pharma partnership Archives - Sanford Burnham Prebys

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A potential new weapon against a deadly, drug-resistant bacterial pathogen

AuthorScott LaFee
Date

January 8, 2024

Acinetobacter baumannii (CRAB)

Carbapenems are a class of highly effective antibiotics that are often used to treat severe bacterial infections. They are usually reserved for known or suspected bacterial infections resistant to other drugs.

Carbapenem-resistant Acinetobacter baumannii (CRAB) is, as the name suggests, impervious to carbapenems; and it has become a major global pathogen, particularly in hospital settings and conflict zones. No new antibiotic chemical class with activity against A. baumannii has successfully emerged in more than 50 years.

In a paper published January 3, 2024, in Nature, a multi-institutional team including Andrei Osterman, PhD, at Sanford Burnham Prebys, with colleagues at Roche—the Swiss-based pharmaceutical/healthcare company—and others, describe a novel class of small-molecule tethered macrocyclic peptide (MCP) antibiotics with potent antibacterial activity against CRAB. Osterman’s lab provided critical data and discoveries related to the drug target and mapping of drug-resistant mutations.

Developing a new class of antibiotics effective against CRAB is critical. The bacterium is resistant to nearly all antibiotics and is difficult to remove from the environment. It poses a particular health threat to hospitalized patients and nursing home residents, with an estimated mortality rate in invasive cases of 40–60%.

The World Health Organization and the Centers for Disease Control (CDC) have both categorized multidrug-resistant A. baumannii as a top-priority pathogen and public health threat.

In the new study, Osterman and colleagues applied an experimental evolution approach to help identify the drug target (the LPS transporter complex) of a new class of antibiotics—a macrocyclic peptide called Zosurabalpin—and elucidate the dynamics and mechanisms of acquired drug resistance in four distinct strains of A. baumannii.

They used an integrative workflow that employs continuous bacterial culturing in an “evolution machine” (morbidostat) followed by time-resolved, whole-genome sequencing and bioinformatics analysis to map resistance-inducing mutations.

In addition to a mechanistic understanding (crucial from a regulatory perspective), the new information also helped reveal the drug-binding site. A related paper in the same issue experimentally verified the findings.

“This comprehensive mapping of the drug-resistance landscape yields valuable insights for a variety of practical applications,” says Osterman, “from therapy optimization via genomics-based assessment of drug resistance/susceptibility of bacterial pathogens to a rational development of novel drugs with minimized resistibility potential.”

A commentary in Nature said the research was “cause for cautious celebration” and urged further development.

Institute News

New COVID-19 drug passes phase 2 clinical trial

AuthorMiles Martin
Date

January 20, 2022

Illustration of red coronavirus particles against a dark blue background

The new treatment, developed by Avalo Therapeutics with Sanford Burnham Prebys researchers, can mitigate lung damage and improve survival in COVID patients.

In a phase 2 clinical trial conducted by Avalo and supported by Sanford Burnham Prebys, a significantly higher proportion of hospitalized patients with COVID-19 remained alive and free of respiratory failure for 28 days after receiving treatment with the new antibody, called CERC-002. Unlike other experimental COVID therapies, CERC-002 does not target the virus itself, instead targeting the immune response associated with the virus to stop the disease from progressing before it becomes fatal.

“At the beginning of the pandemic we thought vaccines were going to be all we really needed. But with variants like omicron, we’re going to have more people that progress to serious illness even with the vaccine,” says study coauthor Carl F. Ware, PhD, director of the Infectious and Inflammatory Diseases Center at Sanford Burnham Prebys. “We need treatments to stop the progression to severe disease and death.”

The findings were published December 6 in the Journal of Clinical Investigation.

COVID-19: a continuing crisis
In the United States, over 840,000 people have died from COVID-19. A large proportion of these deaths have been among the elderly or those who are immunocompromised due to a preexisting condition. And while three quarters of the population has received at least one dose of the COVID-19 vaccine, many remain unvaccinated.

“A lot of us feel safer now that we’ve gotten our shots,” Ware says, “but the threat of the pandemic has not gone away, even for vaccinated people.”

Most people with COVID-19 experience few to no symptoms. However, elderly individuals, people with a concurrent health condition or those who are immunocompromised are susceptible to a condition called cytokine storm, in which their own immune molecules called cytokines flood the body in higher concentrations than usual.

Rather than helping fight the virus, these extra immune molecules wreak havoc, causing patients to develop the deadly respiratory failure characteristic of severe COVID disease.

“The COVID virus gets the immune system amped up by producing these molecules, which is normally how the immune system fights diseases,” says Ware. “But when there are too many cytokines and they’re not doing their job, it can lead to severe damage.” 

Neutralizing the cytokine storm
The new treatment, CERC-002, is a cytokine neutralizer—an immune molecule that recognizes and deactivates a cytokine known as LIGHT, which is elevated in patients with COVID-19. Cytokine neutralization drugs are currently being tested in the clinic, but they are mainly effective in severely ill patients who are already on a ventilator or other organ support.

“There is a critical need for drugs to stop milder cases from progressing to severe,” says Ware. “This treatment targets the cytokine immune response early enough to stop it in its tracks, which no other treatment does right now.”

83 COVID patients were enrolled in the study, half receiving the treatment, and half receiving a placebo. All patients were hospitalized with mild-to-moderate respiratory distress and were also receiving standard-of-care therapy during the trial.

They found that 83.9% of patients who received a dose of CERC-002 on top of standard of care remained alive and free from respiratory distress for 28 days. For patients receiving placebo, the number was only 64.5%.

Looking ahead
As a phase 2 clinical trial, the purpose of this study was to test whether the compound has therapeutic potential in a small number of patients. Now that the drug has proven successful at a small scale, it can be tested on a larger number of patients to ensure its benefits are consistent across the population.

Additionally, because CEC-002 targets the immune response in COVID cases rather than the virus itself, the compound may have applications that extend beyond COVID.

“Cytokine storm is not unique to COVID. It occurs in other infections—even in autoimmune diseases with no active infection, so this treatment may have some utility in these other diseases as well.” 
While there is more work to be done before CERC-002 becomes widely available, it does offer a glimmer of hope during a pandemic that seems never-ending.

“We have made a lot of progress in controlling the pandemic with vaccines and other new therapies, but it’s not over yet,” says Ware. “Treatments like this may bring physicians an option to protect infected people from severe illness.

Institute News

Sanford Burnham Prebys and Roche fight back against antibiotic resistance

AuthorMiles Martin
Date

December 8, 2021

Brown and orange illustration of different shapes of bacteria

Researchers from Sanford Burnham Prebys have teamed up with prominent drug developer Roche Pharma to learn how bacteria develop antibiotic resistance.

Their new results, published in the journal mBio, are one piece of a long-standing collaboration between the two organizations, the goal of which is to mitigate the growing threat of antibiotic resistance by developing more “irresistible” drugs and by helping improve antibiotic prescribing practices.

“The emergence of antibiotic resistance is inevitable for any single drug, new or old. It’s only a question of time,” says senior author Andrei Osterman, PhD, a professor at Sanford Burnham Prebys. “But the precise time is different for every drug and every microbe, so studying when and how resistance to antibiotics evolves gives us powerful information for improving antibiotic treatment.”

Antibiotic resistance develops rapidly

When a patient is treated with antibiotics, most individual bacteria die, but a few cells will survive, usually as a lucky consequence of a random genetic mutation. These survivors go on to multiply into a whole new population of antibiotic-resistant bacteria.

“The development of antibiotic resistance is a strictly Darwinian process, very similar to evolution in larger organisms,” says Osterman. “The difference is that in bacteria, it happens much more rapidly, which makes antibiotic resistance one of the most pressing challenges facing medicine today.” 

Although the speed at which evolution occurs in bacteria makes antibiotic resistance a threat, the researchers were also able to take advantage of this speed to study its development. The team cultured three species of bacteria in a morbidostat, a device that allows bacteria to grow continuously over multiple generations while being dosed with antibiotics. Although theirs was not the first morbidostat device, the team designed a new, more effective version of the system for their experiments.

“It’s like an evolution machine, letting us watch the development of antibiotic resistance in real time and in an environment that more accurately models what happens to bacteria in a clinical setting than other approaches,” says Osterman. “This gives us a clearer and more comprehensive view of resistance than we’ve ever had before.”

Different bacteria develop resistance differently

By observing the bacteria’s evolution in the morbidostat and sequencing their genomes as they evolved, the researchers found that all three species had a similar pattern of resistance development. However, they also found subtle differences in the ways certain genes were expressed, particularly those that help bacteria remove toxins, a critical process in developing resistance.

“It’s like three remakes of the same movie by three different directors, and their comparison gives us a wealth of information to guide the development and use of antibiotics,” says Osterman. 

Understanding resistance is critical to reducing its harm

Working with Roche, the team has completed similar studies on several other classes of antibiotic drugs, which is helping Roche identify promising candidates for antibiotics that are less prone to resistance.

And because antibiotic resistance is often not assessed in drug candidates until years into the process, using resistance to screen for drug candidates this way could save the biomedical industry millions of dollars and help patients benefit from effective drugs sooner.

“A completely ‘irresistible’ drug is a holy grail, something we can never truly achieve,” says Osterman. “But some drugs are less resistible than others, and our methods allow us to figure out which is which in a systematic way.”

In addition to helping develop new drugs, the researchers claim that their findings are easily translatable to the clinic, where doctors can use detailed knowledge of resistance to select optimal drug combinations with less likelihood of failure due to resistance.

“We are moving away from trial-and-error approaches in medicine and moving toward being able to predict exactly what drugs will work best for each patient,” says Osterman. “It is going to take time, effort and money to make this happen, but it will all be worth it if we’re able to alleviate the threat of antibiotic resistance and help save lives, which I’m confident can be done.”

Institute News

Sanford Burnham Prebys drug enters Phase 1 study for the treatment of tobacco use disorder

AuthorSusan Gammon
Date

August 26, 2021

Senior doctor breaking a cigarette

A drug discovered in the lab of Nicholas Cosford, PhD, professor and deputy director of the NCI-designated Cancer Center at Sanford Burnham Prebys, has entered a Phase 1 clinical study.

The compound, SBP-9330, targets a neuronal signaling pathway underlying addictive behaviors and would be a first-in-class oral therapeutic to help people quit smoking. 

The study is being funded by the National Institute on Drug Abuse (NIDA) at the National Institutes of Health (NIH) through a grant awarded to Sanford Burnham Prebys, the Department of Psychiatry, University of California San Diego, School of Medicine, and Camino Pharma, LLC, who will oversee activities related to the Phase 1 study.  

“Smoking continues to be the leading cause of preventable death in the US. Nearly 70% of adult smokers try to quit smoking, but only succeed less than 30% of the time, and often relapse after quitting,” says Cosford, who is also co-founder of Camino Pharma. “It has been 15 years since the U.S. Food and Drug Administration (FDA) last approved a therapeutic for this indication. We hope that SBP-9330 ultimately becomes a viable therapeutic option for smokers to quit for good.”

As a novel selective positive allosteric modulator of the metabotropic glutamate receptor 2 (mGlu2), SBP-9330 is designed to reduce levels of glutamate, a neurotransmitter linked to addiction and relapse behavior. Preclinical studies of SBP-9330, supported by a previous NIDA grant awarded to the same three institutions, demonstrated that the drug candidate reduces nicotine self-administration in animal models and is safe and well tolerated in preclinical safety and toxicology studies.

“We are excited to initiate the first-in-human study of SBP-9330 and are grateful for the investment the NIDA has made in the treatment of tobacco use disorder,” says Gonul Velicelebi, PhD, CEO and co-founder of Camino Pharma. “In the future, we also hope to broaden the indication of SBP-9330 to other types of addiction, such as cocaine, opioid, or methamphetamine use disorders. This is supported by preclinical data in other models of substance abuse as well as the mechanism of action of SBP-9330.”

The randomized, placebo-controlled, double-blind, single-ascending and multiple-ascending dose study is being conducted at a single site in the United States under an Investigational New Drug (IND) application recently allowed by the FDA and will enroll up to 80 healthy volunteers through multiple cohorts. The goal of the study is to determine the safety, tolerability and pharmacokinetic profile of SBP-9330 in humans and to determine a safe dose range for further clinical development SBP-9330 for the treatment of people with tobacco use disorder. 

“We are excited about collaborating in the development of SBP-9330 to treat tobacco use disorder. Each year in the United States, roughly half a million people die from tobacco-related diseases. It is critical to have more therapeutic options if we want to reduce the number of deaths and illnesses related to smoking,” says Robert Anthenelli, MD, UC San Diego professor of psychiatry and one of the co-principal investigators on the NIDA project.

Dr. Cosford has an equity interest in Camino Pharma, LLC. Dr. Cosford’s relationship with Camino Pharma, LLC has been reviewed and approved by Sanford Burnham Prebys in accordance with its conflict-of-interest policies.

Institute News

Graduate student awarded American Heart Association Fellowship

AuthorSusan Gammon
Date

April 14, 2021

Katja Birker, PhD

The heart is the core of life, and for PhD graduate student Katja Birker, it’s the foundation for the beginning of a career.

Birker recently received a prestigious predoctoral fellowship from the American Heart Association (AHA) to continue her research on hypoplastic left heart syndrome (HLHS), a congenital heart disease that affects between two and four of every 10,000 babies born. As of today, the only cure for HLHS is three open-heart surgeries that begin two weeks after birth.

“I’m very grateful to the AHA for supporting my research,” says Birker. “I’ve embarked on a career to study the genes that contribute to HLHS, and this award will help me continue my work that may eventually lead to targeted prevention of HLHS as well as other congenital heart diseases.”

Birker is collaborating with the Mayo Clinic to identify and test whether genes found in HLHS patients—or “candidate” genes—have similar consequences in the hearts of fruit flies—a model organism for cardiovascular research. The research aims to identify novel gene functions and pathways that are likely to contribute to HLHS.

“Many believe that HLHS is a genetic disease, but the genes that are involved are not well known,” says Birker. “The fruit fly is a very good genetic system to model disease because it has many similar genes to humans and a short life span. I’m able to film videos of fly hearts to understand the impact of the candidate genes on heart function.

“My goal is to find genes that can be used in the future for the diagnosis and treatment of HLHS in babies. The research approach could also be used to screen for genes that might be involved in many other types of heart disease,” adds Birker.

The AHA supports early-career scientists with passion, commitment and focus by providing fellowships that fund their pursuit of cardiovascular research. Birker, a graduate student in the lab of Rolf Bodmer, PhD, professor and director of the Development, Aging and Regeneration Program, received her first AHA fellowship in 2018.

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Sanford Burnham Prebys scientist joins historic effort to help children with rare disease

AuthorMonica May
Date

October 3, 2019

Hudson Freeze, PhD

Hudson Freeze, PhD, professor of Human Genetics at Sanford Burnham Prebys, has joined a historic effort that establishes—for the first time—a nationwide network of 10 regional academic centers, Sanford Burnham Prebys researchers and patient advocacy groups to address decades of unresolved questions surrounding congenital disorders of glycosylation, or CDG, a rare disease that affects children. The consortium is funded by a $5 million, five-year grant from the National Institutes of Health (NIH). 

“We are extremely pleased that the NIH is investing in an initiative that will improve the lives of people affected by CDG,” says Freeze, who leads efforts to develop and validate disease biomarkers that will aid in diagnoses, and measuring treatment benefits during clinical trials. “Although globally the number of people living with CDG is relatively small, the impact on the lives of these individuals and their families can be profound. We look forward to working with the patients, families, physicians, scientists and other stakeholders focused on this important study.”

CDG is caused by genetic mutations that disrupt how the body’s sugar chains attach to proteins. First described in the 1990s, today scientists have discovered more than 140 types of mutations that lead to CDG. Symptoms are wide-ranging, but can include developmental delays, movement problems and impaired organ function. Some children may benefit from a sugar-based therapy; however, developing treatments for those who need alternative treatment options has been hindered by a lack of natural history data—tracking the course of the condition over time—comprehensive patient registry, and reliable methods to establish the CDG type.

Working together, the consortium will overcome these hurdles by: 

  • Defining the natural history of CDG through a patient study, validating patient-reported outcomes and sharing CDG knowledge 
  • Developing and validating new biochemical diagnostic techniques and therapeutic biomarkers to use in clinical trials 
  • Evaluating whether dietary treatments restore glycosylation to improve clinical symptoms and quality of life

Freeze will lead the efforts to develop and validate biomarkers for CDG, working alongside the Children’s Hospital of Philadelphia and the Mayo Clinic. The principal investigator of the CDG Consortium Project is Eva Morava, MD, PhD, professor of Medical Genetics at the Mayo Clinic. The patient advocacy groups involved are CDG CARE and NGLY1.org. 

Sanford Burnham Prebys and CDG Care will host the 2020 Rare Disease Day Symposium and CDG Family Conference from February 28 to March 1 in San Diego, which welcomes researchers, clinicians, children with CDG and their families, and additional CDG community members. Register to attend. 
 

Institute News

Immune therapy enters Phase 1 clinical trial

AuthorMonica May
Date

November 15, 2018

Lilly and SBP logos

Sanford Burnham Prebys Medical Discovery Institute (SBP) today announced that the first healthy subject has been dosed in a Phase 1 clinical trial evaluating LY3361237, a biologic that inhibits inflammation by activating an immune checkpoint receptor. LY3361237 arose from a research collaboration between Eli Lilly and Company (Lilly) and SBP formed in 2015 that seeks to discover and develop new immunological therapies. 

Diseases such as lupus, psoriasis and rheumatoid arthritis result from dysfunction of the immune system. Many of these conditions are characterized in part by immune checkpoint failure, resulting in the immune system attacking normal tissue. Previous studies have shown that activating checkpoint receptors can suppress inflammation and restore immune balance—indicating its therapeutic potential. More than 80 diseases are caused by the immune system attacking the body’s own organs, tissues and cells, according to the National Institutes of Health (NIH).  

“Today’s milestone is an important step forward for patients who suffer from autoimmune disease,” says Carl Ware, PhD, director of the Infectious and Inflammatory Diseases Center at SBP. “This advance also illustrates how the fundamental understanding of a biological process—in this case, the role of checkpoint receptors in immune function—can translate to the development of new medicines.”

“Immunological disorders—many of which disproportionately impact women—affect millions of people around the world and remain an area of great medical unmet need,” adds Ajay Nirula, MD, PhD, vice president of Immunology at Lilly. “Our collaboration with SBP is a powerful example of how uniting complementary areas of expertise—deep foundational scientific knowledge from SBP combined with expertise in protein engineering, immunobiology and clinical development from Lilly— can lead to a promising new candidate to treat autoimmune disorders.”

The study will evaluate the safety, tolerability and pharmacokinetics of LY3361237 in healthy subjects. Further information about the trial can be found on ClinicalTrials.gov using the Identifier NCT03695198.

Interested in keeping up with SBP’s latest discoveries, upcoming events and more? Subscribe to our monthly newsletter, Discoveries.

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What SBP Scientists are Researching to Battle Skin Cancer

AuthorHelen I. Hwang
Date

May 16, 2017

Nevus sample from Peter D. Adams' lab

Skin cancer is one of the most common of all cancers, and melanoma accounts for about 1 percent of skin cancers. However, melanoma causes a large majority of deaths from that particular type of cancer. Alarmingly, rates of skin cancer have been on the rise in the last 30 years. Here in Southern California, our everlasting summer comes with a price. Exposure to sun increases our risk to melanoma.

Melanoma occurs when the pigment-producing cells that give color to the skin become cancerous. Symptoms might include a new, unusual growth or a change in an existing mole. Melanomas can occur anywhere on the body.

At Sanford Burnham Prebys Medical Discovery Institute (SBP), we have several researchers working on the causes of melanoma and discovering new ways to treat this deadly disease.

Here is a roundup of SBP’s latest research:

Key findings show how melanoma develops in order to identify potential therapeutic targets

Ze’ev Ronai, PhD
Professor and SBP Chief Scientific Advisor

Ronai’s laboratory has been studying how rewired signaling networks can underlie melanoma development, including resistance to therapy and metastatic propensity. One player in that rewiring is a protein called ATF-2, which can switch from its usual tumor-preventive function to become a tumor promoter when combined with a mutation in the human gene called BRAF.

Ronai’s work on a protein, ubiquitin ligases, led to the identification of RNF125 as an important regulator of melanoma resistance to a common chemotherapy drug. RNF125 impacts melanoma resistance by its regulation of JAK2, an important protein kinase which could play an important role in melanoma resistance to therapy.

Work on the ubiquitin ligase Siah2 identified its important role in melanoma growth and metastasis, and its contribution to melanomagenesis. Melanoma is believed to be a multi-step process (melanomagenesis) of genetic mutations that increase cell proliferation, differentiation, and death.

Work in the lab also concern novel metabolic pathways that are exploited by melanoma for their survival, with the goal of identifying combination drug therapies to combat the spread of melanoma. Earlier work on the enzyme PDK1 showed how it can be a potential therapeutic target for melanoma treatment.

Immunotherapy discovery has led to partnership with Eli Lilly

Linda Bradley, PhD
Professor, Immunity and Pathogenesis Program, Infectious and Inflammatory Diseases Center

Bradley’s group is focused on understanding how anti-tumor T cells can be optimized to kill melanoma tumors. They discovered an important molecule (PSGL-1) that puts the “break” on killer T cells, allowing melanoma tumors to survive and grow. Using animal models, they removed this “break” and T cells were able to destroy melanoma tumors. They have extended their studies and found that in melanoma tumors from patients, T cells also have this PSGL-1 “break”. Bradley’s lab has partnered with Eli Lilly to discover drugs that can modulate PSGL-1 activity in human disease that may offer new therapies for patients.

Knocking out a specific protein can slow melanoma growth 

William Stallcup, PhD
Professor, Tumor Microenvironment and Cancer Immunology Program

The danger of melanomas is their metastasis to organs, such as the brain, in which surgical removal is not effective. By injecting melanoma cells into the brains of mice, we have shown that the NG2 protein found in host tissues makes the brain a much “friendlier” environment for melanoma growth.

Specifically, NG2 is found on blood vessel cells called pericytes and on immune cells called macrophages. The presence of NG2 on both cell types improves the formation of blood vessels in brain melanomas, contributing to delivery of nutrients and thus to accelerated tumor growth. Genetically knocking out NG2 in either pericytes or macrophages greatly impairs blood vessel development and slows melanoma growth.

Mysterious molecule’s function in skin cancer identified

Ranjan Perera, PhD
Associate Professor, Integrative Metabolism Program

Ranjan’s research uncovered the workings of a mysterious molecule called SPRIGHTLY that has been previously implicated in colorectal cancer, breast cancer and melanoma. These findings bolster the case for exploring SPRIGHTLY as a potential therapeutic target or a biological marker that identifies cancer or predicts disease prognosis.

 Drug discovery to help babies has led to a clinical trial at a children’s hospital

Peter D. Adams, PhD
Professor, Tumor Initiation and Maintenance Program

Approximately 1 in 4 cases of melanoma begins with a mole, or nevus. Genetic mutations can cause cells to grow uncontrollably. By investigating how this occurs, we can understand why melanoma develops from some moles, but not others.

Babies born with a giant nevus that covers a large part of the body have especially high risk of melanoma, and the nevus cells can spread into their spine and brain. Adams’ research identified a drug that deters the cells from growing. The drug identified will be used in a clinical trial at Great Ormond Street Children’s Hospital in London, England that may help babies with this debilitating disease.

Discovery of a receptor mutation correlates with longer patient survival

Elena Pasquale, PhD
Professor, Tumor Initiation and Maintenance Program

Pasquale’s work has included whether mutations in the Eph receptor, tyrosine kinases, play a role in melanoma malignancy. Eph receptor mutations occur in approximately half of metastatic melanomas. We found that some melanoma mutations can drastically affect the signaling ability of Eph receptors, but could not detect any obvious effects of the mutations on melanoma cell malignancy.

Bioinformatic analysis of metastatic melanoma samples showed that Eph receptor mutations correlate with longer overall patient survival. In contrast, high expression of some Eph receptors correlates with decreased overall patient survival, suggesting that Eph receptor signaling can promote malignancy.

Institute News

SBP and GSK create new Center for Translational Neuroscience

Authorkcusato
Date

April 20, 2016

Header image

SBP and GlaxoSmithKline (GSK), a global pharmaceutical company, have announced the creation of the SBP-GSK Center for Translational Neuroscience. The new Center, located on the SBP campus in La Jolla, will bring together experts from SBP and GSK to investigate factors that influence brain function and potentially reverse or slow down neurodegeneration, with the aim of identifying and validating new therapeutic targets. Under the three year agreement, GSK will provide funding to create and support a research laboratory. Staffed by SBP scientists, postdoctoral candidates and technicians working alongside neuroscientists from GSK, the Center will be designed to bolster research dedicated to translational neuroscience. Continue reading “SBP and GSK create new Center for Translational Neuroscience”