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Massive-scale proteomics for COVID-19

You’re tackling the unknown. You need as much information as possible.

Access the largest protein profiling platform.
Find patterns no one knew to look for.

With the SomaScan® Assay, you can measure thousands of proteins at once, including >800 proteins involved in immune/inflammatory response. That’s 7x more coverage of COVID-19 associated proteins than any other platform. In response to the pandemic, we’ve simplified our terms, so that researchers who want to analyze COVID-19 samples can get results faster.

Accelerate pandemic response in six ways

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Predict progression

Predict which COVID-19 patients will progress and develop severe illness.

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Identify disease subtypes

Identify COVID-19 disease complication sub-types in those at risk for severe illness.

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Repurpose existing drugs

Repurpose existing drugs by matching them with drivers of COVID-19 progression.

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Identify new drug candidates

Rapidly identify protein targets for new drug candidates for COVID-19.

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Accelerate clinical trials

Accelerate clinical trials for COVID-19 drug candidates.

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Facilitate vaccine development

Find COVID-19 protein expression patterns to accelerate COVID-19 vaccine development.

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Additional resources

WebinarWhat can proteomics teach us about infectious disease?

Dr. Coomb’s group has used the SomaScan Assay to screen >1,300 host proteins in Zika virus-infected cells, both globally and specifically in the central nervous system. Significant findings include the identification of nearly 300 astrocyte proteins that were significantly dysregulated by Zika infections, pointing to pathways that may be involved in neurological complications resulting from Zika, such as microcephaly and Guillain-Barré syndrome. Dr. Coombs’ work in influenza has included extensive proteomic scanning of H5N1, H1N1, and H7N9 in various cell types including induced-pluripotent stem cells. Significant findings include the observation that low-pathogenicity strains induce less profound changes to the global proteome. For instance, avian strains stimulate significant downregulation of key proteins, including those involved in antimicrobial response. Seasonal strains do not elicit the same response. Further, Dr. Coombs’ team found that viral infection in stem cells can reduce pluripotency, activate autophagy, and lead to abnormal differentiation.

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White paperCOVID-19 and the SomaScan® Platform

The battle against Coronavirus disease 2019 (COVID-19) only begins with a test to identify who is infected and who is not. To accelerate an effective response, we have to move beyond the initial diagnosis to prognosis: Who is most susceptible to developing serious, life-threatening symptoms? Currently, there is no way to tell whether an infected individual (or an individual who may become infected) will be asymptomatic or require hospitalization. This wide variation in disease severity is, at least in part, a reflection of the myriad changes that occur within a person’s body as it fights the virus, which in turn reflect the unique biological makeup of that individual.

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PosterUtility of proteomic trajectories of cardiovascular risk and cardiorespiratory fitness to monitor adverse health states throughout post-COVID-19 illness

Cardiovascular involvement is a prominent observation in patients during the acute phase of COVID-19 infection, as well as in convalescence. However, the etiology, trajectory, and underlying biology of cardiac dysfunction across the spectrum of COVID-19 illness is not fully understood. To address this, the CISCO-19 study (NCT04403607) was formed to investigate the multisystem effects of COVID-19 from hospitalized patients

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