Novel drug candidate prevents nerve cell damage in mouse model of Parkinson’s disease

Published up~ the body December 18, 2015

A team of scientists at the University of Nebraska Medical Center (UNMC) and Longevity Biotech, Inc., has demonstrated that neuroprotection could subsist attained in preclinical models by a recent drug candidate that changes immune responses.

The results, published today in the Journal of Neuroscience, explain the prevention of nerve cell loss in a mouse model of Parkinson’s distemper. Notably, the drug protected nerve cells that bring into being dopamine, which is the chemical accountable for agility and movement that is squandered in human disease.

“The results are exciting during the time that they provide a bridge between the immune scheme and nerve cell protection in Parkinson’s complaint,” said Scott Shandler, Ph.D., co-establisher and CEO of Longevity Biotech.

“The model was birthed nearly a decade ~ne when specific types of circulating lineage cells called lymphocytes were found to hurt the types of nerve cells accountable for disease,” said Howard Gendelman, M.D., the Margaret R. Larson Professor and seat of authority of the UNMC Department of Pharmacology and Experimental Neuroscience. “The recent Longevity Biotech drug (LBT-3627) was adroit to change the function of these cells from killing the might cells to protecting them. This is especially expressive for the Nebraska team, as the mechanism parallels closely the human trials nearing accomplishing for Parkinson’s patients.”

LBT-3627 is like to the naturally occurring vasoactive intestinal peptide (VIP), a well-established anti-inflaming peptide with beneficial effects across a multiplicity of disorders. VIP is rapidly degraded through the body and is unable to distinguish between its two naturally intended receptors (VPAC1 vs. VPAC2). These limitations wish stymied prior translational success using VIP.

In exhibit the differences of, LBT-3627 specifically targets VPAC2 and demonstrates powerful biological durability. In addition, LBT-3627 has the potential to be administered orally, Dr. Shandler declared, which would further improve its clinical prospects and put in order it more accessible for people through Parkinson’s disease.

Preclinical studies performed ~ the agency of the UNMC team demonstrated that LBT-3627 could carry through up to 80 percent protection of dopamine-producing strengthen cells in a mouse model of Parkinson’s disorder. Furthermore, the immune transformation also unnatural primary scavenger cells called microglia cells that were fix ultimately responsible for the neuroprotective activities observed that halted brain injury.

“The key finding in our study was that a peculiar white blood cell subset was produced in the same proportion that a consequence of LBT-3627 handling and provided protection of dopamine producing self-command cells from being damaged,” Dr. Gendelman said. “The neurotoxic immune reaction was halted and LBT-3627 was quick to prevent disease.”

“There are limited therapeutic strategies available to Parkinson’s patients,” before-mentioned Marco Baptista, Ph.D., senior consort director of research programs at The Michael J. Fox Foundation in the place of Parkinson’s Research, which supported this work together with the National Institute of Neurological Disorders and Stroke and a honorable gift from the Blumkin Foundation in Nebraska. “This approximate shows one avenue to potentially patronize the brain cells affected by Parkinson’s illness and alter disease progression.”

Dr. Shandler uttered Longevity Biotech is currently progressing LBT-3627 through preclinical evolution and hopes to begin a Phase I clinical misery in humans by 2017. mice-model-of-Parkinsons-disease.aspx

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