Asset Details
Do you wish to reserve the book?
The Combination of a BCL-xL PROTAC and an mTOR Inhibitor Sensitizes Pancreatic Ductal Adenocarcinoma to KRASsup.G12D Inhibitor Treatment
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The Combination of a BCL-xL PROTAC and an mTOR Inhibitor Sensitizes Pancreatic Ductal Adenocarcinoma to KRASsup.G12D Inhibitor Treatment
Do you wish to request the book?
The Combination of a BCL-xL PROTAC and an mTOR Inhibitor Sensitizes Pancreatic Ductal Adenocarcinoma to KRASsup.G12D Inhibitor Treatment
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The Combination of a BCL-xL PROTAC and an mTOR Inhibitor Sensitizes Pancreatic Ductal Adenocarcinoma to KRASsup.G12D Inhibitor Treatment
2026
Overview
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor survival and lacks effective treatments. MRTX1133, a new investigational drug targeting the KRAS G12D mutation, which is common in PDAC, shows promise in preclinical studies but is unlikely to be effective as a single agent. In this study, we combined MRTX1133 with a BCL-xL-targeting degrader (DT2216) and the mTOR inhibitor everolimus for enhanced therapeutic efficacy. The triple combination more effectively killed KRAS G12D-mutant PDAC cells in culture and slowed tumor growth in mice than MRTX1133 alone, which was associated with simultaneously strengthening pro-death signals and blocking survival mechanisms in cancer cells. Notably, the triple combination also showed efficacy against mouse tumors that developed resistance to MRTX1133. These findings suggest that combining MRTX1133 with DT2216 and everolimus could be a more effective treatment strategy for patients with KRAS G12D-mutant PDAC.
Publisher
MDPI AG
Subject
