4.5 Article

Reactive Oxygen Species (ROS)-Activatable Prodrug for Selective Activation of ATF6 after Ischemia/Reperfusion Injury

期刊

ACS MEDICINAL CHEMISTRY LETTERS
卷 11, 期 3, 页码 292-297

出版社

AMER CHEMICAL SOC
DOI: 10.1021/acsmedchemlett.9b00299

关键词

ROS-activatable prodrug; ATF6 activation; ischemia-reperfusion injury; Cyp1A2

资金

  1. Welch Foundation [W-1984-20190330, W-0031]
  2. American Chemical Society Petroleum Research Fund [57370-UNI7]
  3. National Science Foundation [CHE-1726441]
  4. Arnold and Mabel Beckman Foundation
  5. San Antonio Area Foundation
  6. Trinity University
  7. American Heart Association [17PRE33670796]
  8. National Institutes of Health [R01 HL135893, R01 HL75573, R01 HL104535, 1F31HL140850]
  9. Rees-Stealy Research Foundation
  10. Inamori Foundation
  11. ARCS Foundation, Inc., San Diego Chapter
  12. San Diego State University (SDSU) Heart Institute

向作者/读者索取更多资源

We describe here the design, synthesis, and biological evaluation of a reactive oxygen species (ROS)-activatable prodrug for the selective delivery of 147, a small molecule ATF6 activator, for ischemia/reperfusion injury. ROS-activatable prodrug 1 and a negative control unable to release free drug were synthesized and examined for peroxide-mediated activation. Prodrug 1 blocks activity of 147 by its inability to undergo metabolic oxidation by ER-resident cytochrome P450 enzymes such as Cyp1A2, probed directly here for the first time. Biological evaluation of ROS-activatable prodrug 1 in primary cardiomyocytes demonstrates protection against peroxide-mediated toxicity and enhances viability following simulated I/R injury. The ability to selectively target ATF6 activation under diseased conditions establishes the potential for localized stress-responsive signaling pathway activation as a therapeutic approach for I/R injury and related protein misfolding maladies.

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