Pfizer signs drug profiling deal with Nodality
pharmafile | August 10, 2012 | News story | Research and Development, Sales and Marketing | Lupus, Nodality, Pfizer, SCNP
Pfizer has signed a multi-year drug profiling deal with Nodality to help get the best from its autoimmune disease compounds.
Pfizer has bought into San Francisco-based Nodality’s proprietary Single Cell Network Profiling (SCNP) technology, as a tool for the development of Pfizer compounds.
SCNP is a proprietary technology licensed from Stanford University to characterise cell-signalling networks in patients with cancer and other diseases. The multi-year agreement will initially focus on providing biological bases for streamlining the development of potential Pfizer compounds for autoimmune diseases.
The first will focus on lupus, and will include characterising mechanisms of action, disease analysis, and drug profiling. The agreement also gives Pfizer the option to engage Nodality in companion diagnostics development.
The terms of the agreement include an upfront payment, R&D funding, and success-based milestone payments – but further financial details were not disclosed.
Michael Goldberg, interim chief executive of Nodality, said: “We are excited to be working with Pfizer’s world class autoimmune R&D groups to enhance their drug development activities.
“This collaboration, which is Nodality’s second major strategic pharma partnership this year, provides continuing validation of the value the SCNP platform technology can bring to drug development. We look forward to a productive and collaborative relationship with Pfizer’s R&D teams.”
Jose-Carlos Gutierrez-Ramos, senior vice president, BioTherapeutics R&D at Pfizer said: “Our partnership with Nodality exemplifies Pfizer’s commitment to Precision Medicine by providing us with earlier insight into a compound’s potential clinical profile, which can help reduce attrition rates, accelerate development and improve patient targeting.
“There is a tremendous patient need for new medicines that can impact the pathophysiology of autoimmune diseases.”
Ben Adams
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