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Abstract 2249: Development and validation of a pharmacodynamic (PD) assay for TOS-358, the first covalent inhibitor of PI3Kα in clinical development

Autor: John R. MacDougall, Raymond Mak, John Bradley, Allison Simpson, Claire May, Lan Wei, Kendra Ouellette, Marty Olbrot, Jimmy Blair, Neil Dhawan, Wei Chen

Publikováno v: Cancer Research. 83:2249-2249

TOS-358 is a first-in-class covalent inhibitor of PI3Kα and is currently in clinical development in a variety of solid malignancies. We have developed a fit-for-purpose pharmacodynamic assay to evaluate the target occupancy of TOS-358 in in vitro an

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::a4a456949391642472ad772103280841
https://doi.org/10.1158/1538-7445.am2023-2249

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Abstract 4946: TOS-358, a first-in-class covalent PI3Kα inhibitor, demonstrates superior efficacy and does not induce significant hyperglycemia at efficacious doses in multiple animal models

Autor: John R. MacDougall, John Bradley, Raymond Mak, Neil Dhawan, Wei Chen

Publikováno v: Cancer Research. 83:4946-4946

PI3Kα is frequently mutated in a variety of cancer types, and the PI3K-AKT signaling axis also plays a role in insulin signaling and glucose homeostasis. TOS-358 is a highly selective first-in-class covalent inhibitor of PI3Kα and is currently in c

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::ae7d6f1095d79de00e863bdde35d289a
https://doi.org/10.1158/1538-7445.am2023-4946

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Abstract 4945: Inhibition of wild-type PI3Kα signaling is required for durable efficacy in PI3Kα mutant cancer cells due to robust re-activation of wild-type PI3Kα signaling

Autor: John R. MacDougall, Mengqi Zhong, Hanne Merritt, Joselyn S. Del Cid, John Bradley, Raymond Mak, Neil Dhawan, Wei Chen

Publikováno v: Cancer Research. 83:4945-4945

PI3Kα is the most mutated oncogene with a high mutation rate in breast, lung, colorectal, gastric, bladder, and other tumor types. However, current inhibitors have had little efficacy in the clinic due to their inability to achieve maximal PI3Kα ta

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::0b8b74db29ecbdca38ad3648e072349a
https://doi.org/10.1158/1538-7445.am2023-4945

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Abstract 1827: Direct activation of the tumor suppressor protein phosphatase 2A as a therapeutic strategy for TKI-resistant lung adenocarcinoma

Autor: Jaya Sangodkar, Goutham Narla, Sudeh Izadmeher, Neil Dhawan, Neelesh Sharma, Rita Tohme, Michael Ohlmeyer

Publikováno v: Cancer Research. 78:1827-1827

Most lung adenocarcinoma (LUAD) patients develop acquired resistance to tyrosine kinase inhibitors (TKI) via mechanisms enabling the sustained activation of the MAPK and PI3K oncogenic pathways downstream of the tyrosine kinase EGFR. The tumor suppre

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::9d98c923bd4cd1741e43c87ff78d0a51
https://doi.org/10.1158/1538-7445.am2018-1827

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