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In March 2026, I joined the Suzie Pun Lab in the University of Washington Department of Bioengineering. The Pun Lab has a few research areas of interest. These range from using polymers to treat traumatic injuries, targeted drug delivery to kidneys, aptamer discovery and engineering, and cancer therapy. I am currently involved with their cancer therapy research. The goal of this research is to increase the efficacy of in vivo gene therapies for cancer treatment. Currently, ex vivo cell therapies dominate the market. Although, they are very expensive to manufacture. This leads to pricey treatment costs, significantly limiting patient access to such treatments. Instead, if we can find way to administer these therapies in vivo, effectively using the body as a bioreactor, we can significantly decrease the manufacturing cost thus allowing patients more access to such a life changing treatment.
Lab Procedures:
Lipid Nanoparticle (LNP) Formulation
LNP Characterization (size, PDI, charge, encapsulation efficiency)
Dissociation constant (Kd) for aptamer binding
Research Projects
Research Projects
Using Aptamer Conjugated Lipid Nanoparticles (Apt-LNPs) in an in vivo setting
In this project, we wanted to test the ability of Apt-LNPs to deliver a nucleic acid cargo to T-cells in an in vivo environment. Our LNPs encapsulated a mCherry encoding mRNA. mCherry is a flourescent protein. The LNPs were conjugated with various different aptamers. Our aptamers are single stranded DNA that can fold into a specific geometry, allowing them to bind to target molecules with high affinity. We used CD8 and CD62L aptamers in order to help the LNPs target T-cells. Naturally, LNPs will move towards the liver when injected in vivo. The main goal of the aptamer was to help de-target them from the liver, and instead target the T-cell rich spleen.
Initially, the LNPs were evaluated in an in vitro setting. We tested the transduction ability of LNPs conjugated with just the CD8 aptamer, just the CD62L aptamer, both aptamers, and untargeted LNPs. The bispecific LNPs showed greatest targeting of T cells while the unconjugated LNPs showed little targeting. Next, we moved in vivo where we injected these same LNPs intraveneously into mice. Among all the LNPs test groups, there was zero transfection that occured.
Because our aptamers are made of DNA, it is likely that the nuclease enzymes in the mice blood recognized and degraded our LNP-aptamer complex. This degradation must have damaged the LNPs, inhibiting their ability to target and transduce T cells in vivo.
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