Hope Bio’s CTTACC 2023 Recap
What do you get when you send two scientists and two executives to the desert? While you search for a punchline, we’ll supply our experientially discovered answer - you get great and growing industry relationships, breaking news in cell therapy and traumatic brain injury, and a whole lot o’ pictures of a cell culture flask in exotic (by cell culture flask standards) locations.
A huge “thank you” to Scottsdale, Arizona for the extremely warm welcome of Hope Bio’s team (including Philip the Flask), for the 2023 national conference of Cellular Therapies and Transfusion Medicine in Trauma and Critical Care (CTTACC), May 8-11. Hope Bio is particularly grateful to Dr. Charles Cox for presenting an update on a Hope Biosciences-sponsored trial in Traumatic Brain Injury (TBI). The study is an FDA-authorized Phase I/IIa, single center, open label clinical trial for 24 adult patients living with sub-acute or chronic neurological injury. Both men and women were invited to participate, with onset or diagnosis at least six months established. Participants received three infusions of 200 million stem cells over a six-week period, spaced 14 days apart, with status monitored and tested for a year following their last infusion.
Dr. Cox’s findings are summarized in the following points. Wondering what they mean for you or a loved one living with TBI? Explanatory comments break ‘em down. As shared at CTTACC:
1. Hope Biosciences adipose-derived Mesenchymal Stem Cells (HB-adMSCs) are safe.
The stem cells at work in this study are mesenchymal stem cells (MSCs), a type of adult stem cells found in many different tissues. The notation “ad” means the cells in this study are “adipose-derived,” or taken from fat (adipose) tissue. “HB” denotes these cells were cultured by Hope Biosciences, using proprietary technology.
As of this writing, HB-adMSCs have been put to work in more than 35 FDA-authorized studies in dozens of disease and injury conditions. Current and complete studies range in size from a single person to 100 participants, each receiving anywhere from a single treatment to approaching 40 infusions and counting. The shortest study was six months in duration; the longest continued into its third year. Studies have been and are conducted in Sugar Land, Texas at Hope Biosciences Research Foundation, as well as at universities and medical institutes. The TBI trial presented by Dr. Cox at CTTACC was completed at Memorial Hermann Hospital-Clinical Research Unit, in collaboration with The University of Texas Health Science Center, Houston. Findings confirm all other research conducted to date – HB-adMSCs are safe.
2. HB-adMSCs reduce thalamic microglial activation.
Microglia are resident cells of the brain that regulate brain development, neural network maintenance, and injury repair.[1] We have a double-sided relationship with the microglia in our brains. Microglia provide for tissue repair by releasing anti-inflammatory agents, and in instance of TBI can produce protective factors, clear cellular debris, and orchestrate regenerative processes as part of the body’s initial response to restore homeostasis in the brain.[2] Chronically over-activated microglia, however, contribute to neuronal damage by also releasing harmfully inflammatory substances.[3]This is a simplistic explanation – we now know the balance of activation states can vary at different points[4] – but a helpful one for conceptualizing what microglia do in our brains, why they matter, and how their response can change as a result of injury. “Thalamic microglial activation” broadly refers to measurable increased activity in the thalamus, the part of the brain that helps to process information from the senses and transmit that information to other parts of the brain.[5]
Microglia activation is observed in an array of central nervous system (CNS) diseases and conditions, because activation is one way the body coordinates the immune system’s resources during episodes of neuroinflammation; evidence of microglia activation is sometimes part of early diagnosis of CNS disorders, such as multiple sclerosis or Alzheimer’s Disease.[6] TBI has been linked with later development of dementia, including Alzheimer’s; Parkinson’s Disease; immune suppression; various psychiatric disorders; and an overall increase in mortality.[7] Finding that HB-adMSCs reduce thalamic microglial activation is therefore significant both to the immediate and future well-being of those living with TBI.
3. HB-adMSCs improve functional outcomes.
A “functional outcome” is a measurement referring to an individual’s recovery in areas such as vocational, relational, and living skills, rather than strict symptom resolution. In this study, verbal fluency and a “stroop” test (used to measure attention capacity, processing speed, and similar executive processing capabilities) were recorded alongside individualized markers of progress in activities of daily living, such as ability to complete functions required to care for oneself independently. Broadly put, finding that HB-adMSCs improve functional outcomes means treatment with HB-adMSCs improved participants’ ability to function in daily life in ways they find important and meaningful.
4. Inflammatory and microstructural metrics correlate with anxiety and depression and treatment effect.
Individuals living with TBI often suffer debilitating physical, cognitive, and emotional effects (the difficult emotional experience of TBI can be related both to physical damage to parts of the brain structure governing emotions and emotional regulation, and resultant of a formerly healthy individual now living with significant impairment). Seeing a correlation between quantitative values, such as inflammatory markers and microstructural metrics gathered through lab tests and neural imaging, and qualitative patient reports, such as anxiety and depression and quality of life measures, creates a linear relationship between treatment and improvement. This finding both supports the assertion that treatment with HB-adMSCs is the cause of improvement and negates concerns of placebo effect.
The Hope Bio team departed CTTACC convinced that while very big, real world health challenges and threats sometimes seem endless, our country’s great minds, providers, and communities are determined to make a difference. During his CTTACC presentation, Dr. Cox also took a moment to share general announcement of what has since become public news – results of that first TBI study were instrumental in obtaining nearly $5M in Department of Defense funding for a next, larger FDA-authorized Phase II clinical trial to commence soon. One truly final thought from Scottsdale – Hope Biosciences looks forward to being part of big solutions.
[1] Colonna M, Butovsky O. “Microglia Function in the Central Nervous System During Health and Neurodegeneration.” Annu Rev Immunol. 2017 Apr 26; 35:441-468. doi: 10.1146/annurev-immunol-051116-052358. Epub 2017 Feb 9. PMID: 28226226; PMCID: PMC8167938. [2] Loane DJ, Kumar A. “Microglia in the TBI brain: The good, the bad, and the dysregulated.” Exp Neurol. 2016 Jan; 275 Pt 3(0 3):316-327. doi: 10.1016/j.expneurol.2015.08.018. Epub 2015 Sep 3. PMID: 26342753; PMCID: PMC4689601. [3] Gomes-Leal, Wallace. “Microglial physiopathology: how to explain the dual role of microglia after acute neural disorders.” Brain and Behavior. 2012 April; 2, 3: 345-456. https://doi.org/10.1002/brb3.51. [4] Donat CK, Scott G, Gentleman SM, Sastre M. “Microglial Activation in Traumatic Brain Injury.” Front Aging Neurosci. 2017 Jun 28;9:208. doi: 10.3389/fnagi.2017.00208. PMID: 28701948; PMCID: PMC5487478. [5] Torrico TJ, Munakomi S. “Neuroanatomy, Thalamus.” 2022 Jul 25. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 31194341. [6] Woodburn SC, Bollinger JL, Wohleb ES. “The semantics of microglia activation: neuroinflammation, homeostasis, and stress.” J Neuroinflammation. 2021 Nov 6;18(1):258. doi: 10.1186/s12974-021-02309-6. PMID: 34742308; PMCID: PMC8571840. [7] “Donat, et. al. “Microglial Activation in Traumatic Brain Injury,” Frontiers.
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