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229 results on '"Li, Lian‐Sheng"'

1. Menin inhibitor MI-3454 induces remission in MLL1-rearranged and NPM1-mutated models of leukemia

Author

Klossowski, Szymon, Miao, Hongzhi, Kempinska, Katarzyna, Wu, Tao, Purohit, Trupta, Kim, EunGi, Linhares, Brian M., Chen, Dong, Jih, Gloria, Perkey, Eric, Huang, Huang, He, Miao, Wen, Bo, Wang, Yi, Yu, Ke, Lee, Stanley Chun-Wei, Danet-Desnoyers, Gwenn, Trotman, Winifred, Kandarpa, Malathi, Cotton, Anitria, Abdel-Wahab, Omar, Lei, Hongwei, Dou, Yali, Guzman, Monica, Peterson, Luke, Gruber, Tanja, Choi, Sarah, Sun, Duxin, Ren, Pingda, Li, Lian-Sheng, Liu, Yi, Burrows, Francis, Maillard, Ivan, Cierpicki, Tomasz, and Grembecka, Jolanta

Subjects
University of Michigan, Analysis, Models, Genetic aspects, Protein-protein interactions -- Genetic aspects -- Analysis -- Models, Genes, Time, Acute leukemia
Abstract

Introduction The development of acute leukemia is associated with heterogeneous genetic and epigenetic alterations (1, 2), making it difficult to identify new effective therapies for leukemia patients. Despite these challenges, [...], The protein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in acute leukemias with translocations of the MLL1 gene or with mutations in the nucleophosmin 1 (NPM1) gene. As a step toward clinical translation of menin-MLL1 inhibitors, we report development of MI-3454, a highly potent and orally bioavailable inhibitor of the menin-MLL1 interaction. MI-3454 profoundly inhibited proliferation and induced differentiation in acute leukemia cells and primary patient samples with MLL1 translocations or NPM1 mutations. When applied as a single agent, MI-3454 induced complete remission or regression of leukemia in mouse models of MLLI-rearranged or NPMI-mutated leukemia, including patient-derived xenograft models, through downregulation of key genes involved in leukemogenesis. We also identified MEIS1 as a potential pharmacodynamic biomarker of treatment response with MI-3454 in leukemia, and demonstrated that this compound is well tolerated and did not impair normal hematopoiesis in mice. Overall, this study demonstrates, for the first time to our knowledge, profound activity of the menin-MLL1 inhibitor as a single agent in clinically relevant PDX models of leukemia. These data provide a strong rationale for clinical translation of MI-3454 or its analogs for leukemia patients with MLL1 rearrangements or NPM1 mutations.

Published
2020
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2. Selective Inhibition of Phosphoinositide 3-Kinase p110? Preserves Lymphocyte Function*

Author

So, Lomon, Yea, Sung Su, Oak, Jean S., Lu, Mengrou, Manmadhan, Arun, Ke, Qiao Han, Janes, Matthew R., Kessler, Linda V., Kucharski, Jeff M., Li, Lian-Sheng, Martin, Michael B., Ren, Pingda, Jessen, Katti A., Liu, Yi, Rommel, Christian, and Fruman, David A.

Abstract

Background: The class IA PI3K isoform p110α is a promising drug target in cancer therapy yet its role in lymphocytes is not known.Results: Lymphocyte function was minimally affected by p110α inhibition both in vitro and in vivo.Conclusion: Selective inhibition of p110α preserves lymphocyte function.Significance: The study raises confidence that selective p110α inhibitors in cancer therapy will not be immunosuppressive.Class IA phosphoinositide 3-kinase (PI3K) is essential for clonal expansion, differentiation, and effector function of B and T lymphocytes. The p110δ catalytic isoform of PI3K is highly expressed in lymphocytes and plays a prominent role in B and T cell responses. Another class IA PI3K catalytic isoform, p110α, is a promising drug target in cancer but little is known about its function in lymphocytes. Here we used highly selective inhibitors to probe the function of p110α in lymphocyte responses in vitro and in vivo. p110α inhibition partially reduced B cell receptor (BCR)-dependent AKT activation and proliferation, and diminished survival supported by the cytokines BAFF and IL-4. Selective p110δ inhibition suppressed B cell responses much more strongly, yet maximal suppression was achieved by targeting multiple PI3K isoforms. In mouse and human T cells, inhibition of single class IA isoforms had little effect on proliferation, whereas pan-class I inhibition did suppress T cell expansion. In mice, selective p110α inhibition using the investigational agent MLN1117 (previously known as INK1117) did not disrupt the marginal zone B cell compartment and did not block T cell-dependent germinal center formation. In contrast, the selective p110δ inhibitor IC87114 strongly suppressed germinal center formation and reduced marginal zone B cell numbers, similar to a pan-class I inhibitor. These findings show that although acute p110α inhibition partially diminishes AKT activation, selective p110α inhibitors are likely to be less immunosuppressive in vivo compared with p110δ or pan-class I inhibitors.

Published
2012

3. Efficacy of the investigational mTOR kinase inhibitor MLN0128 / INK128 in models of B-cell acute lymphoblastic leukemia

Author

Janes, Matthew R., Vu, Collin, Mallya, Sharmila, Shieh, Marie, Limon, Jose J., Li, Lian-Sheng, Jessen, Katti A., Martin, Michael B., Ren, Pingda, Lilly, Michael B., Sender, Leonard, Liu, Yi, Rommel, Christian, and Fruman, David A.

Abstract

The mechanistic target of rapamycin (mTOR) is a serine/threonine kinase whose activity contributes to leukemia proliferation and survival. Compounds targeting the mTOR active site inhibit rapamycin-resistant functions and have enhanced anti-cancer activity in mouse models. MLN0128 (formerly known as INK128) is a novel, orally active mTOR kinase inhibitor currently in clinical development. Here we evaluated MLN0128 in preclinical models of B-cell acute lymphoblastic leukemia (B-ALL). MLN0128 suppressed proliferation of B-ALL cell lines in vitro and reduced colony formation by primary human leukemia cells from adult and pediatric B-ALL patients. MLN0128 also boosted the efficacy of dasatinib in Philadelphia Chromosome-positive (Ph+) specimens. In a syngeneic mouse model of lymphoid BCR-ABL+ disease, daily oral dosing of MLN0128 rapidly cleared leukemic outgrowth. In primary xenografts of Ph+ B-ALL specimens, MLN0128 significantly enhanced the efficacy of dasatinib. In non-Ph B-ALL xenografts, single agent MLN0128 had a cytostatic effect that was most pronounced in mice with low disease burden. In all in vivo models, MLN0128 was well tolerated and did not suppress endogenous bone marrow proliferation. These findings support the rationale for clinical testing of MLN0128 in both adult and pediatric B-ALL and provide insight towards optimizing therapeutic efficacy of mTOR kinase inhibitors.

Published
2012

4. Targeting KRAS Mutant Cancers with a Covalent G12C-Specific Inhibitor

Author

Janes, Matthew R., Zhang, Jingchuan, Li, Lian-Sheng, Hansen, Rasmus, Peters, Ulf, Guo, Xin, Chen, Yuching, Babbar, Anjali, Firdaus, Sarah J., Darjania, Levan, Feng, Jun, Chen, Jeffrey H., Li, Shuangwei, Li, Shisheng, Long, Yun O., Thach, Carol, Liu, Yuan, Zarieh, Ata, Ely, Tess, Kucharski, Jeff M., Kessler, Linda V., Wu, Tao, Yu, Ke, Wang, Yi, Yao, Yvonne, Deng, Xiaohu, Zarrinkar, Patrick P., Brehmer, Dirk, Dhanak, Dashyant, Lorenzi, Matthew V., Hu-Lowe, Dana, Patricelli, Matthew P., Ren, Pingda, and Liu, Yi

Published
2018
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7. Supplementary Methods, Tables S1 - S3 and S5 - S6, Figures S1 - S12 from Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State

Author

Patricelli, Matthew P., primary, Janes, Matthew R., primary, Li, Lian-Sheng, primary, Hansen, Rasmus, primary, Peters, Ulf, primary, Kessler, Linda V., primary, Chen, Yuching, primary, Kucharski, Jeff M., primary, Feng, Jun, primary, Ely, Tess, primary, Chen, Jeffrey H., primary, Firdaus, Sarah J., primary, Babbar, Anjali, primary, Ren, Pingda, primary, and Liu, Yi, primary

Published
2023
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8. Supplementary Table S4 from Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State

Author

Patricelli, Matthew P., primary, Janes, Matthew R., primary, Li, Lian-Sheng, primary, Hansen, Rasmus, primary, Peters, Ulf, primary, Kessler, Linda V., primary, Chen, Yuching, primary, Kucharski, Jeff M., primary, Feng, Jun, primary, Ely, Tess, primary, Chen, Jeffrey H., primary, Firdaus, Sarah J., primary, Babbar, Anjali, primary, Ren, Pingda, primary, and Liu, Yi, primary

Published
2023
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9. Data from Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State

Author

Patricelli, Matthew P., primary, Janes, Matthew R., primary, Li, Lian-Sheng, primary, Hansen, Rasmus, primary, Peters, Ulf, primary, Kessler, Linda V., primary, Chen, Yuching, primary, Kucharski, Jeff M., primary, Feng, Jun, primary, Ely, Tess, primary, Chen, Jeffrey H., primary, Firdaus, Sarah J., primary, Babbar, Anjali, primary, Ren, Pingda, primary, and Liu, Yi, primary

Published
2023
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10. Figure S2 from KRAS G12C NSCLC Models Are Sensitive to Direct Targeting of KRAS in Combination with PI3K Inhibition

Author

Misale, Sandra, primary, Fatherree, Jackson P., primary, Cortez, Eliane, primary, Li, Chendi, primary, Bilton, Samantha, primary, Timonina, Daria, primary, Myers, David T., primary, Lee, Dana, primary, Gomez-Caraballo, Maria, primary, Greenberg, Max, primary, Nangia, Varuna, primary, Greninger, Patricia, primary, Egan, Regina K., primary, McClanaghan, Joseph, primary, Stein, Giovanna T., primary, Murchie, Ellen, primary, Zarrinkar, Patrick P., primary, Janes, Matthew R., primary, Li, Lian-Sheng, primary, Liu, Yi, primary, Hata, Aaron N., primary, and Benes, Cyril H., primary

Published
2023
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11. Data S1 from KRAS G12C NSCLC Models Are Sensitive to Direct Targeting of KRAS in Combination with PI3K Inhibition

Author

Misale, Sandra, primary, Fatherree, Jackson P., primary, Cortez, Eliane, primary, Li, Chendi, primary, Bilton, Samantha, primary, Timonina, Daria, primary, Myers, David T., primary, Lee, Dana, primary, Gomez-Caraballo, Maria, primary, Greenberg, Max, primary, Nangia, Varuna, primary, Greninger, Patricia, primary, Egan, Regina K., primary, McClanaghan, Joseph, primary, Stein, Giovanna T., primary, Murchie, Ellen, primary, Zarrinkar, Patrick P., primary, Janes, Matthew R., primary, Li, Lian-Sheng, primary, Liu, Yi, primary, Hata, Aaron N., primary, and Benes, Cyril H., primary

Published
2023
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15. Hindered Biaryl Bond Construction and Subsequent Diastereomeric Crystallization to Produce an Atropisomeric Covalent KRASG12C Inhibitor ARS-2102

Author

Yang, Xiaogen, primary, Li, Zhiwen, additional, Xu, Wenwen, additional, Zhu, Guanming, additional, Feng, Xiantong, additional, Zhang, Jun, additional, Zhao, Hongbin, additional, Chen, Yuyin, additional, Kong, Jianshe, additional, Mai, Wanping, additional, Li, Lian-Sheng, additional, Pippel, Daniel J., additional, Ren, Pingda, additional, and Deng, Xiaohu, additional

Published
2022
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17. PI3K-δ and PI3K-γ Inhibition by IPI-145 Abrogates Immune Responses and Suppresses Activity in Autoimmune and Inflammatory Disease Models

Author

Winkler, David G., Faia, Kerrie L., DiNitto, Jonathan P., Ali, Janid A., White, Kerry F., Brophy, Erin E., Pink, Melissa M., Proctor, Jennifer L., Lussier, Jennifer, Martin, Christian M., Hoyt, Jennifer G., Tillotson, Bonnie, Murphy, Erin L., Lim, Alice R., Thomas, Brian D., MacDougall, John R., Ren, Pingda, Liu, Yi, Li, Lian-Sheng, Jessen, Katti A., Fritz, Christian C., Dunbar, Joi L., Porter, James R., Rommel, Christian, Palombella, Vito J., Changelian, Paul S., and Kutok, Jeffery L.

Published
2013
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25. Hindered Biaryl Bond Construction and Subsequent Diastereomeric Crystallization to Produce an Atropisomeric Covalent KRASG12CInhibitor ARS-2102

Author

Yang, Xiaogen, Li, Zhiwen, Xu, Wenwen, Zhu, Guanming, Feng, Xiantong, Zhang, Jun, Zhao, Hongbin, Chen, Yuyin, Kong, Jianshe, Mai, Wanping, Li, Lian-Sheng, Pippel, Daniel J., Ren, Pingda, and Deng, Xiaohu

Abstract

A scaleup route for a first-generation covalent KRASG12Cinhibitor ARS-2102 was devised, featuring an “early cross-coupling” strategy to construct the tetra-substituted atropisomeric biaryl scaffold. An iterative diastereomeric recrystallization enabled an effective chiral resolution of key intermediate 24. A global deprotection followed by chemoselective functionalization afforded ARS-2102 in excellent yield and diastereomeric enrichment. This chromatography-free sequence was successfully executed on kilogram scale.

Published
2023
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27. Development of combination therapies to maximize the impact of KRAS-G12C inhibitors in lung cancer

Author

Molina-Arcas, Miriam, primary, Moore, Christopher, additional, Rana, Sareena, additional, van Maldegem, Febe, additional, Mugarza, Edurne, additional, Romero-Clavijo, Pablo, additional, Herbert, Eleanor, additional, Horswell, Stuart, additional, Li, Lian-Sheng, additional, Janes, Matthew R., additional, Hancock, David C., additional, and Downward, Julian, additional

Published
2019
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29. KRAS G12C NSCLC Models Are Sensitive to Direct Targeting of KRAS in Combination with PI3K Inhibition

Author

Misale, Sandra, primary, Fatherree, Jackson P., additional, Cortez, Eliane, additional, Li, Chendi, additional, Bilton, Samantha, additional, Timonina, Daria, additional, Myers, David T., additional, Lee, Dana, additional, Gomez-Caraballo, Maria, additional, Greenberg, Max, additional, Nangia, Varuna, additional, Greninger, Patricia, additional, Egan, Regina K., additional, McClanaghan, Joseph, additional, Stein, Giovanna T., additional, Murchie, Ellen, additional, Zarrinkar, Patrick P., additional, Janes, Matthew R., additional, Li, Lian-Sheng, additional, Liu, Yi, additional, Hata, Aaron N., additional, and Benes, Cyril H., additional

Published
2019
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34. Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State

Author

Patricelli, Matthew P., primary, Janes, Matthew R., additional, Li, Lian-Sheng, additional, Hansen, Rasmus, additional, Peters, Ulf, additional, Kessler, Linda V., additional, Chen, Yuching, additional, Kucharski, Jeff M., additional, Feng, Jun, additional, Ely, Tess, additional, Chen, Jeffrey H., additional, Firdaus, Sarah J., additional, Babbar, Anjali, additional, Ren, Pingda, additional, and Liu, Yi, additional

Published
2016
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36. Discovery of tricyclic 5,6-dihydro-1 H-pyridin-2-ones as novel, potent, and orally bioavailable inhibitors of HCV NS5B polymerase

Author

Ruebsam, Frank, Murphy, Douglas E., Tran, Chinh V., Li, Lian-Sheng, Zhao, Jingjing, Dragovich, Peter S., McGuire, Helen M., Xiang, Alan X., Sun, Zhongxiang, Ayida, Benjamin K., Blazel, Julie K., Kim, Sun Hee, Zhou, Yuefen, Han, Qing, Kissinger, Charles R., Webber, Stephen E., Showalter, Richard E., Shah, Amit M., Tsan, Mei, Patel, Rupal A., Thompson, Peggy A., LeBrun, Laurie A., Hou, Huiying J., Kamran, Ruhi, Sergeeva, Maria V., Bartkowski, Darian M., Nolan, Thomas G., Norris, Daniel A., Khandurina, Julia, Brooks, Jennifer, Okamoto, Ellen, and Kirkovsky, Leo

Published
2009
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37. 5,5′- and 6,6′-Dialkyl-5,6-dihydro-1 H-pyridin-2-ones as potent inhibitors of HCV NS5B polymerase

Author

Ellis, David A., Blazel, Julie K., Tran, Chinh V., Ruebsam, Frank, Murphy, Douglas E., Li, Lian-Sheng, Zhao, Jingjing, Zhou, Yuefen, McGuire, Helen M., Xiang, Alan X., Webber, Stephen E., Zhao, Qiang, Han, Qing, Kissinger, Charles R., Lardy, Matthew, Gobbi, Alberto, Showalter, Richard E., Shah, Amit M., Tsan, Mei, Patel, Rupal A., LeBrun, Laurie A., Kamran, Ruhi, Bartkowski, Darian M., Nolan, Thomas G., Norris, Daniel A., Sergeeva, Maria V., and Kirkovsky, Leo

Published
2009
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38. 5,6-Dihydro-1 H-pyridin-2-ones as potent inhibitors of HCV NS5B polymerase

Author

Ruebsam, Frank, Tran, Chinh V., Li, Lian-Sheng, Kim, Sun Hee, Xiang, Alan X., Zhou, Yuefen, Blazel, Julie K., Sun, Zhongxiang, Dragovich, Peter S., Zhao, Jingjing, McGuire, Helen M., Murphy, Douglas E., Tran, Martin T., Stankovic, Nebojsa, Ellis, David A., Gobbi, Alberto, Showalter, Richard E., Webber, Stephen E., Shah, Amit M., Tsan, Mei, Patel, Rupal A., LeBrun, Laurie A., Hou, Huiying J., Kamran, Ruhi, Sergeeva, Maria V., Bartkowski, Darian M., Nolan, Thomas G., Norris, Daniel A., and Kirkovsky, Leo

Published
2009
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42. Novel HCV NS5B polymerase inhibitors derived from 4-(1′,1′-dioxo-1′,4′-dihydro-1′λ 6-benzo[1′,2′,4′]thiadiazin-3′-yl)-5-hydroxy-2 H-pyridazin-3-ones. Part 5: Exploration of pyridazinones containing 6-amino-substituents

Author

Dragovich, Peter S., Blazel, Julie K., Ellis, David A., Han, Qing, Kamran, Ruhi, Kissinger, Charles R., LeBrun, Laurie A., Li, Lian-Sheng, Murphy, Douglas E., Noble, Michael, Patel, Rupal A., Ruebsam, Frank, Sergeeva, Maria V., Shah, Amit M., Showalter, Richard E., Tran, Chinh V., Tsan, Mei, Webber, Stephen E., Kirkovsky, Leo, and Zhou, Yuefen

Published
2008
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43. 4-(1,1-Dioxo-1,4-dihydro-1λ 6-benzo[1,4]thiazin-3-yl)-5-hydroxy-2 H-pyridazin-3-ones as potent inhibitors of HCV NS5B polymerase

Author

Ellis, David A., Blazel, Julie K., Webber, Stephen E., Tran, Chinh V., Dragovich, Peter S., Sun, Zhongxiang, Ruebsam, Frank, McGuire, Helen M., Xiang, Alan X., Zhao, Jingjing, Li, Lian-Sheng, Zhou, Yuefen, Han, Qing, Kissinger, Charles R., Showalter, Richard E., Lardy, Matthew, Shah, Amit M., Tsan, Mei, Patel, Rupal, LeBrun, Laurie A., Kamran, Ruhi, Bartkowski, Darian M., Nolan, Thomas G., Norris, Daniel A., Sergeeva, Maria V., and Kirkovsky, Leo

Published
2008
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44. Pyrrolo[1,2- b]pyridazin-2-ones as potent inhibitors of HCV NS5B polymerase

Author

Ruebsam, Frank, Webber, Stephen E., Tran, Martin T., Tran, Chinh V., Murphy, Douglas E., Zhao, Jingjing, Dragovich, Peter S., Kim, Sun Hee, Li, Lian-Sheng, Zhou, Yuefen, Han, Qing, Kissinger, Charles R., Showalter, Richard E., Lardy, Matthew, Shah, Amit M., Tsan, Mei, Patel, Rupal, LeBrun, Laurie A., Kamran, Ruhi, Sergeeva, Maria V., Bartkowski, Darian M., Nolan, Thomas G., Norris, Daniel A., and Kirkovsky, Leo

Published
2008
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45. Novel HCV NS5B polymerase inhibitors derived from 4-(1′,1′-dioxo-1′,4′-dihydro-1′λ 6-benzo[1′,2′,4′]thiadiazin-3′-yl)-5-hydroxy-2 H-pyridazin-3-ones: Part 4. Optimization of DMPK properties

Author

Sergeeva, Maria V., Zhou, Yuefen, Bartkowski, Darian M., Nolan, Thomas G., Norris, Daniel A., Okamoto, Ellen, Kirkovsky, Leo, Kamran, Ruhi, LeBrun, Laurie A., Tsan, Mei, Patel, Rupal, Shah, Amit M., Lardy, Matthew, Gobbi, Alberto, Li, Lian-Sheng, Zhao, Jingjing, Bertolini, Thomas, Stankovic, Nebojsa, Sun, Zhongxiang, Murphy, Douglas E., Webber, Stephen E., and Dragovich, Peter S.

Published
2008
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46. Novel HCV NS5B polymerase inhibitors derived from 4-(1′,1′-dioxo-1′,4′-dihydro-1′λ 6-benzo[1′,2′,4′]thiadiazin-3′-yl)-5-hydroxy-2 H-pyridazin-3-ones. Part 3: Further optimization of the 2-, 6-, and 7′-substituents and initial pharmacokinetic assessments

Author

Li, Lian-Sheng, Zhou, Yuefen, Murphy, Douglas E., Stankovic, Nebojsa, Zhao, Jingjing, Dragovich, Peter S., Bertolini, Thomas, Sun, Zhongxiang, Ayida, Benjamin, Tran, Chinh V., Ruebsam, Frank, Webber, Stephen E., Shah, Amit M., Tsan, Mei, Showalter, Richard E., Patel, Rupal, LeBrun, Laurie A., Bartkowski, Darian M., Nolan, Thomas G., Norris, Daniel A., Kamran, Ruhi, Brooks, Jennifer, Sergeeva, Maria V., Kirkovsky, Leo, Zhao, Qiang, and Kissinger, Charles R.

Published
2008
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47. Novel HCV NS5B polymerase inhibitors derived from 4-(1′,1′-dioxo-1′,4′-dihydro-1′λ 6-benzo[1′,2′,4′]thiadiazin-3′-yl)-5-hydroxy-2 H-pyridazin-3-ones. Part 1: Exploration of 7′-substitution of benzothiadiazine

Author

Zhou, Yuefen, Webber, Stephen E., Murphy, Douglas E., Li, Lian-Sheng, Dragovich, Peter S., Tran, Chinh V., Sun, Zhongxiang, Ruebsam, Frank, Shah, Amit M., Tsan, Mei, Showalter, Richard E., Patel, Rupal, Li, Bin, Zhao, Qiang, Han, Qing, Hermann, Thomas, Kissinger, Charles R., LeBrun, Laurie, Sergeeva, Maria V., and Kirkovsky, Leo

Published
2008
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48. Novel HCV NS5B polymerase inhibitors derived from 4-(1′,1′-dioxo-1′,4′-dihydro-1′ λ6-benzo[1′,2′,4′]thiadiazin-3′-yl)-5-hydroxy-2 H-pyridazin-3-ones. Part 2: Variation of the 2- and 6-pyridazinone substituents

Author

Zhou, Yuefen, Li, Lian-Sheng, Dragovich, Peter S., Murphy, Douglas E., Tran, Chinh V., Ruebsam, Frank, Webber, Stephen E., Shah, Amit M., Tsan, Mei, Averill, April, Showalter, Richard E., Patel, Rupal, Han, Qing, Zhao, Qiang, Hermann, Thomas, Kissinger, Charles R., LeBrun, Laurie, and Sergeeva, Maria V.

Published
2008
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