Sygnature Discovery has launched an in vivo LPS model of inflammation to profile early- stage anti-inflammatory drugs. This will hopefully help create a better understanding of Parkinson’s Disease, Alzheimer’s Disease, multiple sclerosis, and traumatic brain injuries. The model also intends to identify new drugs.
 
Sygnature’s model supports early-stage anti-inflammatory in neuroinflammation, kidney and systemic inflammation. An LPS mouse model has been used as a way to inexpensively produce accurate, and reliable cytokines. Post LPS tissue from the blood, brain or kidney is collected and tested for various pro-inflammatory cytokines. This LPS model sets itself apart from conventional models by including kidney inflammation and neuroinflammation which shows valuable insights into the complex interplay of inflammation in different organs. 
 
“Sygnature’s LPS in vivo model provide that initial step in determining the efficiency of a novel anti-inflammatory. Getting this first in vivo model off the ground is an exciting start, but it is only the beginning of a pipeline of new models planned to test a broader range of immunomodulatory drugs and mechanisms,” says VP of inflammation and immunology John Unitt.
 
This LPS model also allows for an understanding of the pharmacology and processes that establish systemic inflammation. It provides a useful model system to quickly evaluate the efficacy of novel anti-inflammatory drugs in early discovery by measuring key pro-inflammatory cytokines in the blood. Also, Syngature’s model builds on existing in vivo capabilities and strengthens drug target validation to transition from in vitro to in vivo. 
 
“Neuroinflammation like systemic and kidney inflammation involves many of the same inflammatory mediators (cytokines, chemokines). Working across therapeutic teams and Sygnature to establish the LPS model and measure these inflammatory mediators in different parts of the body allows our clients to gain a more holistic answer to their scientific questions. Whether that be a better understanding regarding the mechanism of action, the role of a target on inflammatory processes in multiple body compartments simultaneously, or relevance to a drug efficacy,” commented Max Mirza, VP of Neuroscience. 
 
“This unique approach allows our clients to understand if impacting systemic inflammation can influence neuroinflammatory mediators and potential translatable biomarkers of neuroinflammation.”