Babak Baban is a professor, immunologist and associate dean for research at the Dental College of Georgia at Augusta University where he has served for 13 of his 20 years as a translational and clinical immunologist.
Baban founded Medicinal Cannabis of Georgia, LLC with AU’s Bio-business Incubator, resulting in great strides in pre-clinical research. Through very productive collaborations with AU and DCG, they have published discoveries that brought promise for novel and potential treatments.
He has published 134 peer-reviewed articles, has four patents issued and several pending, and was named a Regents’ Entrepreneurs by the University System of Georgia Board of Regents in 2023.
He earned his Ph.D. degree from University of London in UK.
Areas of Expertise (3)
Regents’ Entrepreneur, Board of Regents, University System of GA (professional)
Distinguished Research Award, The Graduate School, Augusta University (professional)
Honorary Membership, Omicron Kappa Upsilon (OKU), Honor Dental Society (professional)
Membership, Phi Kappa Phi Honor Society (professional)
Featured Podium Presenter Award, Janssen Immunology Symposium, Johnson & Johnson Innovation (professional)
Harvard Business School Online: Certificate, Leadership Principles 2022
Augusta University: MPH, Health Management 2015
Augusta State University: MBA 2008
University of London (UCL): Ph.D. 1998
- American Association for Cancer Research (AACR)
- American Association for Advanced Sciences (AAAS)
- American Association of Immunology (AAI)
- American Association for Bioanalysis (AAB)
- American Diabetes Association (ADA)
- American Society for Microbiology (ASM)
- American Dental Association (ADA)
- American Heart Association (AHA)
- American Association of Dental Research (AADR)
- International Association for Dental Research (IADR)
- European Predictive, Preventive and Personalized Medicine Association (EPMA)
- International Cannabinoid Research Society (ICRS)
- Association for Cancer Immunotherapy (CIMT)
- The International Association For The Study Of Lung Cancer (IASLC)
Media Appearances (4)
The Means Report
From gummies, to vapes to prescriptions, CBD is everywhere. On this edition of The Means Report, we take a close look at this compound that comes from marijuana. It’s not pot. So what is it? And why is it so popular? You will want to hear from Dr. Baback Baban. He’s a researcher at Augusta University. Dr. Baban has done extensive studies on the use of CBD for seizures. More recently he’s looked at how it can be applied to fight lung cancer. Watch our interview and come away more informed about CBD.
Marijuana ingredient could be therapy for a deadly brain tumor, Augusta University finds
The Augusta Chronicle online
One of the active ingredients in marijuana known as cannabidiol or CBD offers some intriguing potential as a therapy, said Dr. Babak Baban, associate dean for research at Dental College of Georgia. CBD does not cause a high, and a drug based on it is already approved by the Food and Drug Administration to treat seizures in children; additionally, it is relatively safe with few side effects, he said. But it has also shown it can be a powerful regulator of the immune system and that is part of what makes it attractive as a therapy for these tumors, Baban said.
Can Cannabis Help Treat Cancer? Researchers Are Getting Closer To An Answer
Babak Baban, an immunologist at the University of Augusta’s Dental College of Georgia, has spent years studying the potential therapeutic applications of the cannabinoid CBD — also called cannabidiol. “As an immunologist, I am naturally interested in any compound that can impact the immune system, health, and diseases,” Baban tells Inverse, noting that cannabis has been used medicinally for thousands of years. “However, the mechanisms responsible for the effects are not known yet.” Additionally, he says, there are many diseases for which CBD could be an effective treatment, so further study of the compound is warranted.
Inhalant CBD offers hope in fight against lung cancer, Augusta University study finds
The study was led by Babak Baban, PhD, associate dean of research, immunologist and professor at DCG and one of the founders of Medicinal Cannabis of Georgia, an Augusta-based biomedical research and development company. Earlier this year, Baban was named a Regents’ Entrepreneur by the University System of Georgia Board of Regents.  “The central core of our research has been studying inflammatory diseases and for that, we picked two different directions: one is centered around chronic inflammation in our system and the other is neurologic diseases such as dementia. Because of their impressive anti-inflammation effects, CBD, CBC and other cannabinoids have attracted our attention,” Baban said.
Inhibiting MicroRNA-141-3p Improves Musculoskeletal Health in Aged MiceAging and Disease
2023 Emerging evidence shows that the microRNA-141-3p is involved in various age-related pathologies. Previously, our group and others reported elevated levels of miR-141-3p in several tissues and organs with age. Here, we inhibited the expression of miR-141-3p using antagomir (Anti-miR-141-3p) in aged mice and explored its role in healthy aging. We analyzed serum (cytokine profiling), spleen (immune profiling), and overall musculoskeletal phenotype. We found decreased levels of pro-inflammatory cytokines (such as TNF-α, IL-1β, IFN-γ) in serum with Anti-miR-141-3p treatment. The flow-cytometry analysis on splenocytes revealed decreased M1 (pro-inflammatory) and increased M2 (anti-inflammatory) populations. We also found improved bone microstructure and muscle fiber size with Anti-miR-141-3p treatment. Molecular analysis revealed that miR-141-3p regulates the expression of AU-rich RNA-binding factor 1 (AUF1) and promotes senescence (p21, p16) and pro-inflammatory (TNF-α, IL-1β, IFN-γ) environment whereas inhibiting miR-141-3p prevents these effects. Furthermore, we demonstrated that the expression of FOXO-1 transcription factor was reduced with Anti-miR-141-3p and elevated with silencing of AUF1 (siRNA-AUF1), suggesting crosstalk between miR-141-3p and FOXO-1. Overall, our proof-of-concept study demonstrates that inhibiting miR-141-3p could be a potential strategy to improve immune, bone, and muscle health with age.
Recombinant human DNase-I improves acute respiratory distress syndrome via neutrophil extracellular trap degradationJournal of Thrombosis and Haemostasis
2023 Background: Respiratory failure is the primary cause of death in patients with COVID-19, whereas coagulopathy is associated with excessive inflammation and multiorgan failure. Neutrophil extracellular traps (NETs) may exacerbate inflammation and provide a scaffold for thrombus formation. Objectives: The goal of this study was to determine whether degradation of NETs by recombinant human DNase-I (rhDNase), a safe, Food and Drug Administration-approved drug, reduces excessive inflammation, reverses aberrant coagulation, and improves pulmonary perfusion after experimental acute respiratory distress syndrome (ARDS). Methods: Intranasal poly(I:C), a synthetic double-stranded RNA, was administered to adult mice for 3 consecutive days to simulate a viral infection, and these subjects were randomized to treatment arms, which received either an intravenous placebo or rhDNase. The effects of rhDNase on immune activation, platelet aggregation, and coagulation were assessed in mice and donor human blood.
Inflammaging, cellular senescence, and cognitive aging after traumatic brain injuryNeurobiology of Disease
2023 Traumatic brain injury (TBI) is associated with mortality and morbidity worldwide. Accumulating pre-clinical and clinical data suggests TBI is the leading extrinsic cause of progressive neurodegeneration. Neurological deterioration after either a single moderate-severe TBI or repetitive mild TBI often resembles dementia in aged populations; however, no currently approved therapies adequately mitigate neurodegeneration. Inflammation correlates with neurodegenerative changes and cognitive dysfunction for years post-TBI, suggesting a potential association between immune activation and both age- and TBI-induced cognitive decline. Inflammaging, a chronic, low-grade sterile inflammation associated with natural aging, promotes cognitive decline. Cellular senescence and the subsequent development of a senescence associated secretory phenotype (SASP) promotes inflammaging and cognitive aging, although the functional association between senescent cells and neurodegeneration is poorly defined after TBI. In this mini-review, we provide an overview of the pre-clinical and clinical evidence linking cellular senescence with poor TBI outcomes. We also discuss the current knowledge and future potential for senotherapeutics, including senolytics and senomorphics, which kill and/or modulate senescent cells, as potential therapeutics after TBI.