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Cancer has been listed as the second leading cause of global death and continues to grow, exerting tremendous burden in individual well-being, public health, economic considerations and scientific advancements. Thus, it’s urgent to find more efficient treatment strategies in anti-cancer field. 

Peptidomimetics have attracted attention as promising drug candidates by mimicking the diverse structure and function of natural peptides, and overcoming the limitations of proteolytic degradation, lower bioavailability, and unfavorable pharmacokinetic profiles. Specifically, the development of selective inhibitors in protein-protein interactions targeting potential anticancer signaling pathways is critical for chemical biology and medicinal chemistry. 

Anticancer signaling pathways are intricate networks and the dysregulation of cell pathways is often associated with the development and progression of cancer. Now targeting the specific proteins in these signaling pathways has become a central focus. Here in my research, we have made efforts in targeting two different hallmarks of cancer cells with sulfonyl-γ-AA peptide which is originally developed in our lab and perfectly adopted for mimicry of the α helix involved in protein-protein interactions. 

One is the design of unprecedented mimetics of (Vascular Endothelial Growth Factor) VEGF-A, which specifically bind with VEGF receptors and could effectively either upregulate or downregulate angiogenesis and impact tumor vascular proliferation and metastasis further. The second one is the investigation of peptide-based inhibitors to disrupt hypoxia-inducible factor 1α (HIF-1α) and p300 binding interaction which mediates hypoxia-response genes’ transcription cascade in tumor cells. The design and optimization of these peptidomimetics improves selectivity and pharmacokinetic properties, propelling them closer to clinical application.

Municipal solid waste in landfills undergoes anaerobic digestion, producing biogas, a significant methane emission source in the US. This biogas is often flared, exacerbating atmospheric carbon levels. My research aims to transform biogas into valuable chemicals and biofuels, leading to waste reduction, greenhouse gas mitigation, and renewable energy production. 

This involves designing amine-functionalized sorbents that can purify biogas in a single step, removing CO2, H2S, and water simultaneously, and enable diesel production through an intensified process to convert purified biogas into liquid hydrocarbon fuels. The amine adsorbent exhibits a 50% higher CO2 uptake capacity than state-of-the-art materials, reducing separation costs by 67%. 

Additionally, the tandem catalytic process integrating reforming and the FTS pathway enables a 54% reduction in capital investment and an 85% increase in yield. The key to this is developing stable, tunable catalysts to achieve the desired selectivity and kinetics for both reforming and CO hydrogenation to produce distillate-range hydrocarbon fuels. The reforming catalyst demonstrated a 4-fold activity increase and 3 orders of magnitude lower coke formation, enabling 160-hour stability. The FTS catalyst surface structure was controlled to boost hydrocarbon yield and limit CO2 emissions. 

Using advanced techniques, I uncovered synergistic active site formation, surface reactivity control, and reaction mechanisms... My work enables sustainable technologies for renewable fuel and chemical production from waste resources.

My research focuses on elucidating the role of Hsp90 co-chaperones in neuropsychiatric disorders, including Alzheimer’s disease (AD) and post-traumatic stress disorder (PTSD). My initial article investigates FKBP52 and Aha1 contributions to the initiation or progression of AD pathogenesis, as a mimic of proteostasis imbalance. Our study provided additional knowledge about the potential mechanisms that may contribute to sporadic AD and reiterates contributions of aging. It also provides a better understanding of how tau accumulation relates to neuroinflammation. 

My second article is a review paper that looks at genetic mouse models of another chaperone protein FKBP51. It provides a universal outlook of at the separate studies done in these mouse models and identifies some limitations and challenges associated with these models. It provided me with the foundation my current research focused on targeting FKBP51 as a therapeutic target for some of these neuropsychiatric disorders.