According to a new study by researchers at the University of Colorado Anschutz Medical Campus, a promising new stroke drug that temporarily inhibits a key protein in the brain without causing lasting damage may significantly alter the treatment of cerebral and global ischemia in the future.
The study was published in the Journal of Biological Chemistry in May.
K. Ulrich Bayer, Ph.D., a senior author of the study and professor of pharmacology at the University of Colorado School of Medicine, stated, “We are one step closer to a new stroke therapy.” Our research demonstrates that the neuroprotective effects were significant, while the potential side effects did not manifest.
Current stroke treatment is to a great extent restricted to separating blood clusters to reestablish blood flow to the impacted district of the cerebrum. However, the drug under investigation here, which was developed on the CU Anschutz Medical Campus, safeguards internal brain function.
“We are one step closer to developing a new stroke therapy, Our findings show that the potential negative side effects did not occur, while the neuroprotective effects were significant.”
K. Ulrich Bayer, Ph.D., professor of pharmacology at the University of Colorado School of Medicine and a senior author of the study.
Ca2+/calmodulin-dependent protein kinase II, or CaMKII, a crucial regulator of learning and memory, was the goal of the researchers’ research. It was thought that altering this protein over time could have an effect on memory and learning capacity.
Working with creature models, the group designated the protein with a neuroprotective peptide known as tatCN19o.
According to Bayer’s statement, “Our team found that tatCN19o did not affect pre-formed memories and only temporarily interfered with learning for less than an hour.”
In addition, they discovered that when administered 30 to 60 minutes after ischemic events and even at extremely low doses, the drug prevented damage to brain cells.
Concentrate on co-creator Carolyn Nicole Brown from the CU Institute of Medication Division of Pharmacology said the brief learning hindrance with the medication in instances of worldwide cerebral ischemia or stroke would be “profoundly satisfactory regardless of whether they were longer enduring than saw here since the treatment is with a solitary intense bolus of the medication.”
“Moreover, the exceptionally brief length of the learning weakness could empower even constant medicines in certain circumstances,” she said, “counting Alzheimer’s illness as only one prominent model.”
Nicole Rumian, Ph.D., a co-author who works in the department of pharmacology as well, noted that while temporarily inhibiting the protein does not result in long-term amnesia, its role in memory maintenance is supported by the findings.
With the drug, Bayer anticipates conducting additional safety studies soon, with human trials beginning in about three years.
He stated, “As a researcher in basic science, I am extremely excited to see my work reach the clinic within my lifetime.”
As the technology’s licensee, Neurexis Therapeutics is currently working on the drug’s late preclinical development.
More information: Nicole L. Rumian et al, Short-term CaMKII inhibition with tatCN19o does not erase pre-formed memory in mice and is neuroprotective in pigs, Journal of Biological Chemistry (2023). DOI: 10.1016/j.jbc.2023.104693
