Dihexa is a nooptropic and a small peptide created by scientists to help reverse certain cognitive consequences of potential trauma-based brain disorders and neurodegenerative conditions such as Alzheimer’s through increased synaptogenesis. The drug is a stable derivative of angiotensin IV, a known peptide, that, when combined with certain analogs, is a precognitive agent that can be administered for neurodegenerative treatment. But in its native stage, the nootropic isn’t capable of crossing over the blood-brain barrier since it doesn’t have the stability for use in a clinical setting.
Chemical Properties and Activities
Professors Alene T. McCoy, Joseph W. Harding and other colleagues in Washington State University based their nootropic development on a previous work showcasing that three terminal amino acids from the Ang IV and its analog, Norleucine1-angiotensin IV, are at the heart of precognitive activities of the peptides. The team then set out to create far smaller and stable derivatives of the Norleucine1- angiotensin IV that kept the active structure of Dihexa intact while making it possible for oral intake and capable of crossing the blood-brain barrier at the same time.
The final compound was Dihexa. Not only was it capable of meeting a number of requirements, but it proved to be active in certain concentrations. That led to significant improvements in cognitive capabilities of learning deficiencies in the scopolamine-treated rat model as well as the Sprague-Dawley rats.
Most importantly, the drug administration was efficient regardless if the animals took directly in the brain, through injection, or by mouth. Comprehensive analysis show that Dihexia’s precognitive activity was in relation to the stimulation of sporogenesis within the hippocampal area of the brain. New dendritic spines led to the creation of functional synapses.
Dinexia was more powerful than the neurotrophic factor; a protein utilized to form neuronal corrections that have yet been created for clinical use.
Dementia is basically a produce of combined diminished synaptic connectivity in neurons as well as neuron wasting of the hippocampus, neocortex, and entorhinal cortex. But previous tries made to build protein neurotrophic factors which include that of Dihexa for therapeutic treatment has been restricted by its incapability of crossing the blood-brain barrier. Plus, the need for manufacturing such agents through recombinant processes is believed to be costly.
Dihexa development seems to have gone over such impediments through its oral intake, anti-dementia activity, pro-cognitive activity, and reduced production costs.