Riggs School Research Symposium

Alborz Mahdavi

Founder and CEO of Protomer Technologies, and Head of Diabetes at Eli Lilly

Dr. Alborz Mahdavi is an entrepreneur, scientist, and biotech founder currently serving as Head of Diabetes at Eli Lilly and Company and Vice President of Lilly Research Laboratories. He previously founded Protomer Technologies, a biotechnology company acquired by Lilly, where glucose-responsive insulins are advancing in clinical trials alongside oral peptide drug programs enabled by a proprietary chemical biology platform. Dr. Mahdavi earned his PhD from Tirrell lab at Caltech and trained the Langer lab at MIT. He was the recipient of the JDRF Varis Agnes International Prize, NSERC fellowship, and the Caltech Demetriades award for best PhD thesis.

Title of the Talk

Translating Ideas into Future Therapies and Building a Biotech Ecosystem

Abstract

In this presentation, I share the journey of translating scientific ideas into therapeutic innovations through my work with Protomer Technologies. I reflect on how we advanced from academic discovery to a successful acquisition, emphasizing the importance of identifying unmet medical needs, building strong scientific and advisory networks, and understanding the biotech landscape. I also discuss key strategies for startup success, including managing risk, designing effective business models, and fostering a supportive innovation ecosystem. Finally, I introduce our platform for controllable protein therapeutics, highlighting its potential to advance precision medicine, particularly in the development of glucose-responsive insulin technologies.

Johnson V. John

Assistant Professor and Principal Investigator at Terasaki Institute for Biomedical Innovation (TIBI)

Dr. Johnson V. John is an Assistant Professor and Principal Investigator at the Terasaki Institute for Biomedical Innovation (TIBI). His research focuses on the design and development of advanced biomaterials and nanotechnology-based platforms for applications in regenerative medicine, drug delivery, and tissue engineering. Dr. John’s work integrates materials science, bioengineering, and translational approaches to develop innovative therapeutic solutions aimed at improving patient outcomes. He leads a multidisciplinary research group dedicated to advancing next-generation biomedical technologies from bench to clinical application.

Title of the Talk

Building Healing from the Bottom Up: Modular Biomaterials in Regenerative Medicine

Affiliation

Terasaki Institute for Biomedical Innovation, 21100 Erwin St, Woodland Hills, CA 91367

Abstract

Traditional scaffold technologies in regenerative medicine have largely relied on bulk materials such as nanofibrous membranes and hydrogels. While effective in certain contexts, these static and homogeneous systems often fail to adapt to the dynamic and heterogeneous microenvironments of injured tissues. Over the past decade, growing efforts have focused on the development of modular biomaterials, which introduce a fundamentally different design philosophy for tissue repair. Rather than forming uniform bulk matrices, modular scaffolds assemble healing environments from microscale building blocks that are injectable, customizable, and inherently microporous. This modularity enables enhanced nutrient and oxygen transport, dynamic cell–material interactions, and the integration of multifunctional therapeutic elements, including growth-factor sequestration, immunomodulatory cues, and mechanically responsive features. Importantly, properties such as porosity, shape, mechanics, and bioactivity can be independently programmed to match specific wound microenvironments. Early successes with microgel-based fillers and microporous matrices highlight a clear shift away from static, one-size-fits-all dressings toward dynamic, adaptive, and modular therapeutics. This talk will place modular biomaterials within the broader trajectory of scaffold evolution and discuss how they are poised not only to accelerate healing outcomes but also to redefine regenerative strategies across diverse tissue types.

Khaja Shameem Mohammed Abdul

Postdoctoral Fellow in the Cardiovascular Signaling Laboratory at Huntington Medical Research Institutes (HMRI)

Dr. Khaja Shameem Mohammed Abdul is a Postdoctoral Fellow in the Cardiovascular Signaling Laboratory at the Huntington Medical Research Institutes (HMRI) in Pasadena, California. He earned his PhD from the University of Ruhuna, Sri Lanka, where he was recognized with two prestigious awards: the Vice Chancellor’s Fellowship from University of Ruhuna and the President’s Research Scholarship from the Ministry of Higher Education.

During 2018-2020, he was a post-doctoral fellow at Guangdong University of Technology, China. Where he discovered cardioprotective effects of a novel drug molecule JC105 which was later patented by the lab. Since 2021, Dr. Khaja Shameem joined HMRI as a post-doctoral fellow, where he investigates the role of protein phosphatases PHLPP1 and PHLPP2 in myocardial aging and injury. His work has been published in multiple peer-reviewed journals, including Journal of Molecular and Cellular Cardiology, International Journal of Cardiology, Journal of Cellular and Molecular Medicine and Biochimica et Biophysica Acta-Molecular Cell Research.

Dr. Mohammed Abdul’s long‑term career goal is to become an independent scientist advancing the field of cardiovascular research. Dr. Mohammed Abdul also contributes to the scientific community as an Editorial Board Fellow for Current Opinion in Physiology and as an Editorial Board Member for The Open Cardiovascular Medicine Journal. Beyond his laboratory work, he has served as a Social Media Ambassador for the American Heart Association and as a communications Committee member for the Society for South Asian Heart Research.

Title of the Talk

PHLPP1: The Missing Link in Nicotine Induced Cardiac Damage

Abstract

Nicotine exposure is known to cause oxidative stress and mitochondrial dysfunction in the heart, yet the molecular mechanisms linking nicotine to cardiomyocyte injury remain unclear. Our work identifies Pleckstrin Homology Domain Leucine-Rich Repeat Protein Phosphatase 1 (PHLPP1) as a key mediator of nicotine induced cardiac damage. We found that nicotine significantly elevates PHLPP1 expression in the adolescent rodent heart and in cardiomyocytes, coinciding with increased NOX4 levels, reactive oxygen species production, and apoptosis. Mechanistic studies revealed that nicotine activates the ERK–4E BP1 signaling axis to promote PHLPP1 protein synthesis, and inhibiting ERK or translation effectively blocks this response. Importantly, PHLPP1 was necessary and sufficient for nicotine induced mitochondrial dysfunction. Together, these findings uncover a novel pathway through which nicotine drives cardiomyocyte injury and highlight PHLPP1 as a potential therapeutic target in tobacco and e cigarette related cardiac injury.