We at Kannalife Sciences, Inc. are pleased to announce the preview of our upcoming peer-reviewed white paper, by Douglas Brenneman, Dean Petkanas, Michael Ippolito, PhD and Sara Jane Ward, exploring neuroinflammatory responses to various LPI structures in DRG and hippocampal cultures and highlighting the critical role of KLS-13019, a potent GPR55 antagonist, in managing these responses. (Click for Full Paper below) Neuropathix, Inc. Kannalife, Inc. Temple University - Lewis Katz School of Medicine Temple University
I am pleased to announce the posting preview to our next peer reviewed white paper describing neuroinflammatory responses to various LPI structures in DRG and hippocampal cultures. Our discovery of KLS-13019 (a potent GPR55 antagonist), plays an important role in managing this response. How is that? LPI is an endogenous signaling molecule for the GPR55 receptor. Well stated literature, and our own discovery has shown that LPI-20:4 produced an increase in inflammatory mediators NLPR3 (inflammasome-3 marker) and IL-1b in neurons from both rat DRG and hippocampal cultures. Our drug brings these IMs back to control levels as KLS-13019 has been shown to decrease LPI-20:4 mediated increases in neuritic IL-1b and NLRP3. Critical to immune response homeostasis is creating balance in situations where the human body could use assistance in preventing early amplifications of the inflammatory response and keeping things from going haywire. Where have we seen this before? The attack on the human body of the foreign pathogen SARS CoV-2 set off a cytokine storm (particularly IL-1b; IL-6; and TNF-a); and this became the major contributor to respiratory collapse and ARDS. Clearly, systemic inflammation is not a good thing, and left unchecked it is the gateway to many neurological, neurodegenerative and chronic disease states. GPR55 elevation plays an important role in the early onset of inflammation as it has been shown to enhance the migration of monocytes, macrophages, and neutrophils. When activated, GPR55 can modulate the release of pro-inflammatory cytokines, such as IL-1b; IL-6 and TNF-a, which are crucial for initiating and amplifying the inflammatory process. This paper is an important basic science portion our neuroinflammatory research. It is an essential publication that lends support to our current work in Peripheral Neuropathy, and Parkinson’s Disease. I hope you will take the time to read this important scientific research as it sheds light on an important mechanism of neuroinflammation and lends credence to what makes our drug KLS-13019 a groundbreaking anti-neuroinflammatory therapeutic. Thank you in advance for your most kind and considerate review.