ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Translational Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1630476
c-MYC mRNA destabilization inhibited lethal pancreatic cancer in-vivo with significant survival outcomes
Provisionally accepted
- 1UTR Therapeutics Inc, New York, United States
- 2UTR Therapeutics Inc., New York, United States
- 3Hunter College, New York, United States
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Pancreatic ductal carcinoma, the most common form of pancreatic cancer and is the deadliest form with an 11% survival rate. There is currently no cure for pancreatic cancer. The mainstay therapy for pancreatic cancer is gemcitabine, capecitabine or FOLFIRINOX as first line therapy for pancreatic cancer. After 21 months, the chemoresistance starts driven by the oncogenic c-MYC signal. This is a significant clinical and cancer biology challenge. The c-MYC oncogene has been shown to be over expressed in the 43.1% and the 31.6% primary and metastatic pancreatic cancer respectively and is the primary driver of the neoplastic changes and progression of pancreatic cancer metastasis. Here, we report the in-vivo down regulation and inhibition of the metastatic c-MYC expressing lethal pancreatic cancer by the mRNA drug the 3'UTRMYC1-18. The drug achieved on-target in-vivo c-MYC dose-dependent downregulation with complete pathological response, inhibition of liver, lung and brain metastasis with significant survival outcome and is safe, stable long half-life, and well tolerated. Mechanistically, the therapeutic efficacy of the MYC mRNA drug was achieved through down regulation of the c-MYC-PD-L1.
Keywords: Pancreatic Cancer, Pancreatic ductal carcinoma, neuroendocrine pancreatic cancer, 3'UTRMYC1-18, c-Myc, PD-L1
Received: 17 May 2025; Accepted: 26 Jun 2025.
Copyright: © 2025 Dorji, Chen, Perera, Aijaz, Li, Matsui and Awah. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Chidiebere Awah, UTR Therapeutics Inc., New York, United States
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