis of leukemic cell lines and primary acute myelogenous leukemia (AML). CDDO-Me decreased the viability of leukemic cell lines, including multidrug resistant (MDR)-1–overexpressing, p53null HL-60-Dox and of primary AML cells, and it was 3- to 5-fold more active than CDDO. CDDO-Me induced a loss of mitochondrial membrane potential, induction of caspase-3 cleavage, increase in annexin V binding and DNA fragmentation, suggesting the induction of apoptosis. CDDO-Me induced pro-apoptotic Bax protein that preceded caspase activation. Furthermore, CDDO-Me inhibited the activation of ERK1/2, as determined by the inhibition of mitochondrial ERK1/2 phosphorylation, and it blocked Bcl-2 phosphorylation, rendering Bcl-2 less anti-apoptotic. CDDO-Me induced granulo-monocytic differentiation in HL-60 cells and monocytic differentiation in primary cells. Of significance, colony formation of AML progenitors was significantly inhibited in a dose-dependent fashion, whereas normal CD34+ progenitor cells were less affected. Combinations with ATRA or the RXR-specific ligand LG100268 enhanced the effects of CDDO-Me on cell viability and terminal differentiation of myeloid leukemic cell lines. In conclusion, CDDO-Me is an MDR-1– and a p53-independent compound that exerts strong antiproliferative, apoptotic, and differentiating effects in myeloid leukemic cell lines and in primary AML samples when given in submicromolar concentrations. Differential effects of CDDO-Me on leukemic and normal progenitor cells suggest that CDDO-Me has potential as a novel compound in the treatment of hematologic malignancies.
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Dissertations / Theses on the topic "CDDOBA"

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Alabran, Jennifer L. "HUMAN NEUROBLASTOMA CELLS RAPIDLY ENTER CELL CYCLE ARREST AND APOPTOSIS FOLLOWING EXPOSURE TO C-28 DERIVATIVES OF THE SYNTHETIC TRITERPENOID CDDO." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1253290381.

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Salif, Harouna. "Effect of CDDO-me on myelopoiesis in naïve mice and in mice undergoing bone marrow transplantation (BMT)." abstract and full text PDF (UNR users only), 2009. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1472976.

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Wong, Michael. "Rational design of small molecule probes for investigating the mechanism of action of the chemotherapeutic agents CDDO and artemisinin." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2006368/.

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Adverse drug reactions (ADR) are a major concern for the pharmaceutical industry and health practitioners as they can cause morbidity and in severe cases mortality. ADRs are one of the major reasons why drugs fail during clinical trials so research directed at predicting ADRs to minimise failure is essential. The CDDO (2-cyano-3,12-dioxo-oleana-1,9(11)-dien-28-oate) and the synthetic endoperoxide series are two promising classes that have potential for the treatment of cancers and malaria and may revolutionise treatment, within their fields, if approved for clinical use. The two main aims that are presented in this thesis are to; (i) design and synthesise novel analogues and chemical probes to identify potential molecular targets for both the CDDO and endoperoxide series (ii) develop appropriate in vitro test systems to help define the molecular mechanism of each class of drug. CDDO-Me (methyl 2-cyano-3,12-dioxo-oleana-1,9(11)-dien-28-oate) is one of the most potent inducers of Nrf2, a transcription factor that regulates the expression of numerous cell defence genes in mammalian cells. Nrf2 is sequestered in the cytosol by Keap1, which ‘senses’ chemical and oxidative stress via its 27 cysteine residues. Although CDDO-Me is one of the most potent inducers of Nrf2, the molecular target and chemical mechanism is still not defined. Current literature suggests that a reversible 1,4 conjugate addition to specific cysteine residue(s) located on the Keap1 protein results in an increase in Nrf2 levels. In order for SAR work to be performed a synthetic route to CDDO and analogues was developed which involved nine steps using oleanolic acid as starting material. Highlights of the chemistry included addition of the ketone using mCPBA and incorporation of the cyano group in steps 3 and 7 of the synthesis. In addition to preparing the target molecule CDDO a number of additional molecules were prepared to define the importance of functional groups in the A and C rings of CDDO. Genetically modified H4IIE rat hepatoma cells transiently transfected with the an Nrf2-sensitive luciferase reporter gene were used to screen the CDDO-Me analogues, including DDO-Me which lacks a cyano group on the A ring, for their ability to induce Nrf2. NMR studies with model thiols were performed to determine the ability of these compounds to form reversible or non-reversible adducts. Mass spectrometry (MS) was used to confirm the NMR data and interpretations. In total, four probes were identified that reacted in a non-reversible fashion: DDO-Me, DDO-Al and DDO-Az (click probe versions of the parent DDO-Me that can be used to facilitate proteomic studies) and CDDO-Epox (a probe with similar overall structure to CDDO-Me but can react at the β-carbon in a non-reversible fashion; this feature should aid proteomic approaches to reactive cysteine residue identification). To further investigate if these compounds were reactive to cysteine residues within a model protein, recombinant human GSTP1 was used as a model protein for chemically reactive molecules. Cys-47 located on GSTP1 has been shown to react with other electrophones and during our studies LCMS has confirmed that all four of the synthesised active probes were capable of attaching covalently to Cys-47 of GSTP1. The emergence of malaria parasite resistance to most available drugs, including the semi-synthetic artemisinin derivatives artemether and artesunate, has led to efforts to create new synthetic peroxides as potential antimalarial agents. Leading examples of synthetic endoperoxides include OZ277 (arterolane), a molecule in phase III clinical trials in combination with piperaquine, and OZ439, a second generation derivative with improved pharmacokinetics and enhanced in vivo antimalarial activity. 1,2,4,5-Tetraoxanes are another class of endoperoxide with proven excellent antimalarial profiles against both chloroquine-resistant and chloroquine-sensitive strains of Plasmodium falciparum and oral activity in murine models of the disease. It is currently widely accepted that endoperoxides have a similar antimalarial mechanism to artemisinin, whereby Fe2+ medicated generation of cytotoxic carbon-centred radicals, results in death of the parasite. It is presumed that C-radicals can react with important key proteins; however, the specific molecular target(s) that leads to eventual parasite death are still unknown. A chemical synthesis of tetraoxane probes that contain a UV chromophore was performed and analogues were subsequently screened for antimalarial activity. The most active tetraoxane identified was exposed to a range of Fe2+ salts and conditions developed to mimic the biological environment. Primary, secondary and novel carbon-centred radical derived products (surrogate markers of bioactivation) were purified using UV-HPLC, characterised and submitted as chemical probes and standards for biological studies. In order for proteomic studies to be initiated, an allyl or azide group was incorporated into a semi-synthetic artemisinin skeleton. The azide (and alkyne) functional group within these probes provides a handle for protein pull down via click chemistry. Azide and acetylenes were chosen over direct linkage to the biotin group to reduce steric hindrance in the semi-synthetic probe. The synthesised click probes were tested for antimalarial activity and were submitted for protein pull down and identification of potential molecular targets. Similarly DDO allyl and azide were synthesised and were tested for Nrf2 induction and further confirmed as viable probes via NMR experiments with simple thiols and GSTP1. In summary, novel CDDO non reversible probes were synthesised and have shown potential as chemical tools to identify the molecular targets/mechanisms by which these compounds activate Nrf2. Tetraoxanes also have been prepared along with artemisinin click probes and the latter have been submitted for click chemistry pull down experiments, within Plasmodium falciparum parasites, to identify potential molecular targets.
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KAUR, ARSHDEEP. "CURRENT DIFFERENCING DIFFERENTIAL OUTPUT BUFFERED AMPLIFIER (CDDOBA) AND ITS APPLICCTIONS IN SIGNAL PROCESSING." Thesis, 2016. http://dspace.dtu.ac.in:8080/jspui/handle/repository/15508.

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In the present dissertation implementation of new active building block Current differencing differential output buffer amplifier (CDDOBA) using IC AD844 has been presented. CDDOBA is a new active building block with two input p and n terminal and two output, +w and -w terminal. CDDOBA can be well thought-out as a collection of inverting and non inverting current mode and inverting and non inverting voltage mode unity-gain cells. Recent advancements in current mode signal processing and advantages of current mode signal processing over voltage mode are briefly described in the second chapter. In this dissertation detailed description of the architecture of CDDOBA and PSPICE simulation of CDDOBA realized with IC AD844 is presented. General first order filters, voltage mode amplifier and differentiator and integrator circuits have been presented as application examples in order to demonstrate the performance of the CDDOBA. The PSPICE simulation results for frequency response are incorporated to verify the theory. A new Biquad filter, employing one CDDOBA as active element and four resistors and four capacitors is proposed.
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SURESHRAO, AMBATKAR HARSHAL. "IMPLEMENTATION OF ANALOG CIRCUITS USING CDTA AND CDDITA." Thesis, 2017. http://dspace.dtu.ac.in:8080/jspui/handle/repository/16081.

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A new CMOS realization of the current differencing differential input transconductance amplifier (CD-DITA) and CD-DITA based voltage mode MISO-type universal biquad filter are proposed. CD-DITA is an extension of CDTA having extra voltage input than CDTA increasing its usability of differential inputs. For a suitable CMOS based implementation of CD-DITA, several CDTA realizations are studied and the suitable one is modified to implement the proposed CD-DITA block. A FVF based DO-CDTA is characterized and its applications in analog signal processing circuits such as basic amplifiers, signal generators such as Schmitt Trigger and KHN filter are also studied. The proposed CD-DITA based voltage mode MISOtype universal biquad filter is realized with two resistors and two capacitors with independent electronic control of natural frequency and quality factor. The proposed filter can implement all five second order low pass, high pass, band pass, band stop, and all pass filter responses without altering the circuit topology. The proposed filter also offers low active and passive sensitivities. In addition, the effects of parasitics and errors on the proposed filter are also investigated. The characteristics CDTA and its applications are verified by PSPICE simulations using TSMC 0.25μm CMOS technology. The characteristics of CD-DITA and validity of proposed universal biquad filter is verified by SPICE simulation using TSMC 180nm technology.
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Chang, Chih-Hui, and 張智輝. "CDDO-Me effect on tumor progression in glioblastoma multiforme." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/7g9rb2.

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碩士
高雄醫學大學
臨床醫學研究所碩士班
106
Glioblastoma multiforme (GBM) is the most common malignant brain tumor. Despite advances treatment include of surgical resection, radiotherapy, and chemotherapy, it is still associated with poor overall survival rate. The C-28 methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO-Me) is a synthetic triterpenoid. In vitro and in vivo studies, CDDO-Me has been found potent of anti-inflammatory and anticancer properties. Although CDDO-Me express cytotoxicity to against a variety of cancer cells including ovarian cancer, prostate cancer, leukemia, breast cancer, lung cancer, and pancreatic cancer in normal cells CDDO-Me exhibit low toxicity. But CDDO-Me effect in GBM is unclear until now. We hypothesis that CDDO-Me is a new drug could inhibit tumorigenesis in GBM. Therefore, there have aims of this study to evaluate the difference of proliferation, migration, and invasion of GBM in vitro under CDDO-Me treatment. We used GBM840 and GBM8901 cell line and treat with difference concentration of CDDO-Me to evaluate difference expression of GBM cell proliferation, migration, and invasion in vitro. We use Western blot to detect N-cadherin, Cyclin D1, Ki-67, 及VEGF expression and find possible pathway. Results show that CDDO-Me significantly inhibite the proliferation of tumor cells at a concentration of 50 nM (P < 0.05) and reduce the ability of tumor cells to migrate and invade. Western blot present of CDDO-Me inhibit N-cadherin, Cyclin D1, Ki-67, and VEGF expression. Further testing of CDDO-Me affects Akt activity but does not interfere with Stat3 activity. According to the above results, CDDO-Me can inhibit the proliferation, migration and invasion of GBM tumor cells at a very low concentration (50 nM). The possible mechanism is CDDO-Me can inhibit N-cadherin, Cyclin D1, Ki-67, and VEGF expression via inhibition of Akt pathway.
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Bynum, James Andrew Jr. "A systems pharmacology approach to discovery of drugs to ameliorate oxidant stress in human endothelial cells." Thesis, 2015. http://hdl.handle.net/2152/31019.

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Ischemia is characterized by reduced blood flow to an area of the body which can then cause cellular injury through the generation of reactive oxygen species (ROS), activation of inflammation, and induction of apoptosis. Although rapid reestablishment of flow is required to prevent organ death, the reperfusion phase of this injury can cause its own deleterious effects often exacerbating the initial insult. The combined action of the two injuries is termed ischemia/reperfusion (I/R) injury. Oxidative stress that results from ischemia/reperfusion injury is a common pathological condition that accompanies many human diseases including stroke, heart attack and traumatic injury. In addition, neurodegenerative diseases including Parkinson’s, Alzheimer’s, and Huntington’s disease appear to involve oxidative stress. Although actively investigated by the medical and pharmaceutical industry; limited progress has been made to ameliorate I/R injury and to date there is no drug approved for treatment for I/R injury. Therapeutic approaches to treat I/R injury have included the administration of compounds to scavenge ROS or induce protective pathways or genetic responses. It was previously reported that caffeic acid phenethyl ester (CAPE), a plant-derived polyphenol, displayed cytoprotective effects against menadione (MD)-induced oxidative stress in human umbilical vein endothelial cells (HUVEC), and the induction of heme oxygenase-1 (HMOX1), a phase II enzyme, played an important role for CAPE cytoprotection. In an effort to improve this cytoprotection, other phase II enzyme inducers were investigated and, 2-cyano-3,12 dioxooleana-1,9 dien-28-imidazolide (CDDO-Im) and 2-cyano-3,12-dioxooleana-1,9-dien-28-oyl methyl ester (CDDO-Me), were found to be potent inducers with a rapid onset of action. CDDO-Im and CDDO-Me, synthetic olenane triterpenoids, developed as anticancer agents were compared to CAPE revealing that CDDO-Im was a more potent inducer of Phase II enzymes including HMOX1 and provided better cytoprotection than CAPE. Gene expression profiling showed that CDDO-Im was more potent inducer of protective genes like HMOX1 than CAPE and additionally induced heat shock proteins. To better understand the mechanism of action of CDDO-IM, a gene expression time-course was undertaken to identify early initiators of the transcriptional response preceding cytoprotection. Application of systems pharmacology identified molecular networks of cell mediating processes.
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Jutooru, Indira Devi. "New Mechanism Based Anticancer Drugs for Treatment of Pancreatic and Bladder Cancers." Thesis, 2010. http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7860.

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Methyl 2-cyano-3,11-dioxo-18b-olean-1,12-dien-30-oate (CDODA-Me) is a synthetic triterpenoid that inhibits growth of Panc1 and Panc28 pancreatic cancer cell lines and activates peroxisome proliferator-activated receptor B (PPARB)-dependent transactivation in these cells. CDODA-Me has also induced p21 and p27 protein expression and downregulated cyclin D1; however, these responses were receptor-independent. CDODA-Me induced apoptosis, which was accompanied by receptor-independent induction of the proapoptotic proteins early growth response-1 (Egr-1), nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1), and activating transcription factor-3 (ATF3). Induction of NAG-1 in Panc28 cells was p38-mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3-K)-dependent, but Egr-1-independent, whereas induction in Panc1 cells was associated with activation of p38-MAPK, PI3-K and p42-MAPK and was only partially Egr-1-dependent. Specificity protein (Sp) transcription factors Sp1, Sp3 & Sp4 are overexpressed in multiple tumor types and negative prognostic factors for survival. Since Sp proteins regulate genes associated with survival (survivin), angiogenesis [vascular endothelial growth factor and its receptors] and growth [cyclin D1, epidermal growth factor receptor], research in this laboratory has focused on development of anticancer drugs that decrease Sp protein expression. Arsenic trioxide, curcumin, 2-cyano-3,12-dioxoleana-1,9-dien-28-oic acid (CDDO), CDDO-Me, and celastrol exhibit antiproliferative, antiangiogenic and proapoptotic activity in many cancer cells and tumors. Treatment of cancer cells derived from urologic and gastrointestinal tumors with arsenic trioxide decreased Sp1, Sp3 and Sp4 transcription factors and cotreatment with the proteosome inhibitor MG132 did not inhibit downregulation of Sp proteins in these cancer cells. Mechanistic studies suggested that compound-dependent downregulation of Sp and Sp-dependent genes was due to decreased mitochondrial membrane potential and induction of reactive oxygen species, and the role of peroxides in mediating these responses was confirmed using hydrogen peroxide, demonstrating that the mitochondriotoxic effects of these compounds are important for their anticancer activities. Moreover, repression of Sp and Sp-dependent genes by CDDO-Me and celastrol was due to downregulation of microRNA-27a and induction of ZBTB10, an Sp repressor, and these responses were also reversed by antioxidants. Thus, the anticancer activity of CDDO-Me and celastrol is due, in part, to activation of ROS which in turn targets the microRNA-27a:ZBTB10?Sp transcription factor axis to decrease growth inhibitory, pro-apoptotic and antiangiogenic genes and responses.
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Book chapters on the topic "CDDOBA"

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Bhardwaj, Kapil, and Mayank Srivastava. "Novel CDDITA-Based-Grounded Inductance Simulation Circuits." In Lecture Notes in Electrical Engineering, 571–82. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6840-4_47.

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Jiao, Min, Yansong Zhang, Yan Sun, Shan Wang, and Xuan Zhou. "CDDTA-JOIN: One-Pass OLAP Algorithm for Column-Oriented Databases." In Web Technologies and Applications, 448–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-29253-8_38.

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Mathis, Bryan J., and Taixing Cui. "CDDO and Its Role in Chronic Diseases." In Advances in Experimental Medicine and Biology, 291–314. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41342-6_13.

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Joshi, Priyanka, Kapil Bhardwaj, and Mayank Srivastava. "Novel Single CDDITA Based Resistively Tunable All-Pass Filter Configuration with Grounded Passive Elements." In Lecture Notes in Electrical Engineering, 645–55. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-2281-7_60.

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Yoshimura, Tsutomu, Shunichi Bandoh, Yoshihiro Nakayama, and Ryoji Asagumo. "Establishment of Composite Durability Data Base (CDDB)." In Durability Analysis of Composite Systems 2001, 83–87. CRC Press, 2020. http://dx.doi.org/10.1201/9781003078784-14.

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Conference papers on the topic "CDDOBA"

1

Khanam, Patan Ayesha, and Mayank Srivastava. "Minimum Component Grounded Inductor Simulator employing CDDITA." In 2019 3rd International Conference on Recent Developments in Control, Automation & Power Engineering (RDCAPE). IEEE, 2019. http://dx.doi.org/10.1109/rdcape47089.2019.8979098.

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Bhardwaj, Kapil, Mayank Srivastava, Kuldeep Panwar, Dinesh Prasad, and Ajay Roy. "Grounded Series R-L impedance Simulator using CDDITA." In 2019 International Conference on Signal Processing and Communication (ICSC). IEEE, 2019. http://dx.doi.org/10.1109/icsc45622.2019.8938336.

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Ogawa, Hiroshi. "An overview on CD Technologies." In Optical Data Storage. Washington, D.C.: Optica Publishing Group, 1994. http://dx.doi.org/10.1364/ods.1994.ma1.

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It has been about 12 years passed since the first audio CD player was released. During these 12 years, various technologies have been developed and many standards have been established in the period of the Red Book for CDDA and the Orange Book part II for CD-R.
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4

Kulkarni, Ajit A., Keith C. Olsen, R. M. Kottmann, Thomas H. Thatcher, HsiMin Hsiao, R. P. Phipps, and Patricia J. Sime. "Novel Triterpenoid CDDO-Me: An Emerging Therapy For Pulmonary Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1942.

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Olsen, Keith C., Ajit A. Kulkarni, R. Matthew Kottmann, Katie Smolnycki, Thomas Thatcher, Rick P. Phipps, and Patricia J. Sime. "CDDO Decreases Expression Of The Pro-Fibrotic Protein Tissue Transglutaminase." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6050.

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Estornut, Cristina, Pilar Ribera, Amparo Bayarri, Paula Montero, and Julio Cortijo. "Omaveloxolone, CDDO-Me and Obacunone as promising therapeutic options in COPD." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.180.

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Xuefang, Zhang, and Yang Yansheng. "Prestacked techniques for unconformity trap reservoir description in the slope of CDDB area." In SPG/SEG 2016 International Geophysical Conference, Beijing, China, 20-22 April 2016. Society of Exploration Geophysicists and Society of Petroleum Geophysicists, 2016. http://dx.doi.org/10.1190/igcbeijing2016-008.

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Xiaoguang, Shi, Zhang Mingzhen, and Zou Dongbo. "A description method for beach-bar sands depositing in unconformity of CDDB area." In SPG/SEG 2016 International Geophysical Conference, Beijing, China, 20-22 April 2016. Society of Exploration Geophysicists and Society of Petroleum Geophysicists, 2016. http://dx.doi.org/10.1190/igcbeijing2016-022.

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Tran, Kim M., Michael B. Sporn, and Karen Liby. "Abstract 820: The synthetic triterpenoids, CDDO-methyl ester and CDDO-ethyl amide, and the histone deacetylase inhibitor vorinostat delay carcinogenesis in a transgenic model of estrogen receptor-negative breast cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-820.

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Deeb, Dorrah, Xiaohua Gao, Scott A. Dulchavsky, and Subhash C. Gautam. "Abstract 3549: Synthetic triterpenoid CDDO-Me induces apoptosis in pancreatic cancer cells by inducing oxidative stress." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3549.

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