Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Valerie Northcutt"'
Publikováno v:
Xenobiotica. 52:1031-1040
Autor:
John Babiak, Nicole Risher, Marla Weetall, Diksha Kaushik, Shirley Yeh, Kylie O'Keefe, Valerie Northcutt, Ronald Kong, Young-Choon Moon, Ellen Welch, Lachlan Molony, Jiyuan Ma
Publikováno v:
Xenobiotica. 52:152-164
Emvododstat was identified as a potent inhibitor of dihydroorotate dehydrogenase and is now in clinical development for the treatment of acute myeloid leukaemia and COVID-19. The objective of this paper is to evaluate the metabolism, pharmacokinetics
Autor:
Neil Gregory Almstead, Joseph M. Colacino, Nicole Risher, Valerie Northcutt, Ronald Kong, Ellen Welch, Jiyuan Ma, Young-Choon Moon, Marla Weetall
Publikováno v:
Drug Metabolism and Pharmacokinetics. 38:100393
Ataluren is an aromatic acid derivative with a 1,2,4-oxodiazole moiety. Ataluren-O-1β-acyl glucuronide is a prominent circulatory metabolite in mice, rats, dogs, and humans following oral administration of ataluren. The objective of this paper was t
Autor:
Elizabeth Goodwin, Valerie Northcutt, Neil Gregory Almstead, Joseph McIntosh, Ronald Kong, Seongwoo Hwang, John Babiak, Jiyuan Ma
Publikováno v:
Drug metabolism and disposition: the biological fate of chemicals. 48(4)
Ataluren is a unique small molecule developed for the treatment of diseases caused by nonsense mutations, which result in premature termination of ribosomal translation and lack of full-length protein production. This study investigated the in vivo m
Autor:
Young-Choon Moon, Marla Weetall, R. Spiegel, Stuart W. Peltz, Samit Hirawat, Neil Gregory Almstead, John Babiak, Liangxian Cao, Valerie Northcutt, Peter Riebling, Joseph M. Colacino, Mandar V. Dali, Thomas W. Davis, Gary Elfring
Publikováno v:
Clinical Pharmacology in Drug Development
PTC299 is a novel small molecule that specifically blocks the production of protein from selected mRNAs that under certain conditions use noncanonical ribosomal translational pathways. Hypoxia, oncogenic transformation, and viral infections limit nor
Autor:
H. Blau, Langdon L. Miller, Malka Nissim-Rafinia, Valerie Northcutt, Batsheva Kerem, Samit Hirawat, Joseph Rivlin, Gary Elfring, Eitan Kerem, S. Armoni, Michael Cohen, Micha Aviram, David Shoseyov, Michael Wilschanski, Yasmin Yaakov
Publikováno v:
The Lancet. 372:719-727
In about 10% of patients worldwide and more than 50% of patients in Israel, cystic fibrosis results from nonsense mutations (premature stop codons) in the messenger RNA (mRNA) for the cystic fibrosis transmembrane conductance regulator (CFTR). PTC124
Autor:
James J. Takasugi, Anna Mollin, Jeffrey Allen Campbell, Meenal Patel, Shirley Yeh, Stuart W. Peltz, Yuki Tomizawa, Young-Choon Moon, Ellen Welch, Allan Jacobson, Gary Mitchell Karp, Huisheng Feng, Anthony Turpoff, Hongyu Ren, Jin Zhuo, S. M. Jones, Atiyya Khan, Valerie Northcutt, Neil G. Almstead, Arthur Branstrom, Feng He, M. Morgan Conn, Guangming Chen, William D. Ju, Wilde Richard Gerald, Samit Hirawat, Christopher R. Trotta, Masataka Kawana, Nicole Risher, Sergey Paushkin, Seongwoo Hwang, Joseph M. Colacino, H. Lee Sweeney, Donald Thomas Corson, Phyllis Spatrick, Elisabeth R. Barton, Panayiota Trifillis, Langdon L. Miller, Westley J. Friesen, Marla Weetall, John Babiak, Jean Hedrick
Publikováno v:
Nature. 447:87-91
Nonsense mutations promote premature translational termination and cause anywhere from 5-70% of the individual cases of most inherited diseases. Studies on nonsense-mediated cystic fibrosis have indicated that boosting specific protein synthesis from
Autor:
Valerie Northcutt, Gary Elfring, William D. Ju, Eileen M. Leonard, Sergey Paushkin, Langdon L. Miller, Seongwoo Hwang, Samit Hirawat, Neil Gregory Almstead, Stuart W. Peltz, Ellen Welch
Publikováno v:
The Journal of Clinical Pharmacology. 47:430-444
Nonsense (premature stop codon) mutations are causative in 5% to 15% of patients with monogenetic inherited disorders. PTC124, a 284-Dalton 1,2,4-oxadiazole, promotes ribosomal readthrough of premature stop codons in mRNA and offers therapeutic poten
Autor:
A. Reha, Jay A. Barth, Carsten G. Bönnemann, Brenda Wong, Stuart W. Peltz, Valerie Northcutt, Jacinda B. Sampson, Kevin M. Flanigan, H. Lee Sweeney, Richard S. Finkel, Gary Elfring
Publikováno v:
PLoS ONE
PLoS ONE, Vol 8, Iss 12, p e81302 (2013)
PLoS ONE, Vol 8, Iss 12, p e81302 (2013)
Background Approximately 13% of boys with Duchenne muscular dystrophy (DMD) have a nonsense mutation in the dystrophin gene, resulting in a premature stop codon in the corresponding mRNA and failure to generate a functional protein. Ataluren (PTC124)