2026-2027 Pre-Doctoral Fellow Projects by Research Category

Clinical and Translational Sciences (includes pharmacotherapy, experimental therapeutics, PK/PD, modeling and simulation)

Raeanne Lanphier, University of North Carolina at Chapel Hill

Mentor: Dr. Klarissa Jackson

Research Title: Revisiting Old Drugs with New Models: Mechanistic and Genetic Insights into Sulfamethoxazole and Trimethoprim- Induced Liver Injury

“Sulfamethoxazole/trimethoprim (SMX/TMP), or Bactrim™, is a widely prescribed antibiotic and remains essential for patient care worldwide. SMX/TMP is associated with idiosyncratic DILI because the mechanism(s) of injury are not fully understood and the occurrence of DILI is unique to the individual. The overall goal of this project is to understand the metabolism of SMX and TMP in the liver and to explore relationships between metabolite formation and drug-induced liver injury (DILI). SMX and TMP can form chemically reactive metabolites that may trigger toxicity and immune responses, such as cytokine release, suggesting that metabolite formation contributes to their toxic effects. Understanding the mechanisms and risk factors behind its rare but serious liver toxicity has direct relevance to both patient safety and drug development. By studying genetic factors, metabolic processes, and immune responses, this project contributes to the characterization of predictive tools that could identify patients at higher risk for adverse reactions.

This project will use in vitro approaches to understand mechanisms and risk factors for DILI in novel and next-generation in vitro models. This includes liver models that combine multiple cell types, providing a more accurate representation of how the liver functions in the body. Aim 1 examines how people differ in the way their liver cells process the antibiotic components SMX and TMP, focusing on genetic differences that affect drug metabolism. Aim 2 studies how these drugs are metabolized and cleared over time using advanced laboratory models of human liver tissue. Aim 3 explores how changing drug metabolism influences immune responses, measuring cytokine release and cell health and toxicity in in vitro systems. Collectively, these aims will provide a better understanding of DILI mechanisms and risk factors for SMX and TMP.”

Andrew Mitchell, Ohio State University, Second Year Fellow

 

Mentor: Dr. Kerry Rogers

Research Title: Strategies to circumvent drug resistance in chronic lymphocytic leukemia

“Chronic lymphocytic leukemia (CLL) is the most common type of leukemia in adults. It affects B cells, which are a type of immune cell that fights infections and are best known for producing antibodies. Normally, B cells are activated when a foreign invader binds to their receptor (called the B Cell Receptor, or BCR). This triggers a series of signals that cause B cells to survive and multiply. However, in CLL, cancerous B cells hijack this process so that the BCR is always active, causing them to multiply and survive when they should not. In CLL, the protein Bruton’s tyrosine kinase (BTK) is stuck in the “on” position, leading to this overactive BCR signaling and making it a target to block as treatment. BTK inhibitors (BTKis) are drugs that bind to BTK and block its function and have been highly effective in treating CLL. So far, four BTK inhibitors have been approved by the US Food and Drug Administration (FDA) and have greatly improved outcomes for patients. However, some CLL cells develop mutations in BTK, preventing inhibitors from blocking BTK and allowing the disease to progress. One type of mutation prevents the drugs from binding to BTK. Another mutation, called “kinase dead,” makes BTK unable to activate other proteins directly but still helps CLL cells survive by supporting BCR signaling in other ways. Because of these resistance mechanisms, new treatments are needed to target BTK in different ways.

Protein degraders are a new type of treatment that may overcome this resistance. There are two main types: PROTACs and molecular glues (MGs). Both work by destroying BTK using the cell’s natural “recycling system,” by tagging it for destruction. PROTACs must directly attach to BTK, but MGs work through brief surface interactions.Our MG, PS26, is being studied for its ability to destroy BTK, including BTK with mutations that make BTK inhibitors ineffective. We think that PS26 will be better at destroying BTK with mutations than PROTACs because it does not need to directly bind to BTK. PS26 could also outperform current treatments because it not only blocks BTK’s signaling role but also removes its scaffolding function. Scaffolding functions allow other protein to attach and correctly position themselves to turn “on,” which supports cell survival. We predict that interfering with the signaling and scaffolding function of BTK will allow PS26 to be effective in treating CLL resistant to current BTK inhibitors.

BTK inhibitors are also commonly combined with a drug called venetoclax for patients with CLL. Venetoclax stops the action of the protein BCL2, and this causes cancerous cells to rapidly die. Although venetoclax is known to work well with BTK inhibitors, it has not been tested with BTK degraders like PS26. We believe PS26 and venetoclax will work better together compared to BTK inhibitors because PS26 stops both functions of BTK. This research will explore how effective PS26 is in overcoming BTK resistance in CLL and whether it can enhance treatment when combined with venetoclax.”

Douglas Nelson, University of Minnesota

Mentor: Dr. Karunya Kandimalla

Research Title: Transport and metabolic dysfunction at blood-brain and gut barriers in Alzheimer’s disease

“My research asks: how do the body’s barrier tissues control what gets in and out, and what happens to nutrient and drug delivery when those controls fail in disease?
I focus on two barriers that are especially important for biopharmaceutics and drug delivery: the blood–brain barrier, which regulates what drugs and nutrients can reach the brain, and the intestinal barrier, which determines how much of an oral drug actually enters the bloodstream. In healthy conditions, these barriers regulate transport, metabolism, and permeability. In Alzheimer’s disease and related metabolic conditions, this regulation breaks down, altering nutrient handling, drug transport, and tissue stability.
My work combines large-scale molecular analysis with targeted experimental measurements to identify which regulatory controls fail, how they fail, and measure the consequences for transport and permeability. By studying both acute disease-related insults (such as toxic amyloid species) and chronic disease states, I distinguish immediate signaling disruptions from longer-term structural changes that reshape barrier function.
At the intestinal barrier, I study how gut microbiota–derived signals regulate epithelial transporters and metabolic enzymes that determine oral drug bioavailability. Differences in these microbial signals help explain why patients receiving the same oral dose can experience markedly different systemic drug exposure.
The long-term goal of this research is to provide a mechanistic foundation for predicting how disease alters nutrient and drug delivery, particularly to the brain, and to identify barrier-level control points that can be leveraged to improve therapeutic effectiveness and reduce variability in drug response.”

Drug Delivery, Bioengineering (includes nanomedicine, devices, biotechnology, protein delivery and characterization, and biopharmaceuticals)

Julia Crowther, University of Michigan, Dr. Paul B. Myrdal Memorial

Mentor: Dr. James Moon

Research Title: Modulating Microglial Activation and Blood–Brain Barrier Integrity: A Multi- Stage Evaluation of Celastrol in Neuroinflammation

“Many brain diseases, such as Alzheimer’s disease and Parkinson’s disease, involve chronic inflammation in the brain. This inflammation damages brain cells and weakens the blood–brain barrier, a protective layer that normally prevents unwanted substances and immune cells from entering the brain. When this barrier breaks down, inflammation becomes worse and can speed up disease progression. The goal of this project is to test whether a naturally derived compound called celastrol can reduce harmful brain inflammation and protect the brain’s protective barrier. To improve how well celastrol reaches the brain, it will be packaged into particles called nanodiscs, which are designed to help drugs enter inflamed brain tissue more effectively. The project will first identify and confirm celastrol’s anti-inflammatory effects in cultured mouse microglial cells. It will then test how well celastrol, delivered using nanodiscs, can reduce inflammation and protect the blood–brain barrier in mouse models of brain inflammation. Finally, the project will evaluate whether celastrol can reduce inflammation in a genetic mouse model of Parkinson’s disease. Overall, this research aims to determine whether improving drug delivery to the brain can make anti-inflammatory treatments more effective, with the long-term goal of developing better therapies for people with neurodegenerative and inflammatory brain disorders.”

Mitchell Kowalke, University of Minnesota, Second Year Fellow

Mentor: Dr. Hongbo Pang

Research Title: Peptide targeting to improve the delivery and therapeutic efficacy of glucocorticoid therapy

“The main goal of my project is to increase the amount of anti-inflammatory drug at the site of action and decrease it in healthy organs/tissues. The drug class I work with is known to have side effects that limits the duration and dosing of the drug. Additionally, this class of drug is known to be immunosuppressive on the body as a whole. This greatly increases the chances for secondary infection. My project will alleviate these issues by delivering the drug in a targeted manner. This will decrease the side effects and global immunosuppression and allow patients to take higher equivalent doses of the parent drug. My project will further devlop existing technology developed by my lab to allow for more widely accepted delivery routes (i.e. oral pill). In addition, another aim of my project is to explore the disease state of rheumatoid arthritis in vivo in order to find disease biomarkers and new molecules that can be used as stronger targeting agents.”

Drug discovery/medicinal chemistry

Olivia Fisher, University of Utah

Mentor: Dr. Thomas Cheatham III

Research Title: Learning the Switch: Machine Learning-Driven Discovery of Conformational Pathways in the TPP Riboswitch

“My project aims to uncover how a specific RNA molecule functions as a genetic switch by changing its three-dimensional shape in response to a small molecule signal. Although it is known that this RNA switch can turn gene expression on or off by folding differently, the detailed pathway of how it moves between these shapes remains poorly understood.To address this gap, I am developing a computational framework that combines physics-based molecular simulations with machine learning to map the RNA’s structural transitions and identify the key intermediate states that enable switching. By capturing how the RNA reorganizes itself at the molecular level, this work seeks to reveal the fundamental principles that allow RNA to sense its environment and regulate genes. Ultimately, these insights will inform the rational design of RNA-based control systems with broad applications in biology, biotechnology, and therapeutic development”

Nina Hawkins, University of Wisconsin-Madison

Mentor: Dr. Weiping Tang

Research Title: Development of Novel Degraders for the Treatment of Cancer

“The driving force of many cancers can often be narrowed down to the improper activity of a specific protein. This can mean either overactivation or overexpression of the protein. One of these proteins is called RIPK1. Overactivation of RIPK1 can result in increased cellular proliferation and evasion of detection by the immune system. To mitigate this, we have developed a small molecule that can take advantage of the natural cellular processes designed to degrade and get rid of misfolded or unnecessary proteins. This small molecule, called a PROTAC can bring RIPK1 in proximity to the complex that will alert the degradation machinery that it needs to be disposed of. We have demonstrated in mouse models, that when RIPK1 degradation is combined with radiation therapy, it sensitizes the tumor cells to killing by the immune system. In this proposal, we plan to develop RIPK1 PROTACs that can specifically act on breast cancer cells that express HER2 on their surface. This can reduce the risks of degrading RIPK1 across the entire body.”

Avery Huber, University of North Carolina at Chapel Hill

Mentor: Dr. Albert Bowers

Research Title: New mRNA Display Based Strategies for Targeting B7-H3 and Other Cancer Cell Surface Receptors

“siRNA is a new type of medicine that can selectively turn off disease causing genes, preventing disease-causing proteins from being made. This type of drug is especially exciting because it can target proteins that traditional drugs cannot. The current challenge, however, is delivery: siRNA must reach the right cells in the body without affecting healthy ones. An FDA-approved drug called GILVAARI (givosiran) shows that this problem can be addressed by leveraging a targeting group that allows the siRNA to be delivered specifically to the diseased cells in the liver. This makes the therapeutic both effective and safe.

My research is inspired by GILVAARI’s success, and I am asking whether similar targeting can be achieved for non-liver cells. I’m particularly interested in delivering siRNA specifically to cancer cells. To do this, I aim to replace the liver-specific targeting moiety in GILVAARI with a peptidic targeting molecule that recognizes B7-H3, a protein with specific expression on cancer and tumor cells within the tumor microenvironment. By attaching our B7-H3 specific peptide to an siRNA specific to MYC (an oncogene that drives cancer cell growth), I hypothesize that we can get cell type specific delivery of the siRNA and achieve cancer cell death.

In these efforts, I also plan to advance the scope of a powerful therapeutic discovery technology, mRNA display. By developing the technology to work in living cells rather than just test tubes, I hope to unlock access to many important cancer targets that are currently difficult (or impossible) to drug. Currently, no targeting molecules exist for B7-H3, so this work could open the door to entirely new cancer therapies.”

Luke Morrissette, University of Michigan, AFPE Regional Award

Mentor: Dr. Anna Schwendeman

Research Title: Development of β-selective LXR agonist-loaded sHDL for the treatment of neuroinflammation and Alzheimer’s disease

“The primary goal of my project is to develop drug-loaded nanoparticles that can deliver a payload to the brain. In doing so, this mechanism will support the treatment of central nervous system disorders, namely neuroinflammation and Alzheimer’s disease. At the core of my project is the development of novel formulations that combine a synthetic nanoparticle carrier with a drug that targets receptors in the brain. To evaluate this goal, I will test my formulations in vitro for their ability to cross the blood brain barrier, engage with their target and produce a meaningful output in the form of anti-inflammatory effects, amyloid beta sequestration and maintaining cholesterol homeostasis.”

Sarah Pogash, University of Maryland, Baltimore

Mentor: Dr. Steven Fletcher

Research Title: Design and synthesis of menin heterobifunctional compounds for the treatment of drug-resistant MLL-rearranged acute leukemias

“Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) are cancers of the blood and bone marrow leading to excess production of abnormal blood cells. The standard of care treatments for acute leukemias (ALs), such as AML and ALL, are moving away from a universal treatment approach to a personalized treatment approach according to differences in what drives the disease in individuals to offer fewer side effects. One such driver in ALs is the rearrangement of the mixed-lineage leukemia 1 (MLL) gene and results in aggressive disease progression and poor patient outcomes. This is a result of a protein-protein interaction between menin and MLL (menin–MLL) that functions to activate genes involved with cellular functions such as proliferation. Within the past year and a half, the FDA has approved two menin inhibitors, revumenib and ziftomenib, both of which work by binding to menin and preventing it from interacting with MLL, arresting the further development of leukemia. However, during clinical trials with revumenib four different mutations developed on menin along the binding site that imparted drug resistance as revumenib no longer binds as tightly and enabling MLL to re-engage menin. Similarly, two of the four mutations to menin identified during clinical trials with revumenib affect ziftomenib binding to menin. Other menin inhibitors that function like revumenib and ziftomenib are in clinical development, but they all target the same binding site, and so it is believed these will succumb to resistance, too. Therefore, different approaches must be undertaken to overcome this limitation. Heterobifunctional compounds such as PROteolysis TArgeting Chimeras (PROTACs) and Regulated Induced Proximity TArgeting Chimeras (RIPTACs) are able to overcome drug resistance observed by traditional FDA approved inhibitors as they do not require tight binding with their target protein. PROTACs are a special type of heterobifunctional compound that induce the degradation of the target protein, while RIPTACs can selectively induce cell death in cancer cells through aggregation. Our goal is to develop a library of menin heterobifunctional compounds in the form of PROTACs and RIPTACs that can be used for the treatment of patients with AML and ALL, including those patients that developed drug resistance to revumenib.”

Caroline Roach, University of Wisconsin-Madison

Mentor: Dr. Jennifer Golden

Research Title: Synthesis and Optimization of Antiviral Quinazolinones and Heterocyclic Derivatives with Activity Against Alphaviruses and Filoviruses

“The goal of my projects is to identify small molecules that successfully inhibit viral infection. Across three different viruses, VEEV, CHIKV, and Ebola virus, I am testing how different changes to the molecules affect how effective they are at stopping the viruses from replicating in cells (known as structure-activity relationships), which is comparable to alleviating infection and symptoms in human patients. To do this, the molecules are synthesized in the laboratory and then run through assays where healthy cells are infected with the virus and then treated with these molecules. A positive result is noted by either cell survival or a visible reduction in the virus detectable on the surface of the cells. Besides antiviral activity, another goal of the project is improving properties that make the molecules more drug-like. These include reducing toxicity to limit unwanted side effects, improving solubility so that it can be administered orally, and making the compounds more stable in the body so that they can have time to reach the sites of infection and interact with the virus.”

Pharmaceutical Technology (includes formulation sciences, dosage form design, materials science, physical pharmacy)

Luke Burroughs, University of Connecticut, Second Year Fellow

Mentor: Dr. Diane Burgess

Research Title: Continuous Manufacturing of Complex Parenteral Drug Products: Next Generation Control, Development, and Standards

“This research project aims to improve the way complex injectable drugs are made using a modern manufacturing method called continuous manufacturing. The project’s goals include:

Understanding the manufacturing process by looking at how different steps in the manufacturing process affect the quality of the final drug product. It’s particularly geared towards the later stages of production, which haven’t been studied as much as the earlier stages.

Improving Drug Quality:
1. Understand how processing parameters like temperature, drug concentration, and flow rate affect the structure of the drug-carrying nanoparticles (liposomes).
2. Figure out how to keep the drug stable in its liquid form during and after manufacturing.
3. Learn how to best filter, concentrate, and add other components to the drug product using a continuous manufacturing process.
4. Investigate analytical technology that can measure drug product properties in real time as it is manufactured to ensure high quality.”

Nila Murali, The University of Texas at Austin, Second Year Fellow

Mentor: Dr. Hugh Smyth

Research Title: Development and Delivery of PEGylated Antibiotics for Enhanced Treatment of Resistant Bacterial Infections

“The goal of my project is to develop advanced antibiotic therapies that can effectively treat stubborn infections caused by bacteria living in protective communities called biofilms. These biofilms act like a shield, making bacteria much harder to reach with traditional antibiotics. By attaching antibiotics to special carrier molecules (polymers), I aim to break through these barriers and deliver the medicine directly to the bacteria. This approach could lead to more effective treatments for infections in the lungs, wounds, and medical devices, improving recovery and reducing the need for stronger or prolonged antibiotic use.”

Pharmacology, Toxicology (includes cell biology, chemical biology, and pharmacognosy)

Sarah Batten, Auburn University

Mentor: Dr. Robert Arnold

Research Title: Integrating multi-omics with preclinical drug development to target novel mechanisms of resistance in cancer

“My project focuses on understanding why certain breast and prostate cancers stop responding to treatments that typically work for treating the cancer. Many of these cancers initially depend on hormones to grow, so doctors use hormone-blocking therapies and/or chemotherapy to treat the disease. Unfortunately, some tumors adapt over time and become resistant, making them harder to treat.

I study proteins that play central roles in helping cancer cells survive stress and resist chemotherapy. Initial research suggests that inhibiting one protein of particular interest, DDX5, could make resistant cancer cells more vulnerable to standard treatments.

My goal is to test new drugs that inhibit these proteins of interest and see whether they make therapy-resistant cancers more responsive to the treatments. I use laboratory cell models, 3D tumor models, and mouse models that closely mimic human cancers to evaluate how effective these drugs are. I also study how cancer cells change at the molecular level when DDX5 is inhibited, helping identify biomarkers that could predict which patients would benefit from these treatments.

Overall, my project aims to develop new strategies to overcome therapy resistance and improve treatment options for patients with aggressive breast and prostate cancers.”

Liam Carman, University of Connecticut, Second Year Fellow

Mentor: Dr. Brian Aneskievich

Research Title: Assessing Biomolecular Protein Condensates as Sites for Restricting Cytoplasmic Progression of Signaling in Chronic Inflammatory Diseases.

“Inflammation, a defining characteristic of many chronic diseases such as Crohn’s disease, colitis, and psoriasis, can be thought of as a signal relay where proteins act in sequence to pass on and sometimes amplify such signals. TNIP1 serves as a safeguard to diminish or quench this signal as a protective measure in the cell, the tissue it is in, and ultimately the individual. Interestingly, TNIP1 protein is distributed throughout the cytoplasm of cells in the form of dots, referred to as puncta. Other proteins have been reported to have this behavior, but none of them to date have a function similar to TNIP1. Literature investigations have shown that these proteins can form liquid droplets within a surrounding liquid environment, much like in a lava lamp. The purpose of my project is to investigate this behavior, starting with samples of TNIP1 protein in solution and assessing what conditions promote or prevent droplet formation. The findings would inform us about what kinds of biochemical or biophysical interactions are important in driving this behavior. We will also examine the effects of other proteins on this behavior, guided by the knowledge that certain other proteins “partner” with TNIP1 in performing its function. Ultimately, we will use the knowledge gained to manipulate TNIP1’s ability to form puncta in cultured cells, and see what effect this has on its inflammation-repressing ability. This will help define a novel way in which inflammation can be restricted and hopefully open up a new area of research for the treatment of chronic inflammatory diseases.”

Kalynn Turner, University of Florida

Mentor: Dr. Leslie Sombers

Research Title: Real-Time, Voltammetric Co-Detection of Serotonin and Glucose Dynamics in vivo Using a Single Microbiosensor

“The brain is a complex organ that controls everything that we think, feel and do. Thus, the brain is comprised of highly structured and overlapping neurotransmitter systems that work dynamically to orchestrate an incredible array of functions. One such neurotransmitter is serotonin, which is hugely important to a range of functions in the central nervous system such as sleep, mood regulation, and cognitive function (1–6). Serotonin also works throughout the periphery to control digestion, appetite, and is an important part of the innate immune cascade (4,6). Impairments in the serotonin system have given rise to a range of neuropsychiatric disorders such as depression, anxiety, hallucinations, and drug addiction (5,7). It’s important to note, however, that these systems do not operate alone. Only studying one neurochemical at a time can be likened to listening to only the violin in a full orchestra. Taking a multi-analyte approach rather than focusing on one analyte at a time holds tremendous promise for a new appreciation of the symphony of neurochemical signaling that orchestrates brain function.

Several methodologies have been employed to study neurotransmitter release, such as serotonin, in the brain; however, electroanalytical strategies offer real-time detection in discrete brain regions (8–14). Since most techniques are specifically optimized to detect only one analyte at a time, there are many understudied neurochemical targets that are hugely important in regulating brain circuit function. One such analyte is glucose, which is considered the major fuel source for the brain (15–18). Despite the apparent importance in brain circuit function, there is little evidence to describe how changes in blood glucose levels affect brain circuit function in real-time. Further, in psychiatric disorders where the brain’s serotonin systems are impaired, such as with chronic depression or anxiety, coincidentally dysregulated blood glucose levels have also been found and these altered levels have been shown to directly, and reciprocally, affect the serotonin system (18–23). To better understand these correlations, our lab has developed a specialized enzyme modified microbiosensor that allows us to study both serotonin and glucose fluctuations at the same space and time. We plan to use these sensors to gain a basic characterization of serotonin and glucose dynamics in rat brain tissue to understand the effect of glucose availability on neurochemical transmission. Further, we hope to characterize what effect glycemic status has on brain glucose availability and serotonin signaling. Lastly, we hope to use these sensors to gain more insight into brain energy homeostasis and how it works to regulate circuit function. Broadly speaking, these studies will lead to the development of improved therapeutic treatment strategies in disorders where both 5-HT signaling and brain glucose metabolism are disrupted.”

Social and Administrative Sciences

Alexcia Carr, University of Texas at Austin, Pre-Doctoral Fellowship in Health Outcomes Disparities

Mentor: Dr. Leticia Moczygemba

Research Title: Factors Related to Medication Access Among People Experiencing Homelessness

“People experiencing homelessness often live with serious health conditions that require access to prescription medications, yet they face many obstacles when trying to obtain and maintain access to those medications. This project will examine medication access as a recurring, multi‑step process that requires repeated engagement with the healthcare system, including medical visits, prescription issuance, and pharmacy pickup, from the perspective of those with lived experience of homelessness. Guided by an evidence‑based framework, the study will explore key stages of medication access, including how people recognize they need care, how they seek help, what happens during medical and pharmacy visits, and what challenges arise once they have their medications.

Kayla Smith, University of Florida, ASHP-AFPE Fellowship

Mentor: Dr. Steven Smith

Research Title: Integrating EHR, Pharmacy, and Claims Data to Advance Real-World Evaluation of GLP1-Receptor Agonists (GLP1-RAs) on Cardiometabolic Outcomes

“Medications known as GLP-1 receptor agonists (GLP1-RAs), such as semaglutide (Ozempic, Wegovy), tirzepatide (Mounjaro), and others, are now widely used to treat a variety of disease states including, but not limited to, diabetes, obesity, and sleep apnea. As a result, their use has expanded at an unprecedented pace, with millions of Americans now taking these therapies. However, because patients obtain GLP1-RA medications through diverse channels, including insurance-covered prescriptions, out-of-pocket purchases (cash fills), online pharmacies, and non-traditional dispensing routes, researchers can’t accurately identify who is truly using them. This uncertainty makes it difficult to evaluate the safety and efficacy of these medications in real world settings.

My project seeks to address this challenge by integrating multiple sources of health information, i.e., electronic health records (EHR), insurance claims, and a national pharmacy fill database, to more reliably capture real-world patterns of GLP-1 medication use.

The project has three key goals:

1. Evaluate the misclassification of exposure to GLP1-RAs using traditional exposure measurement approaches.
I will quantify the extent to which existing data sources, such as insurance claims or EHR prescribing data, miss or misclassify true GLP1-RA use.

2. Describe real-world treatment patterns of GLP1-RA medication use.
Using an optimized exposure measurement approach developed as part of Aim 1, I will examine how long patients remain on GLP1-RA medications, how consistently they adhere to these medications, and investigate reasons for discontinuation. I will also investigate how these treatment patterns change across different ages, racial and ethnic groups, clinical characteristics, and insurance types.

3. Assess GLP1-RAs impact on blood pressure.
Given the high prevalence of hypertension among GLP1-RA users and evidence from randomized controlled trials demonstrating blood pressure-lowering effects, I will use real-world data to evaluate whether initiation of GLP1-RA therapy is associated with clinically meaningful improvements in blood pressure over time.

Overall, this project will strengthen the accuracy of real-world evidence on GLP1-RA medications and support clinicians in identifying which patients are most likely to benefit from these therapies.”