Overview

Many age-related diseases, as well as aging itself, are closely associated with chronic low-level inflammation. We have invented a method for treating, preventing, and/or reversing age-associated inflammation by administering a reverse transcriptase inhibitor (RTI) to patients who have a level of retrotransposable element (RTE)-derived Line-1 complementary DNA (cDNA) that is higher than a reference.

Market Opportunity

Many age-related chronic conditions such as heart disease, cancer, diabetes, Alzheimer's disease, and infection, as well as aging itself, are closely associated with chronic low-level inflammation. Thus, there is a significant need for methods to treat, prevent, and/or reverse age-associated inflammation. In addition, several reports have linked human endogenous retroviruses (HERVs) with diseases such as ALS. Other reports have linked reverse transcriptase (RT) activation with diseases such as Alzheimer’s but without distinguishing whether the RT was of Line-1 or HERV origin. Therefore, there is also a need for a method to detect transcriptionally upregulated RTEs, so as to identify patients at risk of, or afflicted with, age-associated inflammation who might benefit from nucleoside reverse transcriptase inhibitor (NRTI) treatment.

Innovation and Meaningful Advantages

We have invented a method for treating, preventing, and/or reversing age-associated inflammation by administering an RTI to patients who have a level of RTE-derived Line-1 cDNA that is higher than a reference. Our invention also includes a method for detecting transcriptionally upregulated RTEs, so as to identify patients at risk of, or afflicted with, age-associated inflammation who are likely to benefit from NRTI treatment. Direct and sensitive quantification of Line-1 cDNA could also be used to demonstrate effective inhibition of the Line-1 RT enzyme.

Collaboration Opportunity

We are interested in exploring 1) research collaborations with leading pharmaceutical companies; and 2) licensing opportunities with pharmaceutical companies.

Principal Investigator

IP Information

US Provisional Application 63/371,559, Filed August 16, 2022

Publications

De Cecco M, Ito T, Petrashen AP, Elias AE, Skvir NJ, Criscione SW, Caligiana A, Brocculi G, Adney EM . . . and Sedivy J. L1 drives IFN in senescent cells and promotes age-associated inflammation. Nature 2019 Feb 06;566:73-78. doi.org/10.1038/s41586-018-0784-9.

Contact